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The insects flying in circles around your porch light aren’t captivated by the light. Instead, they may have lost track of which way is up, high-speed infrared camera data suggest.

Moths and other insects naturally turn their backs toward light. But when insects turn their backs on artificial light sources, their sense of direction seems to go topsy-turvy, researchers report January 30 in Nature Communications. The insects may lose track of where the ground is, leaving them flying in circles or diving toward the ground.

The findings are the first “satisfying answer to a long-standing phenomenon” of how moths and other insects flock to streetlamps and flames, says evolutionary biologist Florian Altermatt of the University of Zurich who was not involved with the study. “It was also interesting to see that it was an actually rather simple explanation, defying the previous, more complex ones.”  

Those hypotheses range from flying insects being blinded by light and becoming trapped, to insects interpreting light sources as a place to fly for a quick escape. Another idea suggests that the light of the moon serves as a compass, and nocturnal insects mistakenly use human-made lights to navigate the world. These lights can be deadly for insects (SN: 8/31/21).  

Just as pilots flying planes have myriad tools to work out which way is up when they’re gaining speed, flying insects may turn their backs on the sky’s light to keep their feet pointing toward the ground. “It’s a really good idea until somebody invents the LED,” says entomologist Samuel Fabian of Imperial College London, “at which point it’s a very bad idea.”

Fabian and colleagues used high-speed infrared cameras to track how artificial lights affected the flight of a variety of insects. At a field station in Costa Rica, the team watched as wild insects from 10 orders, including moths and flies, circled endlessly around hanging or standing lights. Others flew upward in a steep climb, losing speed until they couldn’t fly any higher. When the light source pointed up, some individuals flipped over and headed for the ground.

During flight, the insects consistently kept lights at their back, even if they ended up crashing. The same was true of moths and dragonflies observed in the lab.

The results “didn’t fit with any of the theories that had been proposed before,” says coauthor Yash Sondhi, an evolutionary biologist at the Florida Museum of Natural History’s McGuire Center for Lepidoptera and Biodiversity. The insects weren’t flying toward the light as they would if it symbolized an escape route. Nor were they flying in smooth spirals, which would suggest the light acted as a compass.

Instead, “it’s a bit like somebody’s grabbed [a pilot’s] joystick and is pulling it in the wrong direction,” Fabian says.

Normal flight was restored when the positioning of a skylike artificial light was opposite the ground. Crash landings were common when the team illuminated a white sheet on the floor. But when a white sheet stretched into a canopy above the floor was bathed in diffuse light, like the sky would be, insects flew through without getting trapped by the light.

In the lab, there were some exceptions. Fruit flies (Drosophila species) — which can fly in the dark — weren’t strongly affected by the light. Oleander hawk moths (Daphnis nerii) could also fly over ultraviolet or LED lights without being thrown off course. In the wild, though, the moths still crash. It’s unclear why, Sondhi says, but one possibility is that the insects might sometimes suppress their response to light. Or it could be something that individuals learn over time.

While it’s clear that artificial light can put insects on a crash course, more research is needed to confirm if it’s happening because insects use the sky’s light for navigation, irrespective of the presence of artificial light, says animal and visual ecologist Brett Seymoure of the University of Texas at El Paso, who wasn’t involved with the research.

Seymoure, Sondhi and other scientists are also teaming up to explore other unanswered questions about light pollution’s effects on insects, such as how susceptible insects may be at different latitudes.

Another question Seymoure and colleagues are exploring is whether putting fixtures on lights, so insects can’t see much light at all, could make streetlights less attractive for flying by insects. “Now that we have the mechanism of how moths are flying to these lights, we can now better design light fixtures that will make it so that they’re not actually doing this behavior,” Seymoure says.

Krystal Tsosie grew up playing in the wide expanse of the Navajo Nation, scrambling up sandstone rocks and hiking in canyons in Northern Arizona. But after her father started working as a power plant operator at the Phoenix Indian Medical Center, the family moved to the city. “That upbringing in a lower socioeconomic household in West Phoenix really made me think about what it meant to be a good advocate for my people and my community,” says Tsosie, who like other Navajo people refers to herself as Diné. Today, she’s a geneticist-bioethicist at Arizona State University in Tempe. The challenges of urban life for Tsosie’s family and others, plus the distance from the Navajo Nation, helped spark the deep sense of community responsibility that has become the foundation of her work.

Tsosie was interested in science from an early age, volunteering at the Phoenix Indian Medical Center in high school with the hopes of eventually becoming a doctor. She remembers seeing posters at the Indian Health Service clinic in Phoenix warning against the dangers of rodents and dust. The posters were put up in response to cases of hantavirus pulmonary syndrome, or HPS, in the Four Corners area. Though the disease had not been identified by Western science until that 1993 outbreak, it had long been known within the Navajo tradition. Learning how Navajo oral traditions helped researchers understand HPS made Tsosie want to work in a laboratory studying diseases, instead of becoming a practicing physician.

Tsosie settled on cancer biology and research after college, in part because of the health and environmental impacts of decades of uranium mining on the Navajo Nation. But after leaving Arizona for the first time after college, Tsosie was confronted with the profit-driven realities and what she calls the “entrenched, systemic racism” of the biomedical space. She saw a lack of Indigenous representation and disparities that prevented Indigenous communities from accessing the best health care. Tsosie began asking herself whether her projects would be affordable and accessible to her community back home. “I didn’t like the answer,” she says.

The need for Indigenous geneticists

So Tsosie returned to Arizona State to work on a master’s degree in bioethics with the intention of going to law school. But the more she learned about how much genetic research relies on big data and how those data are shared and used, the more Tsosie realized there was a huge need for Indigenous geneticists.

Around the world, scientific use of Indigenous genetic data has led to repeated violations of rights and sovereignty. For example, beginning in 1990, Havasupai Tribal members gave DNA samples to researchers from ASU, hoping to understand more about diabetes in their community. Researchers eventually used the Havasupai DNA in a range of studies, including for research on schizophrenia and alcoholism, which the Havasupai say they had not been properly informed about or consented to. In 2010, the Arizona Board of Regents settled with Tribal members for $700,000 and the return of the DNA samples, among other reparations.

The Havasupai case is perhaps the most high-profile example in a long history of Western science exploiting Indigenous DNA. “We have an unfortunate colonial, extractive way of coming into communities and taking samples, taking DNA, taking data, and just not engaging in equitable research partnerships,” Tsosie says.

This history prompted the Navajo Nation in 2002 to place a “moratorium on genetic research studies conducted within the jurisdiction of the Navajo Nation.” It has also, along with the growth of genomics, convinced Tsosie that Indigenous geneticists must play a big role in protecting Indigenous data and empowering Indigenous peoples to manage, study and benefit from their own data. “It’s the right of indigenous peoples to exercise authority, agency, autonomy, and self-direct and self-govern decisions about our own data,” she says.

Tsosie was determined to become one of those Indigenous geneticists, and in 2016, she began dissertation research at Vanderbilt University in Nashville. Around that time, she met Keolu Fox and Joseph Yracheta, two other Indigenous scientists interested in genetics. Fox, who is Kānaka Maoli and a geneticist at the University of California, San Diego, believes Tsosie and others prioritizing Indigenous health and rights represent a paradigm shift in the field of genetics. “Minority health is not an afterthought to someone like Krystal, it is the primary goal,” Fox says. “We have not been allowed to operate large laboratories in major influential academic institutions until now. And that’s why it’s different.”

In 2018, Tsosie, Yracheta and colleagues, with key support from Fox, founded the Native BioData Consortium, an Indigenous-led nonprofit research institute that brings Indigenous scholars, experts and scientists together. The consortium’s biorepository, which Tsosie believes is the first repository of Indigenous genomic data in North America, is located on the sovereign land of the Cheyenne River Sioux Tribe in South Dakota. The consortium supports various research, data and digital capacity building projects for Indigenous peoples and communities. These projects include researching soil health and the microbiome and creating a Tribal public health surveillance program for COVID that has Clinical Laboratory Improvement Amendments certification, as well as hosting workshops for Indigenous researchers.

The work may be even more essential given current genomics trends: With Indigenous nations in the United States restricting access to their DNA, researchers and corporations seek DNA from Indigenous peoples in Latin America.

