- All articles

All articles

- Taxi Drivers Rarely Die of Alzheimer’s—How Complex Mental Maps and Spatial Reasoning Protect Your Brain

- New Observatory Captures More Than Half a Million Galaxies in a Single Image

- Inside the Not-So-Dumb Head of the Dodo Bird

- Viagra May Slow the Spread of Cancer

- This Paradoxical Desert Landscape Is Filled with Fresh Water

- Depression Linked to Shrinking Brain Region in Older Adults

- Could Physics Help Us Solve the Mystery of Aging?

- Pesticide Exposure at Work May Increase Motor Neurone Disease Risk

- Financial Struggle Can Age Your Brain

- Life Originated Twice on Earth

Neuroscience

Taxi Drivers Rarely Die of Alzheimer’s—How Complex Mental Maps and Spatial Reasoning Protect Your Brain

Working with and living in spatially complex environments may help delay cognitive decline, though more research is needed

By Hatim Sharif

7:00 AM CDT on August 9, 2026

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Taxi and ambulance drivers are less likely than workers in almost any other job to die of Alzheimer’s disease. That was the surprising result of a 2024 study examining the death certificates of nearly 9 million people in the United States.

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These findings stopped me in my tracks because those two jobs rely on the same thing as my own work: maps.

I have spent more than two decades staring at maps. Not paper maps on a wall, but digital ones with multiple layers: flood boundaries draped over census blocks, car crash hot spots plotted against road geometry, and satellite readings of rainfall stitched across river basins. Much of my work as a civil and environmental engineer is done through GIS—that is, geographic information systems. Engineers like me hold several spatial relationships in their minds at once, reasoning about where things sit relative to one another across scales ranging from a city block to a whole watershed.

I always assumed that spatial reasoning across map layers was purely professional. But that study on taxi and ambulance drivers made me wonder whether all that mental work might be doing something good to the brain.

Taxi driver brains

Of the 9 million death certificates from January 2020 to December 2022 that researchers examined, taxi and ambulance drivers had the lowest risk of dying from Alzheimer’s disease out of 443 occupations. After adjusting for age, sex, race, ethnicity, and education, roughly 1 in 100 taxi and ambulance drivers died of Alzheimer’s, compared with 1 in 60 people overall.

This pattern did not extend to other driving jobs. The researchers concluded that the key to reducing the risk of Alzheimer’s was not driving itself but continuous real-time navigation: the constant work of locating yourself in space, tracking a destination and updating a mental map as conditions change. Drivers whose jobs relied on fixed or predetermined routes, like bus drivers and aircraft pilots, didn’t seem to experience a similar advantage.

Researchers believe the association between navigation-heavy work and lower Alzheimer’s risk centers on the hippocampus, a part of the brain that governs memory and spatial navigation. It’s one of the first brain regions that Alzheimer’s damages: Problems with spatial navigation and orientation are among the earliest signs of the disease, sometimes surfacing before obvious memory loss.

In one landmark 2000 study, neuroscientists compared the brains of licensed London taxi drivers with those of people who did not drive cabs. Their findings provided the first evidence via structural imaging that regions of the adult brain can measurably change under sustained navigational demand. To earn a license, London cabbies must memorize more than 25,000 streets within a 6-mile radius of Charing Cross, a challenge known as “The Knowledge” that takes three to four years.

Credit: Channel 4 Entertainment / YouTube.

The researchers found that London taxi drivers had measurably more gray matter in the posterior hippocampus, a brain area tied to storing large-scale spatial maps. That volume tracked with experience: The longer someone had driven, the larger that part of the brain. The change was built through practice, not inherited. While people who are good at navigation might gravitate to this kind of job, the job itself does have an impact on the brain.

Together, these two studies make a coherent case: Work that intensively exercises the hippocampus may reshape it, and that reshaping may protect against one of the most feared diseases of aging.

Where map specialists fit in

Cartographers, urban planners, and geospatial analysts spend their working days in sustained spatial reasoning. A geographic information system specialist might use a computer to overlap population data on flood exposure maps to find who is at risk, or read satellite imagery to map land cover after a wildfire. Researchers juggle several layers of data, coordinate systems, and scales at once.

Does spatial reasoning through a screen engage the hippocampus the way moving through a real city does?

While a taxi driver navigates from inside the scene at street level, GIS researchers picture space from above as a map—what cognitive scientists call allocentric reasoning. But these two perspectives overlap in the brain: The hippocampus also builds maps from outside viewpoints, not just from a navigator’s own position.

Research on cognitive maps points toward the same conclusion as the study on taxi drivers. In 2023, researchers ran a machine learning model on more than 22,500 people in a national dataset and were able to predict which ZIP codes had higher rates of Alzheimer’s with 84 percent accuracy based on how complex the environment was. Those living in spatially complex surroundings—the kind that force active map building, such as dense street networks with numerous intersections, diverse points of interest and landmarks, and multiple path options—were less likely to develop Alzheimer’s.

MENTAL MAPS: Living in spatially complex places challenges your brain. Credit: william87 / Adobe Stock.

A follow-up study tied geospatial complexity in one’s environment to greater volume in the brain’s spatial navigation regions. The researchers hypothesized that routinely building cognitive maps exercises the very circuitry that Alzheimer’s attacks first. Repeatedly engaging the cognitive systems involved in spatial navigation could help delay symptoms of disease.

However, these two studies focus on where people live, not the work people do. Whether spatial reasoning through a screen exercises the same circuitry as real-life city navigation remains untested.

Protecting your brain

The implications of whether sustained spatial reasoning protects the brain reach beyond mapmakers and cab drivers. Studies have repeatedly found a link between mentally complex occupations and delayed cognitive decline and lower dementia risk, even after accounting for education.

Research on cognitive reserve—the brain’s capacity to continue functioning despite disease—can help explain why two people with a similar disease burden can show markedly different levels of cognitive impairment. If demanding spatial thinking protects the brain, then how societies design schooling, professional training, and retirement all become questions of brain health.

Spatial reasoning can be trained, and training opportunities are already widespread. GIS and remote sensing instruction are available through geography, engineering, public health, and environmental science programs worldwide.

