The air we breathe is increasingly toxic. The World Health Organization (WHO) estimates that 99 percent of the global population inhales dirty air that exceeds their guideline limits, air that kills about 6.7 million people each year. For perspective, the WHO estimates that there were between 1.8 and 3 million deaths from COVID-19 in the year 2020. Although with the pandemic, official figures are likely an extreme undercount, the fact remains that air pollution is a prevalent, mostly invisible killer.

The problem is only getting worse. In the American Lung Association's 2022 State of the Air report, they found that "nearly 9 million more [American] people were impacted by daily spikes in deadly particle pollution than reported last year." Alarmingly, air pollution's effects are not confined to the breathing, as a growing body of research suggests that air pollution worming its way into the bodies of fetuses and unborn babies vis-a-vis their mothers' lungs.

Indeed, even before drawing their first breath, babies are being exposed to air pollution. It was first discovered in 2018 that air pollution particles can make their way into the placenta, an important organ that forms a protective interface in the uterus during pregnancy. But new research in The Lancet's Planetary Health journal shows for the first time that these pollutants can enter the fetus, exposing unborn infants to toxins before they even breathe for the first time.

The level of estimated pollution exposure strongly correlated with the level of black carbon found in the placenta samples and in cord blood, which accumulates in the umbilical cord.

To determine this, scientists at the University of Aberdeen in the U.K., and Hasselt University in Belgium conducted two studies. In the first, 60 mothers who had just given birth at East-Limburg Hospital in Belgium voluntarily donated their placentas and blood samples, which were analyzed at Hasselt University. Nearly 90 percent of the newborns were white Europeans, so it may not give a picture of what exposure is like in places like, say, New Delhi, India, one of the most polluted regions on Earth.

The researchers analyzed the samples for black carbon, a sooty byproduct of burning fossil fuels and wildfires that long-term exposure has been associated with cardiovascular and respiratory diseases, birth defects and early death. Then, using the volunteers' addresses and public air pollution monitoring data using satellites, they calculated the average level of exposure to toxic air. The level of estimated pollution exposure strongly correlated with the level of black carbon found in the placenta samples and in cord blood, which accumulates in the umbilical cord.

The second study was conducted in Scotland using liver, lung and brain tissue of fetuses. These samples were blasted with specialized white light lasers for just one quadrillionth of a second, but this was enough to illuminate thousands of tiny black carbon molecules.

Together, these results are pretty damning evidence that air pollutants can spread to a fetus and accumulate in worrying amounts that could lead to severe health problems down the road.

"What we have shown for the first time is that black carbon air pollution nanoparticles not only get into the first and second trimester placenta, but then also find their way into the organs of the developing fetus, including the liver and lungs," Paul Fowler, a professor at the University of Aberdeen and one of the study authors, said in a statement. "What is even more worrying is that these black carbon particles also get into the developing human brain. This means that it is possible for these nanoparticles to directly interact with control systems within human fetal organs and cells."

The researchers are quite sure the fetal samples weren't contaminated by the ambient air in the lab because the black carbon was deeply embedded in the organ tissue. The mothers in both studies were also screened against smoking tobacco, so cigarette use didn't skew the results.

"These findings are especially concerning because this window of exposure is key to organ development," the authors wrote. "It is the life stage during which susceptibility for many diseases later in life is programmed."

However, researchers still need to determine what mechanism of action black carbon and other pollutants actually cause disease. The presence of toxins alone isn't enough evidence, although it is a strong indicator. "Nevertheless," the authors conclude, "the exact impact of direct fetal black carbon exposure requires clarification and must be further elucidated in follow-up studies."

"We know that exposure to air pollution during pregnancy and infancy has been linked with still birth, preterm birth, low weight babies and disturbed brain development, with consequences persisting throughout life," Professor Tim Nawrot, a professor of environmental epidemiology at Hasselt University said in the same release. "We show in this study that the number of black carbon particles that get into the mother are passed on proportionally to the placenta and into the baby. This means that air quality regulation should recognize this transfer during gestation and act to protect the most susceptible stages of human development."

There are other ways air pollution may damage an infant's health. A study published in August in the journal Gut Microbes examined 103 Latino babies in Southern California and found that air pollution could influence the gut microbiome, the first time this was shown in infants. Some of these changes have "previously been linked with adverse health outcomes such as systemic inflammation, gastroenteritis, multiple sclerosis, and mental health disorders," the authors reported.