“We are now in the second era of discovery or the second era of colonization,” says Yracheta, who is P’urhépecha from Mexico, director of the consortium and a doctor of public health candidate in environmental health at Johns Hopkins University. “Lots of Indigenous spaces are small and shrinking and we’re trying to prevent that happening by asserting Indigenous data sovereignty not only over humans and biomedical data, but all data.”

Tsosie, Yracheta says, consistently works to bring Indigenous values and accountability to the consortium’s work and has an invaluable combination of skills. “She has a lot of really hard-core scientific background and now she’s mixing it with bioethics, law and policy and machine learning and artificial intelligence,” he says. “We make a really good team.”

Training the next generation

Today, Tsosie leads the Tsosie Lab for Indigenous Genomic Data Equity and Justice at ASU. One lab project involves working with Tribal partners in the Phoenix area to create a multiethnic cohort for genomic and nongenomic data. The data, which will include social, structural, cultural and traditional factors, could provide a more complex picture of health disparities and what causes them, as well as a more nuanced understanding of Indigenous identity and health.

In addition to her own research, Tsosie spends time teaching, mentoring, traveling to speak about the importance of data sovereignty, and serving as a consultant for tribes who want to develop their own data policies. “We’re not just talking about doing research with communities,” she says. “We’re also helping to cocreate legal policies and resolutions and laws to help Tribal nations and Indigenous peoples protect their data and rights to their data.”

At ASU, Tsosie says, she is in the position to push back against some of the prevailing trends in Indigenous genomics, including the tendency to lump Indigenous people together, regardless of environmental, cultural and political factors. “This is an opportunity for my lab to really explore the fact that being Indigenous is not always a biological category. It’s one that’s mediated by culture, and also sociopolitical factors that have sometimes been imposed on us,” Tsosie says.

And while Tsosie’s goals are ambitious, she is equally committed to uplifting the next generation of Indigenous scientists. “Krystal puts in so much time and energy into ensuring that the next generation of students are getting ecosystems where they feel safe and protected to learn about new disciplines,” Fox says. “It’s just so special.”

To Tsosie, empowering Indigenous communities to make decisions about their data and supporting Indigenous students are part of the same mission. “It just makes me happy to think about several academic generations in the future, how many of us will be occupying this colonial space that we call academia,” she says. “Then we can really start shifting this power imbalance towards something that is truly enriching and powerful for our peoples and our communities.”

Bruce the kea is missing his upper beak, giving the olive green parrot a look of perpetual surprise. But scientists are the astonished ones.

The typical kea (Nestor notabilis) sports a long, sharp beak, perfect for digging insects out of rotten logs or ripping roots from the ground in New Zealand’s alpine forests. Bruce has been missing the upper part of his beak since at least 2012, when he was rescued as a fledgling and sent to live at the Willowbank Wildlife Reserve in Christchurch.

The defect prevents Bruce from foraging on his own. Keeping his feathers clean should also be an impossible task. In 2021, when comparative psychologist Amalia Bastos arrived at the reserve with colleagues to study keas, the zookeepers reported something odd: Bruce had seemingly figured out how to use small stones to preen.

“We were like, ‘Well that’s weird,’ ” says Bastos, of Johns Hopkins University.

Over nine days, the team kept a close eye on Bruce, quickly taking videos if he started cleaning his feathers. Bruce, it turned out, had indeed invented his own work-around to preen, the researchers reported in 2021 in Scientific Reports.

First, Bruce selects the proper tool, rolling pebbles around in his mouth with his tongue and spitting out candidates until he finds one that he likes, usually something pointy. Next, he holds the pebble between his tongue and lower beak. Then, he picks through his feathers.

“It’s crazy because the behavior was not there from the wild,” Bastos says. When Bruce arrived at Willowbank, he was too young to have learned how to preen. And no other bird in the aviary uses pebbles in this way. “It seems like he just innovated this tool use for himself,” she says.

Tool use is just one of parrots’ many talents. The birds are famous for emulating, and perhaps sometimes even understanding, human speech. Some species can also solve complex puzzles, like how to invade a secured trash bin, or practice self-control. Such abilities, on par with some primates, have earned parrots a place alongside members of the crow family as the “feathered apes.”

For a concept as abstract as intelligence, it’s challenging to develop a concrete definition that applies across animals. But researchers often point to features once thought to make humans special — enhanced learning, memory, attention and motor control — as signs of advanced cognition. Many of these capabilities are definitely seen in parrots, as well as in the crow family, and other animals like chimpanzees, dolphins and elephants.

“The question is, why is this kind of intelligence evolving multiple times?” says Theresa Rössler, a cognitive biologist at the University of Veterinary Medicine Vienna.

Exploring the parallels between parrots and people could provide clues. “Parrots are our evolutionary mirror image,” behavioral ecologist Antone Martinho-Truswell wrote in his 2022 book, The Parrot in the Mirror. With powerful brains and a proclivity for words, these birds are “the very best example,” he writes, of “nature’s ‘other try’ at a humanlike intelligence.”

It’s taken decades for cognitive scientists to realize this, says Irene Pepperberg, a parrot researcher and comparative psychologist at Boston University. At first glance, parrot brains look quite simple. And given the obvious physical differences and the fact that birds and humans last shared a common ancestor more than 300 million years ago, parrots are not an obvious candidate to help researchers understand human intelligence.

“When I started this work in the ’70s, my first grant proposal came back literally asking me what I was smoking,” Pepperberg says. That’s when she started working with Alex, an African gray parrot who, by the time of his death in 2007, had become renowned for his extensive vocabulary and knowledge of shapes, colors and even math.

Further supporting Pepperberg’s pioneering work, a slew of studies over the last decade highlight parrot smarts — and what these brilliant birds may teach us about how humanlike intelligence can emerge.

A vast skill set

Parrots’ most well-known talent is their affinity for spoken words. Proficiency varies among species, but African grays (Psittacus erithacus) are particularly good at picking up words and speaking clearly, Pepperberg says.

These parrots can repeat up to 600 different words, researchers reported in 2022 in Scientific Reports. While some parrots simply mimic words, it is possible to train birds such as Alex, who had a vocabulary of more than 100 words, to communicate with people.

“It’s not like you can actually sit there and ask them, ‘Why did you do that? What were you thinking?’ ” Pepperberg says. “But because you can [train them to communicate], you can ask them the same types of questions that you ask young children.” Another one of her African grays, for example, can request time alone by saying “Wanna go back.”

Many of parrots’ other cognitive triumphs have come to light only more recently.

Like Bruce the kea, a variety of other parrots are also capable of incredible feats with a tool in claw or beak. Hyacinth macaws (Anodorhynchus hyacinthinus) crack open nuts by holding pieces of wood in their beak or foot to keep the food in just the right position. Palm cockatoos (Probosciger aterrimus) craft drumsticks and rock out to attract mates. Goffin’s cockatoos (Cacatua goffiniana) can recognize individual tools as being part of a set, the only animals other than chimpanzees and humans known to do so (SN: 3/11/23, p. 12).

Overall, 11 of the nearly 400 parrot species, or about 3 percent, have been documented in scientific studies using tools. Crowdsourcing from YouTube videos, Bastos and colleagues uncovered 17 more tool-using species, bringing the total to 28. After plotting the known tool users onto an evolutionary tree, the team estimates that 11 to 17 percent of parrot species may use tools.

Because the ability is more widespread across species than previously thought and found in all but one of the parrot families, it’s possible that tool use originated with the very first parrot, which lived more than 50 million years ago, Bastos argues. Why all the parrots in one major group, the family that includes common pet species like lovebirds and lorikeets, might have lost this proficiency is unclear.

“I’m hoping that future research can reveal why on Earth this one family of parrots doesn’t do it, whereas [every other family] seems to,” Bastos says.

Meanwhile, other researchers are investigating more subtle skills. Some parrots, for example, can practice restraint.

Griffin, one of Pepperberg’s current African grays, can pass a version of the marshmallow test. In the human version, children are offered a marshmallow as an immediate treat but are promised more if they can wait until later to devour it. Offered nuts instead of a marshmallow, Griffin can wait up to 15 minutes for better or more rewards, just like many preschoolers. Exactly what such self-discipline reveals about intelligence is debated, but self-control in humans may be a factor in decision making and planning for the future.

Among humans, how much trust people have in others and other factors such as socioeconomic status can influence responses to the marshmallow test. Different African grays also respond differently, Pepperberg and colleagues reported in August in the Journal of Comparative Psychology.