If sustained engagement with spatial reasoning can help the brain strengthen the circuitry that Alzheimer’s attacks first, its value reaches well beyond the technical skills it builds.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Lead image: Tasnuva Elahi; with image by THANANIT / Adobe Stock

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Hatim Sharif

Hatim Sharif is a hydrologist and professor of civil and environmental engineering and construction management at the University of Texas San Antonio. His research areas include modeling flood hazards, extreme rainfall and water storage.

Astronomy

New Observatory Captures More Than Half a Million Galaxies in a Single Image

The Vera C. Rubin Observatory is off to a fantastic start

By Jake Currie

9:00 AM CDT on August 8, 2026

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At the heart of Chile’s Vera C. Rubin Observatory is the largest camera human beings have ever built. Around the size of a small car, this behemoth weighs more than three tons, and the images it captures are even more impressive—to display the 3,200-megapixel pictures in their full glory would take hundreds of ultra high-definition screens.

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Since it came online in 2024, the Rubin Observatory has been using this extraordinary camera to survey the southern sky as part of its 10-year mission to create a time-lapse record (dubbed the Legacy Survey of Space and Time). Now it’s taken a series of photographs of a region of the night sky known as the Cosmic Evolution Survey Deep Field (COSMOS field), capturing over 650,000 galaxies and more than 75,000 stars.

ACROSS THE UNIVERSE: This video was created by panning and zooming in on a series of stitched-together images of the COSMOS field captured by the Rubin Observatory. Video by NSF–DOE Vera C. Rubin Observatory.

This exceptionally galaxy-rich region was first photographed by the Hubble Space Telescope in 2003. Since then, the COSMOS field has been investigated by telescopes around the world capable of viewing the area in wavelengths that stretch beyond the visible spectrum in both directions.

The are two reasons the Rubin Observatory is turning its attention to the well-studied COSMOS now. First of all, the large number of prior observations makes the region a good reference target to compare measurements from the relatively new telescope. In fact, the image was released as part of an early preview of Rubin’s data. Secondly, Rubin is going to be studying this region extensively during its 10-year mission to contribute a little texture to those other observations, most notably adding the dimension of time.

Read more: “Creating a Cosmic Movie”

“The COSMOS deep image is just the beginning for Rubin in this region,” Rubin Observatory director Bob Blum said in a statement. “Repeated visits to the field over the next few years will demonstrate the power of our survey design for discovery by providing our science community with a huge number of transient and variable objects like supernovae and other explosive transients for follow-up and detailed study.”

In the meantime, it’s certainly off to quite an auspicious start.

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Lead image: Rubin Observatory / YouTube

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Jake Currie

Jake Currie is a writer based in Brooklyn, NY.

Zoology

Inside the Not-So-Dumb Head of the Dodo Bird

Cranial scans reveal a brain with clever sensory adaptations

By Devin Reese

7:00 AM CDT on August 8, 2026

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Dodo birds got a bad rap from the very start. When European sailors landed on the Indian Ocean island of Mauritius, they thought it looked foolish waddling around on the ground with little fear of humans. Thus, they could only think to call it one thing: a “dodo.” Even Linneus in 1766 classified it as Didus ineptus.

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Granted, it was the size of a turkey and completely flightless despite its wings. But a recent study published in the Zoological Journal of the Linnean Society shows that dodos weren’t as inept as they appeared.

Led by researchers at the University of Lethbridge in Canada, the study explored the sensory abilities of the dodo (now classified as Raphus cucullatus), which went extinct in 1662. To do so, they scanned three dodo skulls housed in natural history museum collections in Denmark and the United Kingdom. Two of the specimens constituted the only complete dodo skulls found to date, the internal cavities of which revealed contours of the dodos’ brains.

Read more: “How History Did the Dodo Wrong”

“Although the dodo’s brain disappeared centuries ago, it left an imprint on the inside of the skull,” explained study co-author Christy Anna Hipsley from the Natural History Museum Denmark in a press release. “By digitally reconstructing those spaces and comparing them with the brains of living birds, we can begin to piece together how the dodo sensed, behaved, and interacted with the world around it.”

Pigeons and doves (order Columbiformes) are the dodo’s closest living relatives, and therefore, a relevant comparison point. By comparing the dodo’s brain imprints with those of 36 living Columbiformes, the researchers found the forebrains, which handle memory and cognition, to be proportionately similar in size. Pigeons have remarkable cognitive abilities, such as long-term image recognition; so, the behavior of dodo birds that wobbled over to 16th-century sailors may have stemmed more from their predator-free history than any lack of intelligence.

One distinction of dodo brains was their smaller optic lobes (more than 3.5 times tinier than those of pigeons), indicating vision that works in low light (for example, dawn, dusk, and the dead of night). Furthermore, the high-domed skulls of dodos were reminiscent of certain owls. Their olfactory bulb imprints also hinted at keen senses of smell that, coupled with a pronounced upper beak for probing their surroundings, would have supported low-light activity as well.

Nothing dumb about that.

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Lead image: Roelant Savery / Wikimedia Commons

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Devin Reese

Devin Reese is the executive editor of Natural History and a science writer based in Alexandria, Virginia.

Health

Viagra May Slow the Spread of Cancer

And statins can help

By Jake Currie

4:00 PM CDT on August 7, 2026

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Viagra was something of an accident. Developed by Pfizer, sildenafil was a promising drug to relieve chest pain and high blood pressure, but male test subjects noticed certain, uh, side effects. So the drug company went with it, giving it the brand name Viagra and the rest is history. Now sildenafil might have another use preventing the metastasis of cancer cells, according to a new study published in Cancer Research.

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Sildenafil works by blocking the activity of phosphodiesterase type 5 (PDE5), an enzyme that breaks down cyclic GMP (cGMP), a second messenger involved in a lot of cell functions that also relaxes blood vessel walls. With PDE5 inactive, cGMP accumulates, your blood vessels dilate, and you’re off to the races (so to speak).

Researchers led by a team from the Weizmann Institute of Science in Israel treated mouse and human cancer cells (cultured from a variety of cancers) with sildenafil and monitored what happened. They discovered cGMP has a side hustle, just like sildenafil. It binds to a protein that transports cholesterol in cells, which can be used to build cell membranes. These membranes come in handy for cancer cells when they’re striking out to seek their fortune in other parts of the body, and they’re particularly vulnerable to supply disruption from elevated cGMP activity, the researchers found.

Read more: “Can Cancer Be Treated by Changing Its Cells?”