"Overall, we saw that ambient air pollution exposure was associated with a more inflammatory gut-microbial profile, which may contribute to a whole host of future adverse health outcomes," senior author Tanya Alderete, assistant professor of Integrative Physiology at University of Colorado, Boulder, said in a statement.

Alderete recommended that mothers avoid walking near high-traffic areas, investing in an air filtration system, opening the windows and breastfeeding as long as possible.

"Breast milk is a fantastic way to develop a healthy microbiome and may help offset some of the adverse effects from environmental exposures," Alderete said.

However, as Salon previously reported, microplastics were recently found in human breast milk for the first time. Breastfeeding is still recommended, of course, but it underscores the ubiquity of pollutants when it comes to reproductive and infant health. It is critical to address this growing issue, as the future health of our children is literally at stake.

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The device looks less steampunk and more 21st-century science fair project. But make no mistake—it’s Naert’s reinterpretation of a 19th-century thought experiment known as Maxwell’s Demon. To look for violations of the second law of thermodynamics, in 1867 Scottish physicist James Clerk Maxwell proposed the concept of a “demon” that could interact with microscopic particles. In a nutshell, the second law states that without the input of additional energy, heat always flows from a hot region toward a cold one. Imagining a demon that could disrupt the flow forces physicists to contemplate what the second law actually means.

“We can get inside the working of the second law by such thought experiments,” says Naert. “And we built it for real.”

Maxwell’s contemporaries had uncovered the second law while investigating the most efficient way to convert heat—from burning coal, for example—into the motion of pistons and turbines. But this principle turns out to have far broader implications than for just steam engines. It’s why ice always melts in a drink at room temperature, but the drink never turns into ice. Put another way, the second law indicates that certain processes in nature can proceed only in one direction. Such irreversible processes distinguish the past from present—what physicists call “the arrow of time.” “This is really the principle that describes why we get old,” says Naert.

The second law “is so much of our experience,” says physicist Harvey Leff, a professor emeritus at California State Polytechnic University, Pomona. “We observe it when we put our hand near a fire and are like, ‘Oops, that’s hot,’ and move our hand away.” Any exceptions, like a refrigerator where heat flows from cold to hot, requires a power source.

But what does it mean for something to be hot or cold? To answer that question for steam and other gases, 19th-century physicists developed the concept of temperature to describe the average speed of numerous particles bouncing around in random directions—some faster, some slower. (Later, they would discover the particles were atoms and molecules.) Hotter temperatures mean particles moving at a faster average speed.

The goal of a steam engine is to convert the chaotic motion of hot water vapor into motion in a defined direction, such as the vertical motion of a piston. To create orderly motion, the second law says that you need to keep the gas in two regions at different temperatures. If the gas were all at the same temperature, the vapor particles would move in random directions, and that random motion would not push the piston in a specific direction.

Maxwell sought potential violations of the second law, as scientists do when someone proposes that a principle should apply to all of nature. Specifically, he tried to devise a theoretical engine that exploited gas at a single temperature. In 1867, he presented a thought experiment, commonly depicted as a box with two compartments containing the same gas at a single temperature. The gas molecules bounce around at a range of speeds following a specific distribution.

But what if a little demon resided at the partition between the two compartments and sorted the molecules according to speed? One compartment would end up with faster molecules on average, corresponding to a hotter temperature, while the other compartment would contain slower molecules on average, corresponding to a colder temperature. The demon would have created two regions of different temperatures. Heat would again flow from hot to cold, making it possible to generate motion in a particular direction, which someone could use to move a piston.

Thus, the demon seems to have created an engine from a gas at one temperature, violating the second law. “Maxwell’s Demon was one of the greatest threats to the second law,” says physicist Nicole Yunger Halpern of the University of Maryland.

For more than a century, physicists have contemplated the thought experiment, and in recent years have even converted it into real-life machines. Naert’s device emulates Maxwell’s Demon, except instead of randomly bouncing molecules, he uses randomly bouncing steel beads.

The beads shake around the container to hit a rotating blade in different directions. Naert has engineered it such that the blade turns a dynamo to generate an electric current—but only when the blade rotates in a particular direction. He can then use that current to turn a motor, for example. Like Maxwell’s Demon, the contraption turns chaotic motion—analogous to heat—into orderly motion.

It’s surprising that the device could generate orderly motion at all, according to Yunger Halpern, because the machine is so large. Most real-world constructions of Maxwell’s Demon use microscopic particles such as atoms or electrons.