A parrot named Pepper started out waiting for a larger treat, Pepperberg says. “Then she realized, ‘Wait a minute, if I take the smaller treats [really quickly], I get to go back to playing with my human, and I prefer that to the [big] treat.’ ”

Unlike Griffin, who receives near-constant interaction with people, Pepper is often left to her own devices. Because Pepper spends more time alone, perhaps she considers it unacceptable or unpleasant to wait to take a treat when people in the room are ignoring her.

The beauty of a bird brain

A bird’s brain looks nothing like a primate’s. Most primate brains have curves and crinkles that twist into the elaborate patterns of the cerebral cortex. The nerve cells packed within these wrinkles help people think, remember and learn. A bird brain, on the other hand, “looks like a blob of protoplasm,” the jellylike substance that fills cells, Pepperberg says. Because of this simple-looking brain, it was long thought that to have a bird brain was to be stupid.

But Pepperberg knew that was wrong. When she gave scientific talks in the 1980s about parrot accomplishments, people would say, “But it can’t be happening, there’s no cerebral cortex,” she recalls. “I was like, you’re the neurobiologists. Go find it.”

By the early 2000s, scientists had discovered that, in fact, parts of the avian brain are akin to the mammalian neocortex, the largest part of the cerebral cortex. Subsequent work has found that, compared with mammals, avian brains have “a higher total number of neurons for the same amount of skull space,” says neurobiologist and geneticist Erich Jarvis of Rockefeller University in New York City.

Parrot brains are especially densely packed. Some species even have more neurons than some large-brained primates. This density may facilitate the formation of brain circuits not found in other animals, Jarvis says.

One of those circuits seems to be a major information highway comparable to one in human brains, says comparative neuro­biologist Cristián Gutiérrez-Ibáñez of the University of Alberta in Edmonton, Canada.

Human brains transfer information from the cerebral cortex to the cerebellum — a “little brain” at the back of the skull that in part coordinates movement — through clusters of neurons known as the pontine nuclei. This connection is crucial for cognitive functions like learning how to talk or making tools.

In birds, the similar pathway connects the avian equivalent of the neocortex to the cerebellum, Gutiérrez-Ibáñez and colleagues reported in 2018 in Scientific Reports. In addition to the pontine nuclei, birds shunt information through a second conduit, the SpM. It’s unclear what info gets transmitted via the SpM, Gutiérrez-Ibáñez says. But among birds, the parrot SpM is particularly large in size — a tantalizing hint that it may contribute to parrot intelligence.

Parrot and human brains may also share genetic underpinnings, a team of researchers including Jarvis and behavioral neurobiologist Claudio Mello reported in 2018 in Current Biology.

Parrots have acquired duplicate copies of various genes, some of which are known to be important for brain development and speech in people, says Mello, of Oregon Health & Science University in Portland. More copies could mean more ability. But parrot smarts may come down to how genes in the brain are regulated in addition to gaining more or new genes. Unlike other studied birds, parrots have genetic mutations in regions of DNA that provide instructions to switch genes on or off, perhaps to activate certain genes crucial for brain function and cognition.

This is reminiscent of humans, Mello says. We have mutations in these same gene regulators while other apes don’t. In us, the changes allow the regulators to kick-start genes related to growing big forebrains, a region important for complex cognition. If the same is true in parrots, it could point to a shared evolutionary process for humanlike intelligence.

The evolution of intelligence

To figure out the evolutionary origins of parrots’ brainpower, scientists have to go way back — all the way to the mass extinction that ended the Age of Dinosaurs. In the aftermath, as modern avian groups emerged, some birds rapidly evolved big brains.

That’s what paleontologist Daniel Ksepka and colleagues found by analyzing the skull casts of more than 2,000 living bird species, 22 extinct bird species and 12 nonavian dinosaurs. A large brain relative to body size is one indication, albeit imperfect, that an animal might be intelligent. Parrots, as well as members of the crow family, ended up with some of the largest brains of any birds.

Dinosaurs and early birds had similar sized brains relative to their bodies, the researchers reported in 2020 in Current Biology. By the time of the mass extinction 66 million years ago, both groups were already beginning to form forebrains. Rapid environmental change in the wake of the asteroid impact that may have sparked the mass extinction could have pushed some avian brains further on the fast track to growth, says Ksepka, of the Bruce Museum in Greenwich, Conn.

“The day after [impact] is going to be really hard,” he says. And then came forest fires and changes in the atmosphere and temperature as dust blocked out the sun.

Adaptable animals with relatively large brains — a group that probably included parrot ancestors — may have had a leg up over those without. Animals that figure out how to open pinecones with their beaks, say, will do better than the ones waiting for the next crop of berries that might never come, Ksepka says.

Today, having a big brain is just one thing humans and parrots have in common. In general, they also share long lives, monogamy and learning to sing or talk from others, a trait known as vocal learning. Researchers are investigating how these traits might relate to the evolution of intelligence. Right now, there are more hypotheses than answers.

For example, one line of thinking suggests vocal learning and a need for complex forms of communication may have paved the way to greater intelligence. Parrots “have very large, flexible vocal repertoires,” says behavioral ecologist Lucy Aplin of the University of Zurich and Australian National University in Canberra. “They can learn new vocalizations throughout their lives.”

It’s unclear what most parrot calls mean. But some parrots make signature sounds that declare who they are or what groups they belong to, Aplin says. If parrot talkativeness is indeed a driver of cognition, “that then begs the question, why do they need such complex communication, which then ties it back to their social systems,” she says.

Parrots live in large, cohesive groups. So having a good memory and enhanced intelligence may help the birds maintain relationships and strategically climb up the social ladder. Sulphur-crested cockatoos (Cacatua galerita), for instance, live in groups of hundreds of individuals yet maintain hierarchies that don’t seem to be based on physical characteristics. “The assumption is that they must be doing it based on memory, which is a big cognitive load,” Aplin says.

The possible connection between big brains and parrots’ social natures is a question that Aplin’s team is beginning to explore using MRIs of parrot brains. The goal, she says, is to identify how brain size as a whole — as well as regions particularly important in cognition — vary among species that differ in level of sociality.

In the case of songbirds, species with more complex vocal skills are better at solving cognitive puzzles in the lab, Jarvis and colleagues reported in September in Science. Jarvis, who is also a Howard Hughes Medical Institute Investigator, speculates that the same is probably true among parrots.

Parrots and songbirds, as well as humans, have neural circuits involved in song and speech that evolved from nearby pathways that control body movements. Instead of controlling muscles that move wings or arms, the circuits are connected to sound-producing organs. Parrots have more sophisticated vocal communication skills than songbirds, thanks to an additional copy of this same circuit, Jarvis and colleagues reported in 2015. The extra dedicated brain space hints that vocally adept parrots may therefore be better problem solvers than songbirds. So far, Jarvis has only tested songbirds’ problem-solving skills.

Parrots’ dexterity in maneuvering objects with their feet may also relate to the evolution of intelligence, Gutiérrez-Ibáñez and colleagues reported in August in Communications Biology. “[Hand-eye coordination] is like a stepping stone into intelligence and higher cognitive ability,” he says.

Take primates. Monkeys and apes with better motor skills tend to have bigger brains, researchers reported in 2016. Finesse with handling objects as tools is key for accessing challenging food sources, like using sticks to crack open nuts or to pull ants out of anthills. Good motor skills, Gutiérrez-Ibáñez says, are also probably key for understanding an item’s physical properties, and big brains can mentally manipulate those objects.

Parrot intelligence in the wild

How parrot intelligence plays out in the wild is mostly unknown. What scientists know about parrot smarts largely comes from captivity, where the absence of predators and the abundance of food might free up mental space, Pepperberg says.

Captive parrots are probably best viewed as what can be, not necessarily what always is. “We say humans are brilliant, and we point to Einstein, we point to Beethoven, we point to Picasso,” Pepperberg says. While the average human might struggle with calculus, musical theory or painting masterpieces, we still say Homo sapiens does great things.

It’s also possible that scientists are just missing the cognitive feats of wild parrots. It’s difficult to get wild parrot studies off the ground because the birds can fly away, and researchers can’t easily follow. (New Zealand’s kākāpō, the only flightless parrot, is the exception.) “Researching these highly mobile animals is a challenge in the wild,” says Rachael Shaw, a behavioral ecologist at Te Herenga Waka – Victoria University of Wellington in New Zealand.