The team also looked at 20 years of health records from more than 40,000 male cancer patients ages 35 to 65. Those who had filled prescriptions for sildenafil before getting a cancer diagnosis had a 26 percent higher survival rate five years out. Combining sildenafil with statins, which also reduce cholesterol production, increased the five-year survival rate to 32 percent.

“We have uncovered a new biological pathway that links a well-known signaling molecule to cholesterol regulation within cells, and shown how this pathway can be harnessed to interfere with the ability of cancer cells to form metastases,” study author Ayelet Erez said in a statement. “Beyond their therapeutic promise, our findings highlight that cancer biology is shaped not only by mutations in tumor cells but also by the patient’s metabolic state and by medications they’re already taking for other conditions.”

It’s yet another reason to take the little blue pill.

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Lead image: KeronnArt / Adobe Stock

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Jake Currie

Jake Currie is a writer based in Brooklyn, NY.

Environment

This Paradoxical Desert Landscape Is Filled with Fresh Water

Dunes and lakes as far as the eye can see

By David Nield

3:00 PM CDT on August 7, 2026

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To fully appreciate the spectacular contradictions of Lençóis Maranhenses National Park in northeastern Brazil, you really need to see them from above—namely, from images taken by the NASA Landsat 9 satellite.

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What makes the region such a paradox, as these shots show, is that it mixes vast sandy dunes with an astounding number of freshwater lagoons. Basically, it’s a desert with an oasis everywhere you turn.

COMPLEX ECOSYSTEM: The dunes in Lençóis Maranhenses National Park, which you can see in the tan section of this photo, are surrounded by ocean and forests. Within the dunes, the many lagoons can be seen as a subtle pattern of what look like blue specks in the tan. Image by NASA Earth Observatory/Michala Garrison.

The dune fields cover some 350 square miles, approximately the size of New York City, and the dunes themselves can reach heights of nearly 100 feet, pushed across the terrain by blustery trade winds from the east during the dry season.

Adding to this surreal landscape is the supply of quartz sand, which has built up over hundreds of thousands of years and been pushed and pulled by changing sea levels. Then there’s the rain—around 50 inches per year, or a little more than you could expect in Seattle and more than double San Francisco’s annual allowance.

Read more: “The Amazing, Autotuning Sandpile”

The dunes, surrounded by the mangrove and restinga forests that make up the rest of the park, are also right in the middle of three distinct biomes in Brazil: the Amazon rainforest, the Cerrado savanna, and the shrublands and forests of the Caatinga.

All of those factors contribute to the dramatic images you see here, captured last month when the lagoon levels peaked. Of note as well are the eye-catching shifts in lagoon colors, caused by different depths of water, and the buildup of sediment, algae, and dissolved organic matter.

SAND SHUFFLE: The conveyer belt of dunes is slowly expanding to the west. It moves about 13 to 82 feet each year, which sounds slow, but is pretty fast for dunes. Image by NASA Earth Observatory/Michala Garrison.

Home to more than 850 species, the park was declared a UNESCO World Heritage site in 2024, and NASA’s satellites are keeping a close eye on it. The dunes are traveling west at a rate of 13 to 82 feet per year (a fair clip for dunes), and the dune field as a whole has extended westward by nearly a third of a mile over the last two decades.

Satellite imagery also helps explain the park’s name: In Portuguese, Lençóis Maranhenses means “the bedsheets of Maranhão”—an apt description of how these dunes and lakes appear from the sky.

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Lead image: NASA Earth Observatory / Michala Garrison

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David Nield

David Nield has written about science and technology for more than 20 years. His work has appeared in a wide range of publications, including Wired, Popular Science, The Guardian, and Gizmodo.

Neuroscience

Depression Linked to Shrinking Brain Region in Older Adults

The memory center of the brain show signs of decreasing volume

By Jake Currie

1:00 PM CDT on August 7, 2026

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No one knows what causes Alzheimer’s disease. There are plenty of risk factors associated with the neurodegenerative disease, like inflammation, smoking, and genetics, but so far no single culprit has emerged. A new study published in Translational Psychiatry, however, investigated the link between Alzheimer’s and another risk factor, depression, leading to some surprising results.

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Neuroscientists led by a team from the University of Southern California analyzed high-resolution MRI scans from more than 2,000 healthy adults between the ages of 50 and 90. Around a third of them (630) had been diagnosed with depression, and these subjects showed a significant decrease in volume in their hippocampus. The entire hippocampus wasn’t affected, though, just a smaller subfield responsible for retrieving memories, reconstructing memories from partial information, and distinguishing between similar experiences.

BRAIN CHANGES: Atrophy in a specific part of the hippocampus has been observed in both adults with depression and adults with Alzheimer’s disease. Image by Stevens INI.

“This study shows why it’s important to look beyond the total size of the hippocampus,” study co-author Meredith N. Braskie said in a statement. “Depression wasn’t related to smaller volume throughout the entire region. The association was concentrated in a particular set of subfields, giving us a more precise picture of how depression may relate to brain health during aging.”

To investigate the link to Alzheimer’s, the team used PET scans to look for the telltale buildup of amyloid and tau proteins in the brain. They also factored in whether the subjects carried the APOE ε4 gene, another risk factor for the disease. Somewhat surprisingly, they found that none of these factors were related to the relationship between depression and the shrunken hippocampal regions.

Read more: “Can You Overdose on Happiness?”

While that might seem like an anticlimactic result, the study sheds light on what’s going on in the brains of older individuals who suffer from depression, and that could prove to be an important part of the Alzheimer’s puzzle. Or as study co-author Arthur W. Toga explained, “Understanding how depression relates to specific memory systems may help researchers identify people at risk, clarify the pathways connecting depression and dementia, and ultimately guide more personalized approaches to protecting brain health.”

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Lead image: Orapun / Adobe Stock

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Jake Currie

Jake Currie is a writer based in Brooklyn, NY.

Physics

Could Physics Help Us Solve the Mystery of Aging?

Some scientists say the answers may lie in thermodynamics and other mathematical principles

By Kristen French

11:00 AM CDT on August 7, 2026

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Why do some giant sea creatures live hundreds of years, while small land animals such as insects may live only a matter of months? Why does a living thing’s ability to overcome wear and tear generally decline over time?

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These and other questions about the nature of aging remain deeply mysterious even to those who have studied them for decades. But physicists think they might have some quantitative tools that can help.

A few months ago, some 160 scientists across physics, biology, and medicine met in Singapore for the first ever global conference on the physics of aging, or gerophysics. It’s a niche discipline whose first glimmerings arose in the 1960s but that is only now coming into its own. The scientists gathered in Singapore talked about how to develop a predictive and testable science of aging using certain concepts such as thermodynamics and network theory. Together, they intend to establish mathematically precise definitions of terms like aging and healthspan and to find simple mathematical principles that can explain the complex processes that contribute to longevity.

I spoke with Max Unfried, a research fellow at the National University of Singapore's Centre for Healthy Longevity, and one of the organizers of the gerophysics conference as well as a founder of the field itself about the maximum lifespan of humans, why bears and bats may unlock the secrets of successful aging, and the importance of thermodynamics to the future of medicine.

What does physics have to do with aging?

One thing is that biology cannot make its own rules. Everything has to obey the laws of physics. The fundamental processes that occur when a star dies are probably also relevant when a human or other organism dies. Currently gerontology is primarily described in terms of biology. You have your genes, you have your proteins, and these things change with age. If you’re a physicist, you might describe that process in different ways, perhaps in terms of thermodynamics.

Physics can also bring questions of systems stability or instability to the conversation. Does an unstable system increase mortality? If you combine this with the biological way of thinking, you might notice that genes, proteins, and lipids change in a linear fashion with age. But as these molecular components change in a linear way, a person’s mortality risk and rate of disease goes up exponentially. One question is, how can a bunch of linear processes create something exponential? That’s probably not a question biology by itself can answer, because you have emergent phenomena, new dynamics that need explanation. Some fundamental laws of physics might help.

Why do you think this field of gerophysics is only coming together now?

The first paper in the field was published in the 1960s, which attempted to use statistical physics to describe aging. Over the past 65 years, you had individual attempts to bring a little bit more of physics thinking into the field of aging biology and gerontology. But it never reached a critical mass. Some scientists in Germany and the United States did a little bit, and these efforts got attention, but the ideas never spread. Then, in the past 10 to 15 years, we slowly have more physicists coming into the aging space, people thinking more about network dynamics.

Three years ago, I started a workshop at one of the large aging meetings, and people liked it, so we started a conference. And now we finally have people that understand each other, a peer group. Not physicists, and not biologists, but gerophysicists. These are people that come from physics, engineering, and mathematics, who share a fundamental language of mathematical modeling and physics thinking and are applying it to aging biology. Within physics there are different subdisciplines: Some people come from a thermodynamic lens and think more about entropy, and other people come from a stability science perspective. Still other people study network science and want to understand how network connectivity is lost in aging and what that means for resilience. Now they can all talk to each other and discuss those ideas and get feedback.

A lot of predictions that gerophysics makes are probably not what biology would have expected, which probably has relevance for how we measure aging and how we target aging with treatments.

Read more: “The Longevity Skeptic”

Why would biologists not have expected some of the predictions that gerophysicists make?

There are a few areas where physics has surprising things to say about aging: maximum lifespan and stable versus unstable lifespan.

Let’s start with maximum lifespan. For humans, it’s around 120. It’s just like a barrier that can’t be crossed. But if you had 10 times more humans or 100 times more humans, would we actually see humans live until 200? We just don’t know. Biology can’t answer that question. But physics models like the stress response model collapse at around 120 or 150 years of age, which gives you an indication that this is probably the limit for human lifespan with our existing blueprints. Humans just won’t be able to live to 300, even if we had infinite humans. For most people, the max is 110, 115, and the people who live to 120 are extreme outliers.

The second thing is work from the Uri Alon group at the Weizmann Institute of Science, who modeled different animals according to their “stability,” and found they come in two broad categories: stable animals and unstable animals. Unstable animals decline more rapidly toward death. Stable animals live in a state of equilibrium for longer and die later.

Assume you have a U-shaped bowl that represents resilience. And in that bowl, you have marbles, and they roll around in there, which represents your daily fluctuations of blood pressure, heart rate variability, and glucose levels. In a stable animal, the marbles all roll around in there, but they don’t fly out of the bowl. Now, assume that aging erodes the bowl, making it flatter. Now, those marbles, as they change, are much more liable to exit. The flatter the bowl, the less stable it is, and the more likely the animal is to develop disease and die. Ecology has similar analogies for how ecosystems fail.

What’s an example of an animal that’s stable versus an animal that’s unstable?

Luckily, humans are fairly stable animals. That’s why we live a long time. Our diseases come only in late age. Most of them appear around 50 or 60. The problem is that most of the animals we use in the lab are unstable: mice, drosophila, C. elegans. That’s why mice are very short-lived. They usually all get cancer. This makes them good for cancer research, but not good for longevity or aging drug trials, because all the things that you modify in a mouse aren’t relevant to human aging. But the entire academic biomedical ecosystem depends on mice, so what the field has to do is find the shortest-lived stable animal that we can use to test our theories and drugs. That’s going to cost more money and require new infrastructure.

Lifespan stability has implications for drug targets. Returning to the bowl, our current drugs address the marbles, but physics might aim to treat the shape of the bowl instead.  Targeting the marbles might give us up to 15 years of additional healthy life, which is pretty good. But it’s different from trying to increase maximum lifespan. To change maximum lifespan you have to target the bowl, which increases your resilience. This resilience is related to thermal fluctuations, entropic damage, random damage, whose root cause is life itself. It’s not possible to target the damage caused by thermal fluctuations because they’re random and uncorrelated. If we were to cure all those fluctuations in the marbles, but do nothing about this thermal damage, you’d get a 110-year-old without diseases who still died. They wouldn’t have any cancer. They won’t have Alzheimer’s. Their brain will work. They’ll be super fit for their age. But they’ll still be frail.

If aging obeys physical laws the way that falling objects obey gravity, does that mean that it’s inevitable in the same way?

Inevitable is a hard word. Most things age. You have a few creatures, those long-lived animals that show negligible senescence, where mortality doesn’t increase with age. Humans follow an exponential trajectory called Gompertz law, where your risk of dying doubles every eight years. A few creatures, like the naked mole-rat, seem to have a constant mortality rate. Trees have a constant mortality rate in most cases. There seems to be something that doesn’t increase mortality in these cases.