Cognitive biologist Alice Auersperg of the University of Veterinary Medicine Vienna and colleagues solved that problem by capturing wild Goffin’s cockatoos in Indonesia, placing them in a field-based aviary and then releasing them after studying how the cockatoos make and use sets of wooden tools to get seeds out of sea mangos.

Shaw and colleagues are working to improve another challenge of field studies — recognizing individual birds — by developing facial recognition software, which could also be useful in conservation. More than 100 parrot species are endangered or threatened because of habitat loss and the pet trade.

Studying parrot intelligence could help conservation efforts, Bastos says. A study from 2018 found that wild keas in New Zealand learned to use sticks to tamper with egg-baited traps intended for stoats — a relative of weasels that preys on keas. Some birds got stuck inside the boxes and died. Understanding the bird’s cognitive limits could lead to new, kea-proof trap designs.

Sometimes wild parrots aren’t in forests but in people’s yards. Across the Tasman Sea from New Zealand, in Sydney, sulphur-crested cockatoos can learn from one another how to break into trash bins for food (SN: 10/8/22, p. 10). People retaliate with tricks of escalating difficulty to keep the birds out.

These urban bird populations highlight the adaptability of parrots, Aplin says. Sydney has sprung up around cockatoos’ native habitat. “We can’t assume that cities are empty spaces where we only have to account for human wants and needs. We also have to be thinking about the animals that we’re supporting specifically in those cities.”

Some Goffin’s cockatoos escaped from the pet trade into urban settings in Singapore, where there is now a stable population. Seeing how the birds adapt in real time is “super exciting,” Rössler says. Scientists could learn how the new surroundings might spark new innovative behaviors. “That’s the evolution in the making.”

Swallow the wrong microbe, and you might end up in the hospital with a needle or two in your arm — and plenty of itty-bitty bacterial needles poking at you from the inside. That’s because many bacteria that make us sick use microscopic, syringelike structures to inject our cells with proteins that wreak havoc from the inside. Now, researchers have shown how these microbes load their nanoscale needles with proteins.

Tracking individual proteins as they jittered around inside living bacteria revealed the microbes use a shuttle bus–like system to load their syringes: shuttle proteins travel random paths within the microbes’ interiors, grabbing cargo destined for injection as they go and dropping it off at the syringes, scientists report January 3 in Nature Microbiology. Knowing how these bacterial needles work could help scientists learn how to disrupt them — or commandeer them for medical applications, like using bacterial needles to inject cancer cells with targeted drugs while leaving healthy tissue unscathed.

Shuttling proteins to the syringe is “a really novel molecular mechanism that was not known before,” says microbiologist Andreas Diepold of the Max Planck Institute for Terrestrial Microbiology in Marburg, Germany.

Under the microscope, the syringelike structures, called a type-III secretion system, look like hollow needles just wide enough for a single unfolded protein to slither through, Diepold says. A microbe’s entire surface might be covered in such needles, giving the bacterium the look of a sinister little pincushion. Scientists know the protein structure of these nanoscale needles quite well. But “we don’t know the basic question of how they recruit whatever is injected,” he says.

Previous studies suggested that a ring of proteins at the base of the secretion system, where it attaches to the bacterial cell membrane, might act something like a sorting platform that grabs target proteins and loads them into the syringe. But that work wasn’t done in living cells, says microbial geneticist Kelly Hughes of the University of Utah in Salt Lake City, who was not involved in the new study.

Other studies in live cells, including recent work by Diepold and his colleagues, hinted that the components of the sorting platform might not stay put at the bases of the syringes. Instead, they might wander around the gel-like jumble of fluids, proteins and other biological bits enclosed within a bacterium’s cell membrane, picking up and dropping off target proteins as they go — like shuttle buses.

The new study put the shuttle-bus idea to the test by using fluorescence microscopy to track the movement of individual sorting platform proteins in Yersinia enterocolitica, a stomach bug that lurks in undercooked pork. Maps of the proteins’ paths show them wandering random, zigzag paths through the cells. And experiments with mutant Y. enterocolitica that lack injectable proteins revealed that the shuttle-bus proteins move more quickly in the mutants — without any injectable targets to bind to, the shuttle-bus proteins don’t get weighed down by cargo and can diffuse faster through the cells. This showed that the sorting platform proteins don’t just wander; they also pick up passengers along the way.

“What I loved about this paper was that it was all set in vivo,” in living cells, Hughes says. “You get these beautiful pictures. And you know, a picture’s worth a thousand words.”

Unraveling more of the outstanding mysteries surrounding these microscale needles will make it easier for scientists to throw a wrench in these machines, or to tinker with them. This type of secretion system, one of a handful of different types of needles bacteria have at their disposal, is widespread across different species of bacteria, Diepold says, so they’re good targets for new types of antibacterial drugs (SN: 3/30/22).

They’re also promising tools for medicine and biotech, Hughes says. But as much as they look like medical syringes, bacterial syringes work differently — and scientists still don’t know exactly how bacteria push proteins through their needles. It’s also unclear how the proteins that load up the needles recognize their targets. “We want to understand the riddle of how these systems work,” Diepold says. “We want to understand which solutions evolution came up with to allow bacteria to infect us.”

Each morning after breakfast, Scott Broadbent takes a plastic bottle from the refrigerator in his home in Alameda, Calif., pops the top, and drinks the contents, 2.5 ounces of milky liquid. “It has sort of a pineapple creamy flavor,” he says. “It’s really not bad.”

The bottle might contain ketone ester, a supplement meant to help the body burn fat instead of carbohydrates. Researchers are now testing whether it might also slow the aging process. Or Broadbent might instead be getting a placebo. He is part of a clinical trial at the nearby Buck Institute for Research on Aging to assess the supplement’s safety and side effects in older adults.

A retired chemist who used to work for pharmaceutical companies, Broadbent is 70 and in excellent health today, but he worries about the future. He’s not necessarily afraid of dying, but he doesn’t want to be sick and in pain as he grows older. His dad had Parkinson’s disease. Broadbent survived prostate cancer and recently developed tinnitus, which spooked him and sparked anxiety attacks. “I thought if I had to live like this the rest of my life, I don’t know if I’d want to do it,” he says.

Some scientists think there’s a better way. These researchers — part of a burgeoning field called “geroscience” — aren’t seeking immortality. The focus is much more pragmatic: By addressing the root causes of aging, they hope to stave off the disability and diseases that can make old age so miserable. They want to help people feel healthy for longer, compressing the years of illness that often accompany old age into a much shorter time frame. “Let’s build a medicine that would be safe enough for someone in midlife to take almost like a supplement, like a daily vitamin, but with much more profound biological effects,” says James Peyer, CEO of Cambrian Bio in New York City.

Just don’t call these potential medicines antiaging therapies. “That term is associated with an industry that is trying to sell products to the public to separate people from their money,” says S. Jay Olshansky, a demographer and geroscientist at the University of Illinois Chicago. The antiaging market includes everything from face creams meant to zap wrinkles to pills that promise to turn back the clock. “It’s bogus,” he says. Geroscientists instead are doing legitimate research at respected research institutions to find medicines that can slow the aging process. Many of the compounds under study show promise in mice and even humans, and some are in clinical trials.

Better health in old age is not just about individual benefits. By 2030, 73 million baby boomers in the United States will be 65 or older. By the same year, experts project, there will be a billion people 65 and older globally. And though people are living longer, they are not necessarily living healthier than previous generations.

“There’s this fear of what is this going to do to our health care system,” says Laura Niedernhofer, a geneticist and researcher studying aging at the University of Minnesota in Minneapolis. “And it goes well beyond just health care. We don’t have the nursing homes. We don’t have the personal care staff to deal with this at all.” Drugs to help keep older adults healthy, active and independent would be a societal boon.

But whether developing such drugs is even possible remains to be seen. Getting the medicines to market means securing more funding, overcoming stumbling blocks related to study design and combating near constant hype.

How did geroscience begin?

The advent of modern medicine and public health has more than doubled the average human life span — from about 30 in the early 1800s to more than 70 today. “This is perhaps one of the biggest things that has happened to humankind, period,” says Jamie Justice, a geroscientist who heads the health domain at the XPRIZE Foundation, which holds competitions to spur technological developments and announced a new prize related to aging in November. “We are a lot less dead than we used to be because of where public health and modern medicine has gotten us.”