The issue is, all those organisms are living systems that are far from thermodynamic equilibrium. We’re not talking about normal thermodynamics—we’re talking about non-equilibrium thermodynamics in dissipative systems. They have to spend or dissipate energy to keep local order in the organism. If aging is fundamentally caused by this entropy, a universal tendency of everything to break down, then maybe aging itself is a kind of universal force, similar to gravity.

Then the argument is that nature found some tricks, some genetic blueprints, to extend life. And the question is, can nature build something much better than that, especially in living systems? Currently, the longest-lived animals are 200 to 400 years old, so it seems to be possible to live that long for some animals, but this comes with certain side effects, and almost all of the long-lived animals reside in cold water, which results in fewer thermal fluctuations and less entropy.

Maybe if you want to live to 200 years, you have to become a whale and find solitude in the deep ocean. Or maybe we can learn something from the long-lived animals. Maybe we can find genes or proteins that, if we have enough of them, can provide additional lifespan. Maybe we have to go into germline editing. It would be too late for people already alive, but we can edit the future in the germline to make newborns more stable across their lifetimes.

You mentioned one big question the field is trying to answer is how can a linear molecular process lead to a compounding death rate. What are the other big questions that the field is interested in answering?

Currently, we have 200 or 300 theories of aging. It’s telomeres one year. It’s reactive oxygen species the next year. It’s something else the year after that. In a way, all those theories have linear effects, but none of them fully explains aging. If you have hundreds of theories, nobody really understands it, and probably each of them is partly true. But physics can tell you how all those different linear aging theories fit together.

But what other open questions are there? Some things are far from settled. We currently have two popular models that describe the stability of mortality, and they’re approximations. I hope they’ll get better in the future. I also hope that stochastics will come more into the aging space. We’re exploring that. One area that’s really coming in more is from thermodynamics—especially the subfield of stochastic thermodynamics, which is very interesting. It’s not a mainstream field yet.

About 30 years ago or so, people in the physics community started thinking: “Okay, thermodynamics really deals with microscopic objects. It’s like all your gas atoms in a box.” Stochastic thermodynamics asks the questions of what happens to thermodynamics on a small scale where fluctuations matter. They started figuring out certain equations that give you ideas of entropy at a small scale, which is where a lot of our molecular damage lives. This field is currently heavily focused on thermodynamic computing. Silicon Valley is building companies on that, and many of those people work on quantum computing.

You could look at biology as just information being delivered between different proteins and molecules. Does the thermal noise make distorted signals, and how does this change with age? This has to be figured out, and this has to move into biology and aging biology.

I believe the future of medicine will be thermodynamic. This is very long term. I’m talking 50 to 100 years. Currently, biomedicine is very crude. It tries to modulate biology on the physiological level, but you take a drug and it hits multiple targets at once. We don’t even really understand which target it hits. We kind of hope it’s the one, but we need much more precision. Physics could help us deliver precise energetics to precise locations in the body. But we need much better tools to study a lot of those things, because we don’t have the instruments that could measure some of those things, especially in biological systems.

Another question is around the fact that there seems to be this plateau at old age. Very old people above 100 or 110 have a constant mortality rate. It’s a high mortality rate. You have a 50-50 chance of dying every year, compared to the doubling of your mortality risk every eight years before that. Maybe physics can help us explain why, as well as what really makes certain people age faster than others. There’s a lot of variability. Also, what impact did evolution have?

This recent paper about the impact of somatic mutations on lifespan, which was published a few weeks ago, got some traction. It tried to answer how much extra lifespan would we get if we eliminated all somatic mutations, which are changes in the DNA of a body cell that happen after conception. And at what age does it really become relevant? We should be able to rank what we should target and say, “Well, you know, if somatic mutations only start killing us at around age 150, maybe we can put them off a little bit?” We could focus instead on what kills us at age 110—or earlier.

Read more: “This Is Life at 400”

What kind of research do you think is most pressing right now in gerophysics?

From a drug development perspective, and a pragmatic perspective, the best way forward currently is to figure out what we can learn from longest-lived animals and try to see if we can implement it in humans. Let’s be inspired by nature. It’s probably an easier task than to try to develop something from scratch.

Is there one animal in particular you think is most promising in that regard?

I probably would put my hope into bats. They’re one of the largest groups of mammals, the second largest group after rodents. There are more than 1,500 species of bats. That’s the first thing. The second thing is that there are a lot of bats that live vastly longer than their body size should predict. A lot of bats are the size of a mouse or smaller, and some of them live up to 40 or 50 years. That’s quite impressive. And then, what we know is that they’re very good with pathogens. They’ve got enhanced immune systems that allow them to live with a heavy viral load.

The immune system plays a big role in human aging. If we could learn how bats control their immune systems so that they don’t spike into cytokine storms—maybe we could improve the human immune system. That probably helps with cancer and viruses and a lot of other things.

The naked mole-rat is also very fascinating. Similar story. It’s a very small animal, very long-lived, very cancer-resistant. And then, bears and other hibernating animals are very interesting. If a human were to do what a hibernating bear does, they’d have to go to the doctor: Half of the year, you binge eat, and the other half you just lay around and don’t eat at all. It’s like a seesaw between obesity and anorexia. If a human laid around like a bear, they’d get thrombosis. The bear wakes up, and they’re kind of good to go.

I’ve just started a new research organization on this subject called the Thalion Initiative. To study these things from a physics perspective, you need data. Right now we don’t have enough data for all of those animals where we could say, “Are they stable? Are they unstable? How fast do they age?”

What we’re trying to build is like a CERN for aging biology, a biomedical mega-project that focuses on aging biology, and especially on the things that nature already figured out. We want to build this super large dataset of over 200 different species. For each of the species, get many specimens across every age group, from young to old, and then measure everything that we currently are able to measure: the genes, transposomes, the methylomes, the proteomes, lipidomes, and inflammation markers. Then we could see molecular changes across evolution, across animals, and see what controls lifespan, what gives them stability.

We know that complex systems become better through stress and noise, so we probably should observe modularity and resilience in longer-lived species.

You just held the inaugural conference for the field earlier this year. One of the focuses of the conference was using artificial intelligence to screen compounds for longevity effects. Why is AI a useful tool in this space?

Biology is always in a very high-dimensional space, and what AI is really good for is compressing everything into a few variables. It can take all those features of biology and, for example, put all of the inflammatory molecules into a single effective variable, all the heart-related ones into another, which is helpful for some physics modeling.

But it also depends on data, and there’s a lot of unstructured data in biology. Some of it is good for simple modeling, but other data isn’t good enough for AI yet, so we need approaches that collect more data to make AI useful.

Could physics help us separate lifespan from healthspan or sickspan?

Yes, it can, and that’s probably the strongest thing it offers right now. The marbles are probably the healthspan, and the bowl is the maximum lifespan part. Realizing those are two different things is an important starting point. Because two different species can have vastly different maximum lifespans, but can have similar diseases. A human and a mouse both get cancer but the humans have a maximum lifespan 40 times longer. That probably tells you the biology is somewhat different. Maximum lifespan is probably subject to a bunch of other evolutionary constraints. It probably also tells you why, for instance, caloric restriction has a lot of benefits in mice but probably won’t have much benefit in humans.

It will be important to bring evolution back into the biology of aging, because while evolution is the central dogma of biology, it gets ignored when it comes to drug discovery. We have cancer therapies, and if you only give one cancer drug to a person, the cancer becomes resistant. If you throw different drugs at the cancer, it’s actually more likely to die because it cannot adapt to all of them. That’s basic evolutionary thinking, but something like that holds for aging as well.

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Kristen French

Kristen French is an associate editor at Nautilus. She has worked in science journalism since 2013, reporting and writing features and news for publications such as Wired, Backchannel, The Verge, and New York Magazine. She has a masters degree in science journalism from Columbia University.

Health

Pesticide Exposure at Work May Increase Motor Neurone Disease Risk

A new review looked at 1,734 people with ALS. But it couldn’t separate pesticide from other risk factors, such as head trauma.

By Rachel Tan

9:00 AM CDT on August 7, 2026

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Being diagnosed with amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, can be devastating.

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ALS is the most common form of motor neurone disease, a neurodegenerative condition that affects people’s ability to speak, eat, breathe, and swallow. It is debilitating and progresses rapidly: on average, people survive just 2 to 3 years after a diagnosis. Most people are diagnosed between the ages of 40 and 70.

A new study, published earlier this week, has found that being exposed to pesticide at work can increase the risk of developing ALS by 61 to 71 percent. The study brings together the findings of eight other studies—but not all of them assess risk in the same way. Here’s why we need to interpret the findings with caution.

What we know about ALS causes

Men are around 20 percent more likely to develop ALS than women.

The disease occurs sporadically in over 90 percent of patients, meaning the large majority have no known family history or identified genetic cause. The remaining 10 percent of cases are familial, meaning the person has a known genetic variant or family history of ALS.

However, it’s not well understood exactly what triggers both the sporadic and familial forms of the disease, although an interaction between genes and environment is likely.

Over the last few decades, researchers have been investigating exposure to pesticides as a possible trigger.

Several studies have found associations between being exposed to pesticides and a higher risk of developing ALS. However, a causal relationship has not been established.

What the new study did and what it found

This new study pooled data from eight separate studies, five from the United States, one spanning Canada and France, one from Italy, and one from Australia.

It asked a simple but important question: Does having ever being exposed to pesticides at work raise someone’s risk of developing ALS?

The answer, based on this combined analysis, was yes.

Overall, people who had ever had any exposure to pesticides (including fungicides, herbicides, and insecticides) at work were 61 percent more likely to develop ALS, compared to those who hadn’t.

Pesticide exposure appears more strongly linked to ALS risk in men than in women in this analysis. But the evidence is too limited to know whether this reflects a true biological difference, or gaps in how exposure was measured for women.

The risk was slightly higher with exposure to herbicides (a type of pesticide), which was associated with a 71 percent heightened risk of developing ALS.

ALS affects an estimated 8 in every 100,000 Australians. So a 61 to 71 percent increase would mean a small number of new cases.

But these numbers don’t reflect how devastating and debilitating this disease is for families and communities affected by ALS. There is currently no cure.

But here’s why we should be cautious

This review was able to assess the link between pesticide and ALS in a large sample, by combining 1,734 ALS cases across the eight studies. This is more than any single study could provide alone.

But combining studies in this way inevitably introduces some inconsistencies, as each one has been conducted independently, using different methods. So it’s hard to control for the differences.

Several of the studies in the review found a link between developing ALS and other separate risk factors, such as head trauma or being exposed to other kinds of toxins. But the analysis couldn’t fully disentangle these risk factors from pesticide exposure. This means we can’t tell how much someone’s exposure to pesticide contributed to them later developing ALS, or whether it was due to the other contributing factors too.

One study also assessed military veterans exposed to Agent Orange, a herbicide the United States used as a weapon during the Vietnam War. This kind of exposure is likely quite different to typical occupational pesticide exposure today. But the new review didn’t assess this separately.

Most of the included studies also relied on self-reported exposure, meaning participants had to recall and estimate how much pesticide they’d likely been exposed to. These studies tended to show a stronger link between pesticides and ALS than studies that independently measured exposure.

As the authors of the new study noted, this means recall bias may have played a role. People who already have ALS, or who already suspect a link between pesticides and the disease, may be more likely to remember and report being exposed to pesticides.

So, what does this all mean?

Overall, the study supports the case that being exposed to pesticide at work increases your risk of developing ALS.

These findings highlight the need for more rigorous research into the specific details. We need to understand which chemicals or pesticide ingredients may be responsible, and whether the risk is related to dose. This means understanding whether being exposed to pesticides over a longer time, or at a higher dose, might further increase your risk.

Someone’s risk of developing ALS is likely influenced by a combination of factors, including genetics and environment.

The way multiple exposures to risk factors accumulate and interact over a person’s lifetime may also play a role; for example, if you work with pesticides every day and have also been exposed to other toxins, had a severe head injury and/or a have genetic predisposition.

This is known as a “multistep” model of disease development and it isn’t currently possible to determine someone’s personal risk profile with precision.

The picture is still evolving. More evidence will help regulators and employers make better decisions about safe exposure levels and potential risk mitigation strategies.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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RT

Rachel Tan

Rachel Tan is a neuroscientist based at the Brain and Mind Centre at the University of Sydney. She is a current FightMND Mid-Career Research Fellow and a former NHMRC Fellow. Her research focuses on understanding the pathological brain changes that give rise to neurodegeneration in patients, with the goal of uncovering what goes wrong in the brain, and why these diseases develop and progress differently in each person, to advance biomarker discovery and targeted interventions.