There’s a downside, of course. We’re living long enough to see the frailty and illness that comes with old age. Cells stop dividing, DNA degrades, the immune system falters. We become increasingly vulnerable to disease. Many of us spend our last decades beset by medical maladies — broken bones, weakness, dementia, cancer, heart disease and more. Doctors can do little more than play whack-a-mole, beating back illnesses one at a time.

For decades, scientists thought the gradual decline that comes with old age was unavoidable. But experiments in the 1980s and ’90s suggested that the process might not be so fixed.

In one notable experiment, Cynthia Kenyon, a molecular biologist at the University of California, San Francisco, and colleagues found that mutations in a single gene in the roundworm C. elegans could double its life span. Typical 13-day-old worms barely moved. “The animal is clearly in the nursing home,” Kenyon said in a 2011 TED Talk. The mutant worms moved as if they were much younger, and they lived longer too.

For researchers interested in human health, this and similar findings from other teams led to a profound realization: Perhaps the aging process is malleable. If so, scientists might be able to develop therapies to attack the root of aging rather than simply combating the pileup of diseases.

By the late 2000s, “the whole perspective of the scientific community changed,” says Felipe Sierra, who was then a program officer at the National Institute on Aging in Bethesda, Md. Aging biology moved from a phase of description into a phase of molecular investigation. Sierra wanted a name to bring the field together. He landed on geroscience, a word he had first seen in a grant proposal by another researcher studying aging, Gordon Lithgow. “Gero-” comes from the Greek word for old man. It wasn’t difficult to convince other researchers to get on board. “Everybody listened to me because I was in charge of the money,” says Sierra, now chief scientific officer at Hevolution Foundation, a nonprofit that funds geroscience research.

What compounds might fight aging?

Though there are no proven therapies for people yet, geroscientists are eyeing several compounds that can slow the aging process, at least in worms, fruit flies and mice. Some have already been tested in humans, and many more clinical trials are under way. Which will work? “Let me see. Let me look at the crystal ball,” Sierra jokes. “Who knows?”

Perhaps the best studied is rapamycin, a compound first discovered in a soil sample collected in 1964 from Rapa Nui, or Easter Island. Today, people who receive organ transplants take the drug to help keep their immune systems from rejecting the foreign tissue. But rapamycin also prolongs life in yeast, flies and mice. And it’s being tested in people in clinical trials. How it counters aging isn’t entirely clear. The drug inhibits a protein complex called mechanistic target of rapamycin, mTOR for short, which plays a role in cell growth and protein synthesis. This inhibition appears to have wide-ranging effects, including reducing inflammation, clearing old and damaged cells, and altering cellular metabolism — some of the key processes that researchers think are to blame for the aging process.

Rapamycin isn’t the only drug to impact mTOR. Researchers at the biotech company resTORbio tested other mTOR inhibitors in elderly adults to try and improve immune function. About 250 people participated in the clinical trial, which tested two mTOR inhibitors alone and in combination compared with a placebo. In 2018, the team reported that those who received the drugs had fewer infections and mounted a better response to the flu vaccine. The company tried one of those compounds in a subsequent study, though, and it failed to show an effect on self-reported respiratory illnesses. resTORbio no longer exists, but the company’s chief medical officer, Joan Mannick, hasn’t given up on mTOR inhibitors. She cofounded a new company called Tornado Therapeutics, based in New York City, that is working to develop new rapamycin analogs, or “rapalogs.”

Another promising class of drugs targets cells that have stopped dividing but don’t die. These senescent cells release chemical signals that can trigger inflammation, disrupt tissue repair and harm neighboring cells. In some cases, these signals even prod neighbors to become senescent too.

The drugs, called senolytics, aim to eliminate senescent cells by prompting them to commit suicide. After showing promising results in mice, senolytics are now being tested in humans. More than 25 clinical trials have either been completed or are under way.

One of the most commonly tested senolytic regimens is a combination of two compounds: the anticancer drug dasatinib and quercetin, an antioxidant that occurs naturally in grapes, berries and other fruits and vegetables. Other research efforts plan to compare fisetin, a compound found in strawberries and apples, with a placebo to see if it has an impact on frailty and markers of inflammation in the blood.

Unity Biotechnology, based in San Francisco, is focused on senolytic therapies exclusively. The company’s most advanced compound, called UBX1325, targets a protein abundant in the blood vessels and retina that regulates cell death. Preliminary results from a trial in patients with diabetic macular edema, a thickening of the retina related to diabetes, suggest that the compound can improve eyesight.

Diet is also known to profoundly affect the aging process. Studies have found that the low-carb ketogenic diet, for example, can help mice live longer. But restrictive diets can be hard to follow and have side effects. Broadbent followed the ketogenic diet for a month or so, but his cholesterol levels went dramatically up. Ketone ester, the compound Broadbent might be downing each morning for the Buck Institute’s clinical trial, may mimic the longevity benefits of such diets.

When the body runs out of glucose to use for energy, the liver creates another source by converting fat into molecules called ketone bodies. “If we don’t eat for a day or so, we’ll start to make ketone bodies,” says John Newman, a geriatrician at the Buck Institute who is leading the trial. “And we’ll make more and more the longer that we starve in order to fuel our bodies.” These compounds are more than just fuel. They help regulate inflammation and control other cellular processes, many of them involved in the aging process. Drinking ketone esters, which quickly break down, is a way to deliver the ketone bodies without the diet.

Among the dozens of clinical trials testing potential gerotherapies, very few are yet assessing their ability to prevent the onslaught of diseases that come with aging. Instead, the goal is establishing safety or seeing whether a compound can nudge some biomarker in the right direction. And many of the potential treatments under study are natural compounds or existing drugs that are already off patent, which might leave drug companies hesitant to invest in future trials or to seek approval from the U.S. Food and Drug Administration or other regulatory agencies.

What’s more, as James Kirkland, a geriatrician at the Mayo Clinic in Rochester, Minn., points out, many of the clinical trials happening now will fail. “In fact, most will,” he says. That’s just a part of drug development.

For now, some companies are bolstering their chances of success by pursuing many options. Cambrian Bio, the parent company of Tornado Therapeutics, for example, is “taking a number of different shots on goal,” Peyer says. “We don’t know which drug is going to really be the first multidisease preventative.”

What are the barriers to progress?

One of the big challenges for geroscience is to figure out how to show that a compound prevents age-related diseases in people. Scientists would have to give the drug to healthy people and then track their health as they age, an expensive and time-consuming endeavor. “In mice, it takes us four years. In humans, it would take decades and tens of thousands of people,” Niedernhofer says.

An easier path to the clinic would be to develop these therapies as a treatment for a single disease rather than a multidisease preventive. “That’s something that the FDA is very comfortable with,” says Nathan LeBrasseur, a researcher studying aging at the Mayo Clinic. Once the drug is approved for one indication, it would be much easier to seek approval for others — and potentially widen to a preventive. “The absolute irony of all of this is, to try and advance geroscience, we’re going right back to the old way of doing things, which is one disease at a time,” Niedernhofer says. For example, Unity is developing its lead antiaging candidates as therapies for a variety of eye diseases.

One group of researchers, however, has developed a clever work-around. Rather than treating healthy people and waiting for them to age, the team has devised a study that will recruit people who have one age-related disease and assess whether a drug reduces the time it takes to develop another. In this case, the researchers have chosen the diabetes drug metformin. Metformin has a long safety record, and studies suggest it can impact heart disease, cancer and cognitive decline. Metformin may even reduce the risk of long COVID. The precise mechanisms that underpin these effects aren’t entirely clear. The study, called Targeting Aging with Metformin, or TAME, will look at things such as cardiovascular events, cancer, cognitive decline, dementia and death.

But nearly eight years after investigators first announced the 3,000-person trial, they’re still trying to get together funding. Metformin is cheap and readily available, no longer protected by a patent, so drug companies have no incentive to develop it for aging. Nir Barzilai, director of the Institute for Aging Research at the Albert Einstein College of Medicine in New York City, who is leading the study, has started telling people the trial will start in January. “And as long as I don’t say which year, it will be true,” he jokes.

Part of what holds the field back is society’s approach to medicine, says Justice, of the XPRIZE Foundation. “We have a model of medicine that prioritizes treatment of diseases,” she says. “You get one disease. You treat one disease. You restore homeostasis.” But that approach isn’t relevant for aging. Geroscientists also have to fight society’s views of aging. The mind-set is “things get old. It just happens. There’s nothing you can do, just let it go,” Justice says. “I think that is actually a fundamentally ageist view, as if people who are older don’t have a right to health.”