Health

Financial Struggle Can Age Your Brain

Persistent poverty can accelerate cognitive decline starting in your 50s

By Kristen French

7:00 AM CDT on August 7, 2026

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A series of overlapping crises has pushed many people living in high-income countries over the edge in recent years. A combination of rising inflation and weakened social services plus climbing longevity across Europe and the United States has meant that many adults are perpetually struggling to make ends meet. A record number of households in the United Kingdom, for example, are reporting financial adversity. This could be very bad news for public health.

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A massive new study led by researchers at University College London (UCL) suggests that people who experience either persistent money struggles or persistent low income in early and middle adulthood may face worse cognitive performance at the age of 53, cognitive decline from ages 53 to 69, and worse brain health from ages 69 to 71.

The study, published in the journal Innovation in Aging, looked at data from 2,759 people in the U.K. who turned 80 this year and have been followed since birth in 1946. A subset of the people followed in the study, known as the MRC National Survey of Health and Development, or the 1946 British cohort study, also sat for brain scans. These links between financial struggle and cognitive aging remained even after accounting for factors that might have skewed the results such as childhood cognition, education level, and childhood disadvantage.

I spoke with corresponding author and UCL data scientist Jacques Wels about how financial hardship actually ages the brain, how the findings fit into the larger story about how society shapes our health, and how much control we have over our cognitive aging.

What inspired you to do this study now?

The department where I work is dedicated to aging research as it relates to a dataset called the National Survey of Health and Development, which for decades has tracked people born during a single week in 1946. This cohort turns 80 years old this year. It’s the oldest cohort in the U.K.

This group can offer a lot of information on aging, which is something that other large cohort studies don’t have because they include mostly younger participants. It’s one of the only studies where we can not only track people over their lifetimes, but also have brain scans, which allows us to look at the relationship between aging and brain health. In fact, we really want to thank this cohort of people. Without them, we wouldn’t be able to do this important research.

Read more: “What Do People Think About?”

You found that people with persistent financial hardship are more likely to have cognitive decline in their 50s and worse brain health as they progress into their 70s and beyond. What do you think is going on here?

One important thing is that most studies on cognitive decline focus on individual behaviors, whether you’re drinking, smoking, or behaving in other unhealthy or healthy ways. Alternatively, they focus on genes, like the APOE gene, that help to explain cognitive decline. We thought it would be important to go beyond these behavioral explanations or genetic explanations and look at what society does to your brain. What society does is to generate potential inequalities over a person’s lifetime, and most of the time these are economic inequalities.

Based on what you found in the study, is there something about the stress induced by persistent financial struggles that is different from other kinds of stress?

There’s a lot of debate about oxidative stress and whether stress can have an impact on inflammation, for example, but we didn’t address that. What we addressed is the accumulation of poverty over the lifespan, and what we observed at first after 50 and 60 years old in terms of cognitive decline, was a strong and statistically significant association. Now on the mechanisms, we can make assumptions. The first assumption is the one you mentioned: stress. The second one is cognitive load. When you’re really worried, you don’t have much time to sit on a bench and play chess with a friend. What you can think about with your brain isn’t the same when you struggle versus when you don’t struggle.

Are you saying that thinking about playing chess is better for your brain than worrying about money?

Yeah, that fits within the behavioral pattern, you know? There are even some studies that say that doing crosswords, and similar kinds of games, is good for brain development. If all of your time is spent worrying about money, you don’t have time to think about things that are fun. And thinking about fun is good for your brain.

Do you have a sense of where financial adversity would rank in the overall picture of risk factors for cognitive decline, like diet, exercise, and social isolation?

I don’t think we could rank them, no. We would need the proper statistical techniques. Don’t forget also that addressing these different variables over the lifespan is really difficult using this kind of study.

What we were able to do, though, is to look at childhood adversities. There are a few studies that show that what happens in your childhood explains what happens in terms of cognitive decline after 50. What we show in this study is that actually, this accumulation of poverty over the lifespan and its impact on brain health is independent of childhood adversity. So we go beyond the framework of childhood adversities, which is an important finding. It means that even if it was bad during your childhood, there’s still a possibility that if you have a chance to do better in life, your brain will not be affected as much.

But distinguishing between the different variables you mentioned, social isolation and loneliness, would be fascinating. That’s not something we did, so I wouldn’t be able to rank them, but I can say that the effect of persistent financial hardship is quite strong.

The cohort you were studying were all born in 1946 and lived through different economic conditions than people alive today. To what extent do you think the patterns would hold for, you know, Gen X or millennials?

It’s very likely that the pattern will hold, but the way this pattern spreads over the population might be different. In this cohort, most of the effects are observed among men and not so much among women, which is interesting. But we need to remember that it was really a male-dominated society back then, where the men were working more than the women.

In younger generations, men tend to be healthier, while women tend to be less healthy than they used to be. As a result, in these younger generations, we might actually observe a relationship that’s a bit stronger between financial hardship and cognitive decline among females and probably a bit weaker amongst males. But people who are younger than 50 aren’t old enough yet to see cognitive decline. We would see that in the near future.

Similarly, your study sample is all British and white and skews a bit healthier. Do you think that the findings for the U.S. or the global south would look significantly different?

I need to be very cautious here. My first answer is, I don’t know. My second answer is, it’s not so much about the brain measurements. That isn’t a problem and could be replicated across countries. But the experiences of poverty are going to be quite different, and the accumulation of financial issues over the life course might also be different in other kinds of contexts. In the case of the U.S., it might be a bit worse in terms of income inequalities compared to the U.K. Whether this accumulates over the lifespan, I’m not sure. I tend to think it does, so I’d say that maybe the link between persistent financial hardship and cognitive aging will be stronger in the U.S. But that’s a hypothesis. U.S. researchers should do the same study we did and tell us what they think.

On the global south, it’s a very important question, but it depends which country we’re talking about. It depends on the level of inequalities. It depends on employment regulations as well, because employment is a main driver of financial stability over the lifespan.

Yes, I imagine so many factors could play into this lifespan picture, including the way families are structured, the way social support works.

The potential role of the welfare state is something we didn’t address here. I’m not saying the welfare state is the answer to everything, but it definitely plays a role.

You pointed out something very interesting, which is that this cohort, although it’s a great cohort, is very white dominated. We don’t have information about ethnicity because the number of non-white people born in the U.K. in 1946 was small. But it’s a multidimensional process where low household incomes are associated with ethnicity a lot in some countries. Understanding how this accumulates would be interesting, but it’s too early to tell.

Read more: “We’re Killing Ourselves with Work”

You conclude that supporting financially vulnerable adults could potentially help prevent dementia. What kind of support do you think would be most successful?

It’s an interesting question. The study shows an association between long-term poverty and brain decline. So what is the answer? We need to tackle long-term poverty or at least provide more security to people. And then it’s about what kind of society we want to live in. I’m not the first one to say that. When you provide more security to people, they tend to be healthier, and they tend to live longer, and they tend to have fewer health issues, and they tend to cost less to society.

But one important thing is to understand the pathways better. You mentioned social isolation. We know that financial deprivation and poverty are linked to social isolation, and social isolation is linked to cognitive decline. So we would like to better understand how these different variables interact and accumulate over the lifespan, and understand the mechanism for how financial instability explains brain health. We need to understand that to act because just saying that we need to provide more security isn’t a good answer in terms of public policy. We also need to understand the mechanism.

How does this study fit into the broader conversation about social determinants of health?

The definition of social determinants of health depends on whom you talk to, but it’s basically the idea that it’s not only the behaviors and the genes, but it’s also the society that shapes your health. The value of this specific study is to establish a structural association between what you observe in the lab and something that happens later. The weakness of this study, to be absolutely transparent, is that we can’t explain why we observe those relationships. But this study is one of the first to establish a relationship that seems to be causal between financial hardship and cognitive decline. It was important to establish it. The next steps will be to try to explain why the relationship works the way it does.

Personally, I believe we need to be more critical of the social determinants of health framework. Yes, poverty is linked to poor health. We know that. But why? How? The point of the social determinants of health framework is to focus on the determinants. A determinant is something that determines, so it’s a deterministic approach, an approach from the 1950s. That’s what social science tried to avoid for more than 40 years.

My problem with the social determinants of health is that we treat people as subjects. They are subjects, and they are victims. They aren’t agents of their own destiny. Of course, we’re all both. We’re both subjects and agents. My question is, to what extent do people actually have something to say and to what extent can they contribute to changing society in one way or another?

We never pay attention to what actually happens within the workplace, for example, but the kind of work you do, the kind of employment contract you have, even how unions function, have a big impact on your health. A very bad paper on unions was published in the United States in 2020, with a weak methodology, but in general, unions are something that people never pay attention to. It’s really not “lefty,” what I’m saying, because unions could have a negative impact, and they do in some countries and for some specific groups. But we need to understand better the mechanisms at work and move away from a deterministic approach.

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Kristen French

Kristen French is an associate editor at Nautilus. She has worked in science journalism since 2013, reporting and writing features and news for publications such as Wired, Backchannel, The Verge, and New York Magazine. She has a masters degree in science journalism from Columbia University.

Evolution

Life Originated Twice on Earth

New research traces the origins of our metabolism back in time

By Jake Currie

5:00 PM CDT on August 6, 2026

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The evolution of life is an incredibly improbable event, and as far as we know, it’s only happened once in our solar system—or so we thought. According to a new paper published in Science Advances life has actually evolved twice, right here on Earth.

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Before life existed on our planet, the areas around hydrothermal vents in the ocean created the kind of primordial soup conducive to its evolution. But how did life emerge from the muck? To find out, an international team of researchers led by scientists from Heinrich-Heine University in Germany investigated the origins of the suite of chemical reactions life uses to, well, exist.

One “non-negotiable property of life,” the authors write, is our metabolism, the more than 400 complex chemical reactions organisms use to convert energy in a usable form. So to trace the origins of life, they traced the evolution of the enzymes responsible for those reactions back in time.

The genes for these enzymes are highly conserved (meaning unchanged) until you get to a certain point: the split between bacteria and archaea. While archaea are single-celled prokaryotes like bacteria, they differ enough from both bacteria and the rest of life to warrant their very own domain. They also inhabit some of the most extreme environments on Earth (including our guts).

Read more: “High on Ayahuasca, Bruce Damer Saw How Life on Earth Began. He May Very Well Be Right”

“The surprise is that the enzymes that catalyse those reactions aren’t conserved across the evolutionary divide that separates bacteria and archaea,” study co-author William Martin of Heinrich-Heine University said in a statement. “We found that the last universal ancestor of all cells, LUCA, possessed enzymes for only about half of the reactions of metabolism.”

How then did the LUCA metabolize energy?

According to the team, the rest of its metabolic enzymes weren’t enzymes at all. Instead, LUCA used transition metals littered around hydrothermal vents to serve the same catalytic process. “The closer we look, the more clearly we can see that early biochemical evolution was a hybrid of enzymatic and metal catalysts,” explained study co-author Joseph Moran from the University of Ottawa.

That means whatever existed before LUCA relied entirely on metals to harness energy.

As they transitioned from leaning on their environments to metabolize energy to become more self-sufficient, bacteria and archaea each evolved their own new enzymes to replace the metals in these reactions. “The new data leave only one conclusion,” Martin said. “The bacteria and archaeal lineages made the transition to the free-living state independently. Only free-living cells are alive. Let’s call it by name: We are looking at one origin of the genetic code, but two origins of life.”

After all, the evolution of life may be an improbable event, but if the conditions are ripe for it to happen once, why not twice?

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Jake Currie

Jake Currie is a writer based in Brooklyn, NY.

Table of Contents

Nautilus: 2026 Aug 9

All articles

Taxi Drivers Rarely Die of Alzheimer’s—How Complex Mental Maps and Spatial Reasoning Protect Your Brain

New Observatory Captures More Than Half a Million Galaxies in a Single Image

Inside the Not-So-Dumb Head of the Dodo Bird

Viagra May Slow the Spread of Cancer

This Paradoxical Desert Landscape Is Filled with Fresh Water

Depression Linked to Shrinking Brain Region in Older Adults

Could Physics Help Us Solve the Mystery of Aging?

Pesticide Exposure at Work May Increase Motor Neurone Disease Risk

Financial Struggle Can Age Your Brain

Life Originated Twice on Earth