Geroscientist Matt Kaeberlein of the University of Washington in Seattle agrees. No one would argue that we shouldn’t develop therapies for Alzheimer’s or cancer because these diseases are a natural part of getting older. So, he asks, why would this argument hold for aging? “I don’t really see what the field is trying to do as any different than trying to cure disease,” he says. “It’s just a much more efficient and effective approach, or it’s likely to be.”

Kaeberlein thinks dogs, because they age much faster than people, could bridge the gap between lab studies in mice and therapy approval. “You can do longevity clinical trials in dogs that you can’t do in people,” he says. And companion animal medications are regulated much like human medications. The Dog Aging Project, which Kaeberlein codirects, is testing rapamycin in 500 middle-aged dogs to assess its impact on the heart, the immune system, cancer incidence and cognition.

But even if geroscientists find compounds that treat the decline that comes with aging, it’s not clear whether they will compress the period of age-related illness — that’s the goal — or simply delay it. It’s also uncertain whether such therapies might add to the average life span and, if so, how many years. John Davis, an ethicist at California State University, Fullerton, worries about how such increases might affect demographics. If the average life span jumps to 120 years, the effects aren’t too pronounced, he says. If it goes far longer, there is the potential for “really spectacular increases in population on a planet that I personally feel is already overloaded.” And then there are concerns about how longer life might impact existing inequalities. “Billionaires who live longer have more time to accumulate even more wealth,” Davis adds.

Beware the antiaging hype

There’s another potential obstacle: hype.

No one can say with any certainty that there will be a pill to prevent aging. Yet that hasn’t stopped some companies and less scrupulous researchers from cashing in. The public’s interest in escaping aging makes overselling results enticing. In 2019, for example, the FDA warned consumers against receiving infusions of plasma from young donors, which some companies offered for $8,000 a liter. The treatment was based on promising mouse studies that gave older mice blood from younger mice, either via transfusions or by connecting the two animals’ circulatory systems. The young blood appeared to rejuvenate the older animals’ muscles, livers and brains, but the benefits haven’t been proved in human patients.

The internet is likewise rife with supplements and even prescription medications with purported antiaging benefits. Many of the pills being touted as age-reversing miracle drugs are the same compounds geroscientists are currently testing in trials. “[Companies] start trying to sell it to the public before it’s been tested for safety and efficacy,” Olshansky says. That can make it especially difficult for consumers trying to sort fiction from fact.

LeBrasseur is concerned that if scientists oversell their progress, they run the risk of losing public trust. And a rush to clinical trials might lead to safety problems. “If something bad happens, that’s going to set the entire field back,” he says. “I just think we have to be patient and humble.”

A student of Newman’s, at the Buck Institute, asked him recently how geroscience has changed clinical practice. “The honest answer is it hasn’t at all,” he says. “We’re still building the data. We’re still running the clinical trials waiting for it to come in. And this all takes time.”

But Broadbent, and many others, aren’t satisfied waiting for settled science. He likes to do his own research, and ketone ester seems like a good bet. The particular product he may be drinking as part of the clinical trial is now being sold as a supplement, and he plans to continue taking it after the trial ends. “I’ll sign up right away,” he says. “I’ll be on an annual subscription.”

Many scientists are convinced that the geroscience revolution is coming. Until then, there’s a tried-and-true method for improving your health span. It’s the advice any doctor will give you: Eat a balanced diet, exercise, get vaccinated and avoid tobacco and alcohol.

A sledgehammer dealt the final blow to New York City’s dream of a paleontology museum.

On May 3, 1871, workers broke into the workshop of famed British artist Benjamin Waterhouse Hawkins. Inside, they came upon a plaster skeleton of a towering duck-billed dinosaur — modeled after the first dinosaur fossil unearthed in New Jersey 13 years earlier — alongside a statue of the beast as it would have appeared in life.

These were the first 3-D renderings of any North American dinosaur, a testament to the continent’s geologic past that scientists were only just beginning to understand. But the public would never see the skeleton or the statute.

The workers wrecked the workshop. Plans and drawings were torn to pieces. Sledgehammers shattered the dinosaurs.

In the more than 150 years since, this vandalism has remained one of the most infamous events in paleontology. The story passed down through the years is that the workshop was destroyed on the orders of New York political boss William Tweed in a malicious act of political and religious vengeance.

Tweed viewed dinosaurs as “inconsistent with the doctrines of received religion,” a paleontologist noted later in 1940. The destruction is cited as one of the early battles between a traditional Christian worldview and a growing scientific understanding of Earth’s deep past.

The loss of Hawkins’ dinosaurs has “always been a shock to the paleontological community,” says Vicky Coules, an art historian at the University of Bristol in England. It’s been thought that Tweed “was basically against the whole concept of dinosaurs,” she says.

But the story might be due for a rewrite. Recent historical sleuthing by Coules and her Ph.D. adviser Michael Benton, a paleontologist at the University of Bristol, suggests that the demise of Hawkins’ dinosaurs was not religiously motivated, or even ordered by Tweed.

Instead, the story that paleontologists tell about this affair may say more about the history of anti-evolution sentiment during the 20th century than in the 1800s.

Who was Benjamin Waterhouse Hawkins?

Today, dinosaurs are everywhere, the most iconic creatures of the prehistoric past. Their place in the public imagination is in no small part due to Hawkins.

Hawkins dedicated his career to depicting the natural world, even helping Charles Darwin illustrate the 1839 book The Voyage of the Beagle (SN: 1/16/09). In 1854, Hawkins’ most famous artwork went on display when the Crystal Palace reopened in London. Thousands flocked to this showcase of (sometimes looted) wonders from across the British Empire. A natural history section featured life-size statues of dinosaurs made by Hawkins.

This was several years before Darwin published his theory of evolution and only about a decade after the term “dinosaur” had entered the lexicon. For many people, seeing Hawkins’ statues was the first time they had come face-to-face with the concept of deep time (SN: 6/4/19).

Displaying dinosaurs in the flesh was “enormously innovative,” Benton says. “No one had attempted anything like this before.”

The exhibit made Hawkins the de facto expert on depicting prehistoric life, and in 1868, the Board of Commissioners of Central Park — the group in charge of developing New York’s new green space — asked Hawkins to build similar statues. They were to be the centerpiece for the park’s planned Paleozoic Museum, dedicated to American paleontology.

At this time, most of the major dinosaur discoveries were happening in Europe or its colonies. American scientists had yet to dig into the ample bone grounds of western North America, and most of the continent’s major paleontological finds — including Tyrannosaurs rex — were still at least a decade away (SN: 3/30/23). 

But a small number of fossils were starting to come out of the East Coast, including a dinosaur with a flat, beaklike snout named Hadrosaurus found in New Jersey. The Paleozoic Museum, the Central Park commission thought, would give Americans a chance to prove that they too had a prehistory worth remembering. Hawkins’ Crystal Palace statutes “hit [the public] between the eyes,” Benton says. Now, “New York wanted that.”

Hawkins accepted the job. He would dedicate the next few years to a museum that would never open its doors.  

The story that paleontologists tell

In the 1860s, New York was a city on the rise. One of the men riding that high was William Tweed, a state senator who dominated the city’s political scene. Tweed stripped power from all who opposed him. In May 1870, for instance, he dissolved Central Park’s board of commissioners and created a new group filled with his cronies.   

By year’s end, the new commissioners canceled the Paleozoic Museum and moved to discontinue their relationship with Hawkins — without paying him.

The museum’s demise had been simmering in the background for months. Already, Hawkins’ workshop had been relocated from a government building to a shed in the park. The move made room for the growing collection of the upcoming American Museum of Natural History, which, unlike the publicly funded Paleozoic Museum, had the private financial backing of New York’s wealthiest citizens, including the banker J.P. Morgan.

Plans for the two museums coexisted for a while. But eventually, the park commissioners decided that a museum dedicated solely to paleontology and funded by the public was just too big a burden to take on. It didn’t help that at least one member of the park commission was also on the committee for the American Museum of Natural History.

In March 1871, the New York Times — which frequently ran stories critical of Tweed — reported on the loss of the Paleozoic Museum, which Hawkins had lamented at a public meeting.

Two months later, the artist’s dino models lay in pieces.

“Hawkins was distraught,” Coules says. The destruction sent ripples through the scientific community, eventually becoming one of the foundational stories in the history of American paleontology, she says.

And the villain in the story: Tweed.

The Times article allegedly sent Tweed into a rage, and he ordered one of his cronies to descend “upon the Paleozoic Museum with vengeance in his soul,” paleontologists later wrote.

But it wasn’t just the bad press that supposedly angered Tweed. “There was always a rumor that there was some sort of creationist angle to it,” says paleontologist Carl Mehling of the American Museum of Natural History.

This version of the story, which paleontologists have repeated since at least the 1940s, rests on Tweed and his men referring to Hawkins’ dinosaurs as “pre-Adamite” animals and an incident in which one of Tweed’s followers told Hawkins he should focus on living animals. The argument fits into a common perception that emerged during the mid-20th century that religion and prehistory were often at odds in the late 19th century.

This is where the Central Park story begins to unravel.

Rethinking the Central Park dinosaur scandal

Last year while Coules was working on her Ph.D., she read up on Hawkins and things weren’t adding up.

For one, the timing of events didn’t make sense. Why would Tweed wait two months after the Times article to retaliate against Hawkins? When Coules dug up the newspaper story, she found it on Page 5, with no mention of Tweed in the article.

“My first question was, why on Earth would you be upset about that?” Coules recalls.

Tweed had bigger things to worry about. At the time, he had been accused of everything from bribery to money laundering. (Tweed was eventually arrested in late 1871 and died in prison several years later.) So it seemed odd that Tweed, who was fighting for his political life, would take such offense to a story buried so deep in the paper.

Coules started to suspect another culprit: Henry Hilton. Tweed appointed Hilton, a top lawyer to New York’s wealthiest men, to the new board in charge of Central Park in 1870. Hilton took to the role immediately, regularly visiting the park to search for areas of improvement.

Some of these “improvements” were head-scratchers. Hilton had workers paint a bronze statue of the biblical Eve entirely white, permanently damaging the metal. His penchant for destructive whitewashing — he ordered a similar treatment for a whale skeleton destined for a museum — became a joke in the press. 

One day while going through her notes at a café, Coules came across park commission meeting minutes from the day before the models were destroyed. In that meeting, the committee resolved to remove Hawkins’ workshop “under the direction of the Treasurer” — Henry Hilton. 

“I was like, wow! Look at this!” Coules says. Hawkins himself blamed Hilton for the vandalism. Coules found New York Times articles from the period in which Hawkins implicated Hilton.  

But why did Hilton want the dinosaurs destroyed? Coules’ research didn’t pick up any hint that religion was a major motivation. Rather, she argues, Hilton “had a strange relationship with artifacts,” as demonstrated by his whitewashing habits.

Hilton would also go on to harbor other destructive tendencies — swindling a wealthy widow out of her fortune and running her late husband’s business into the ground.

Hilton had “quite strange ideas [that managed] basically to piss off everybody,” says Coules, who published her findings with Benton last year in the Proceedings of the Geologist’s Association.

That Hilton’s “strange ideas” would be behind the Hawkins incident makes sense to Ellinor Mitchel, an evolutionary biologist at the Natural History Museum in London and coauthor of a book on Hawkins’ Crystal Palace dinosaurs. “I think that’s the way of much of history, that it turns it’s sort of out human strengths and weaknesses that pivot the direction of things,” she says.   

But not everyone is so sure. “It seemed quite convincing to me that Hilton played an important role,” says Lukas Rieppel, a science historian at Brown University in Providence, R.I., and author of a book on dinosaurs during America’s Gilded Age. But “it’s very hard for historians to know the private motivations of people who died over 100 years ago.”

Still, Coules’ work convincingly shows religion wasn’t a motivating factor.

For one thing, “pre-Adamite” was simply a way to refer to deep time, Benton says. So even if Tweed and Hilton did refer to Hawkins’ models in this way, it would have been more descriptive than derisive. What’s more, natural history — including paleontology — was seen as a respectable, middle-class occupation in the 19th century. “Natural history was seen as an expression of piety,” Rieppel says. “So a way that one could express one’s devotion to God [was] by learning about God’s works in the natural world.”

In fact, the idea that the world was ancient was widely accepted at the time, Benton adds. A more inflexible view of creationism, in which evolution is false and the world is only a few thousand years old, really started to gain steam only in the 20th century, he says.

Religion’s supposed role in the Hawkins’ saga may have been introduced by paleontologists writing about this incident in the mid-20th century, who may have been projecting their experiences with creationist movements into the past, Rieppel says. From there, the story stuck.

Hawkins’ lasting influence

The loss of the Paleozoic Museum might have been for the best. It would have been “obsolete almost immediately and I fear almost comical,” Mehling says — soon overshadowed by bigger discoveries from the American West.

But that doesn’t mean that Hawkins’ models didn’t have value, Mehling says. Dinosaur statues may now be the stuff of tacky roadside attractions and miniature golf courses. But in the 19th century, Hawkins’ statues were key to opening the public’s imagination to an ancient world that was quite different from the present.

Hawkins’ display was so awe-inspiring that in 1905, when the American Museum of Natural History unveiled its 20-meter-long Brontosaurus, it displayed the skeleton upright (SN: 4/7/15).

And Hawkins’ work continues to influence how people think of dinosaurs. While doing research for the Paleozoic Museum, Hawkins strung together the fossil pieces of Hadrosaurus into a standing skeleton and displayed it in Philadelphia. Before this, fossils had only ever been displayed flat on a table or kept in drawers. Visitors flocked to see the strung-together skeleton, overwhelming staff at the institution where it was housed.

The tradition stuck. And today, most museums display their fossils using Hawkins’ method.    

A peek inside

Neutron tomography can help scientists capture 3-D images of the insides of fossils and artifacts without damaging them. The technique can uncover hidden features within dense material that X-ray scanning can’t detect, James R. Riordon reported in “Seeing into the past” (SN: 11/4/23, p. 18).

Reader Rob Janes asked how the 3-D images are captured.

In neutron tomography, scientists blast beams of neutrons at an object they want to study, Riordon says. Detectors on the other side of the object record the proportion of neutrons that make it through without being reflected or absorbed along the way. Using that data, computer algorithms create virtual slices of the object, which can then be assembled to provide 3-D views of the object’s interior, he says.

Reader Heidi Wilson asked whether neutron tomography has been used on ancient manuscripts that can’t be unfolded.

X-ray computed tomography has been the go-to method for analyzing ancient manuscripts, Riordon says. The artifacts are generally made of low-density material, such as papyrus or parchment, that X-rays can effectively image.

One recent exception, reported in 2021 in Archaeometry, is a medieval amulet made of a folded lead scroll that contains inscriptions. Since X-rays cannot easily penetrate particularly dense materials like lead, the researchers turned to neutron tomography to virtually unfold the sheet and reveal the inscribed runes. “Although ancient metal manuscripts are comparatively rare, neutrons offer a way to read them without risking the damage that opening them up would cause,” Riordon says.

Thinking about loneliness

Social scientists are learning more about how feeling detached from animals, places and routines — not just people — can cause loneliness. These revelations may lead to new interventions, Sujata Gupta reported in “What is loneliness?” (SN: 11/4/23, p. 24).

“While reading [this story], I found myself once again thinking about the demise of the front porch in our communities…. Having grown up in a small town in western New York that came into its own in the mid-1800s, front porches are to be found on most of the older homes,” reader Jim Sobek wrote. “A few years ago, while in town for a week of bicycling, I spent an evening with cousins on their front porch. As we whiled away the evening in conversation, neighbors out for their evening walks stopped by to talk for a while and then went on their way, only to be replaced by other neighbors also taking their evening constitutionals. Warm greetings and friendly conversation were exchanged between neighbors who knew each other well.”

Many modern homes “have large backyards, large decks, some pools and always-spacious air-conditioned interiors, but at best only a small covered concrete front stoop,” Sobek continued. “The residents often do not speak with neighbors, and sometimes don’t even know who their neighbors are.” While these homes are more comfortable, Sobek wonders whether they have also contributed to the loneliness and loss of community that some people now feel.

Correction

In “Clear the air,” the unit of the x-axis in the graph titled “Methane emissions in 2022, by source” was labeled incorrectly (SN: 11/18/23, p. 18). It should have been million metric tons, not metric tons.

Ask thousands of teens whether frequent use of certain substances brings a high risk of harm, and they mostly nail it: a majority say yes for cigarettes, alcohol, cocaine and heroin. But there’s one substance that many skip over — cannabis.

Only 35 percent of 12- to 17-year-olds perceive a “great risk of harm” from smoking marijuana once or twice a week, according to the National Survey on Drug Use and Health.

It’s a sentiment that some of their parents may share. Parents often don’t understand that the products used today “are not what they knew when they were in high school,” says Kelly Young-Wolff, a licensed clinical psychologist and research scientist at Kaiser Permanente Northern California Division of Research in Oakland. If their children are using cannabis, parents may think, “‘it’s not that bad, at least they’re not using this other drug that’s worse.’”

But the cannabis products available now are leaps and bounds more potent — which may increase the risks for addiction and psychosis — than in the past. Marijuana plants have been bred to contain more delta-9-tetrahydrocannabinol, or THC, the main psychoactive chemical. In 1995, the total percent of THC by weight of marijuana plant material was around 4 percent; now marijuana with a THC potency of 20 percent or more is available. Trouncing that are concentrated cannabis products, including wax, budder and shatter, which can have a THC potency as high as 95 percent.

Cannabis is legal for adults to use recreationally in 24 states and Washington, D.C., and is allowed for medical use in 38 states and D.C. The widespread availability of cannabis “promotes the idea that it’s safe,” says pediatrician Beth Ebel of the University of Washington School of Medicine and Seattle Children’s Hospital. But that “is an incorrect assumption.” THC can impact brain chemistry “in a way that wasn’t intended,” Ebel says. “Some of the worst effects can have lifelong health consequences, especially for a young person.”

Concentrated cannabis products can be so extremely potent, and so different from what’s been known as cannabis, that “we need to start calling them something else,” says neuroscientist Yasmin Hurd of the Icahn School of Medicine at Mount Sinai in New York City. “These are new drugs.”

How does THC affect the adolescent brain?

As is true for other drugs, adolescence is an especially risky time to use cannabis. “The adolescent brain is still developing into early adulthood,” Hurd says. During this period, connections within adolescents’ brains are forming, getting reinforced or being pruned. “Your brain is trying to figure out, ‘what is important that I need to learn, and what is important that I need to retain,’” Ebel says, and this process is “negatively affected by THC.”

THC binds to one of the main receptors, called CB1, of the endocannabinoid system. This complex system influences many functions in the body. In the brain, the endocannabinoid system plays a crucial role in the organ’s development and helps to regulate anxiety, pain, memory, the motivation of behaviors and more.

The endocannabinoid system also contributes to structural changes that occur as developing teen brains mature. But THC can interfere with the system’s signaling during this key time and leave an imprint on the brain’s structure.

Studies in animals have found that exposure to THC in adolescence can reduce CB1 receptors in the brain and lead to long-lasting problems with memory and learning. One of the areas the psychoactive chemical alters is the prefrontal cortex, which matures during adolescence and is integral to problem-solving and emotional regulation. In adolescent rats injected with THC, nerve cell protrusions that connect with other nerve cells were prematurely cut back, disrupting the circuitry of the prefrontal cortex, Hurd and colleagues reported in Molecular Psychiatry in 2019.

There’s also evidence in people that THC changes teens’ brains. Researchers analyzed close to 1,600 magnetic resonance images of the brains of nearly 800 adolescents, taken at 14 and 19 years of age, on average. There was an association between cannabis use over the five years and an accelerated thinning of the prefrontal cortex, the researchers reported in JAMA Psychiatry in 2021. Cortical thinning is expected in adolescence and is likely tied to the pruning of underused connections. But accelerated thinning means that process isn’t following the normal developmental plan. The researchers hypothesize that the accelerated thinning might be connected to the premature loss of nerve cell protrusions that was described in the rat study.

Marijuana use is linked to mental health harms

Using cannabis puts teens’ mental health at risk. That’s true even for someone using cannabis recreationally. Adolescents ages 12 to 17 whose cannabis use did not meet the threshold for a substance use disorder were about twice as likely to develop depression or have suicidal ideation as those who didn’t use cannabis, according to a study of more than 68,000 adolescents published in May in JAMA Network Open.

The risks increase for those with cannabis use disorder, which is diagnosed when someone’s use interferes with daily life, but they aren’t able to stop using, among other symptoms. The JAMA Network Open study reported that adolescents with cannabis use disorder were 2.5 and 3 times as likely to have depression or suicidal ideation, respectively, as those who didn’t use cannabis.

Beginning cannabis use as a teen is more likely to lead to dependence than starting as an adult, just like alcohol, cocaine and nicotine. Compared with young adults, adolescents are more susceptible to dependence within a year of taking up marijuana. Eleven percent of those ages 12 to 17 progressed to cannabis use disorder by 12 months, but only 6 percent of those ages 18 to 25 did, researchers reported in 2021 in JAMA Pediatrics. After three years, the prevalence was 20 percent of adolescents versus 11 percent of young adults.

Yet many teens are turning to marijuana as a coping mechanism. A study of what motivated high school seniors to use cannabis found that reasons related to coping — such as to escape problems, relieve tension or deal with anger — approximately doubled in prevalence during the last four decades, researchers reported in 2019 the Journal of Studies on Alcohol and Drugs. For a project on how cannabis legalization for adults in California has impacted adolescent health, Young-Wolff has talked to clinicians who care for adolescents. They’ve told her that many of their patients who use cannabis are doing so to self-medicate, to try to relieve symptoms of depression or anxiety.

Ebel has seen this too. But as the drug wears off, users are more anxious than they were before, she says. “It drives a cycle that drives increased use.”

When marijuana is a part of a teen’s everyday life, it can change their future trajectory. A study of young people in Australia and New Zealand compared the frequency of cannabis use before the age of 17 with how participants had fared by age 30. Those who used cannabis daily were more likely to become dependent on cannabis, use other drugs and attempt suicide, and less likely to finish high school, compared with teens who had never used, researchers reported in 2014 in the Lancet Psychiatry.

Cannabis addiction is also tied to the development of the psychiatric disorder schizophrenia. A study of nearly 7 million Danish people ages 16 to 49 found an association between cannabis use disorder and schizophrenia, researchers reported in May in Psychological Medicine. The association was stronger for males overall and especially at the ages of 16 to 25 years old. The researchers estimate that in 2021, without cannabis use disorder, around 15 percent of cases of schizophrenia in males and 4 percent in females would not have occurred.

The risks of using concentrated cannabis products

Although smoking the marijuana plant is still the most common way teens use cannabis, vaping cannabis concentrates is on the rise. A study of high school seniors reported that from 2015 to 2018, among past-year cannabis users, smoking decreased from 95 percent to 90 percent, while vaping increased from 26 percent to 34 percent. Daily use was also more common among those who vaped, at 29 percent, verses those who smoked, at 18 percent, researchers reported in JAMA Pediatrics in 2020.

There is early evidence that high-potency products are associated with an increased risk of psychosis, a symptom of schizophrenia. In a study of adults, daily use of high-potency cannabis products led to nearly five times the risk of psychosis compared with people who didn’t use cannabis, researchers reported in 2019 in Lancet Psychiatry. For the purposes of the study, high potency was defined as having 10 percent THC or higher.

There are also reports of a rise in cannabis hyperemesis syndrome, a complication of high potency cannabis use that leads to abdominal pain, nausea and repeated vomiting. A Canadian study found that emergency department visits for the syndrome increased 13-fold from 2014 to 2021.

Ebel says concentrated cannabis products are largely unstudied and “pose new and alarming health risks.” Hurd says that because we don’t know the full impact on health from high potency products, users are essentially the test subjects.

So as with other substances, public health officials recommend that parents talk with their kids about the risks of cannabis use. Especially with indications that teens are turning to cannabis to self-medicate, “if you notice a change in your child’s behavior, try to find out what’s going on,” Young-Wolff says. It’s also important for parents to consider the messages they send about marijuana, she says. The clinicians Young-Wolff has talked to have noticed that parents are using cannabis more and that they’ve become more permissive about teen cannabis use. “That can really make it hard to get this message to the kids to not use,” she says.

So, for adults who are taking part in the new legality of marijuana: “If you are going to use cannabis,” Young-Wolff says, “don’t use in front of your children.”