To be clear, Naert’s device does not violate the second law of thermodynamics, nor does Maxwell’s Demon. Physicists, pondering the demon over decades, have delivered multiple explanations for why it doesn’t. One is that in order to sort the beads, the demon has to be cooler than the rest of the gas, says Naert. Thus, the container of gas particles is not a single temperature, which contradicts the premise of the thought experiment.

In the case of Naert’s device, the rapidly bouncing steel beads are at one temperature, whereas the electronic component that converts the beads’ motion into the rotation of a blade is another temperature.

So why recreate Maxwell’s Demon? Physicists have used the thought experiment to explore common concepts in wildly different contexts. For example, in the 20th century, it led physicists to discover the physical nature of information. In order for the demon to sort molecules by speed, it needs some way of knowing the particles’ speed. The demon would need to store that knowledge and erase that information. From these ideas, physicists figured out that information isn’t just some abstract concept that we humans harness to communicate. It’s the physical state of some object, like representing the voltage across a transistor as a bit of information—a key concept now fundamental to the study of computing.

In addition, the second law of thermodynamics signifies the statistical nature of the universe. Its building blocks are not stars, planets, humans, or bacteria—they’re the atoms and molecules that make us up. You can think of the atoms in the universe as a deck of cards, constantly being shuffled and reshuffled. By the end of the reshuffling, the deck will have no semblance of order. But instead of dealing with a deck of 52 cards, the universe has a deck on the order of 1082 atoms.

Or if you want to be more manageable, consider the 1024 molecules in a cup of coffee. If you drop a sugar cube into that coffee, those sugar molecules have so many more ways of redistributing themselves throughout the coffee than staying in cube form. Or consider someone who releases perfume in a room. That perfume will rush to fill the space. This illustrates the concept of entropy, often described as “disorder.” The most likely arrangement of atoms has the highest entropy. A deck of cards sorted according to the four suits has lower entropy, for example, than one that is not. Similarly, dissolved sugar molecules cannot re-cube, and the perfume cannot rush back into the vial, without some external intervention requiring energy.

Ultimately, the second law of thermodynamics says that energy moves around in nature to increase entropy. “If you ask what physics is, you might just say it is the study of energy,” says Leff. “What’s happening as far as I can see is that energy keeps redistributing itself.”

However, as people invent new technology, it’s not always clear how the second law applies. For example, seemingly straightforward concepts like temperature get complicated. Naert’s steel beads are at room temperature in the conventional sense, defined according to the average speed of their constituent molecules. This is the same temperature that you might associate with how it would feel to touch the bead. But Naert has identified another property of his system, which he interprets as a different type of temperature, defined not by the speed of its constituent molecules, but that of the glass beads bouncing around. It’s mathematically analogous to conventional temperature, as both involve the speed of discrete particles, but has no relation to whether you will burn or cool your hand when touching it. Naert plans to work with theorists to better understand what this type of temperature means, along with measuring and understanding the role of entropy in his device.

In addition, physicists have had to revisit the second law as researchers build smaller and smaller devices, such as quantum engines—made of a few atoms. They want to know, for example, whether the second law limits these quantum engines in the same way as conventional macroscopic engines, says Yunger Hapern.

Naert’s personal motivation to build this machine was intellectual curiosity, but he thinks that studying the second law in macroscopic contexts could potentially lead to more efficient machines for harvesting energy from ocean waves, for example, as it illustrates the conversion of chaotic macroscopic motion into orderly motion that could be used to charge a battery or move a turbine. In addition, he sees his device as a teaching tool. “This is incredibly close to the original idea from the 19th century,” he says. But because he uses beads instead of molecules, “you can see everything because it’s in centimeters.” With his new device, Naert has invited Maxwell’s Demon to confuse and enlighten us at a new scale.

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An intense jet of energy in space appears to be traveling seven times faster than the speed of light—a feat that is considered physically impossible in our universe. Though this rapid pace is only an optical illusion, according to a new study, it still represents a blast of energy shooting towards us at very nearly the speed of light.

The Hubble Space Telescope (HST) has captured incredible views of the jet—which was ignited by an unprecedented collision between two hyperdense objects, called neutron stars—that led to one of the most important breakthroughs in astronomical history at the time it was discovered in 2017.

While the jet did not actually break the cosmic speed limit, it raced right up to the edge of this impassable threshold, reaching at least 99.97 percent of the speed of light, which translates to about 670 million miles per hour. Scientists led by Kunal Mooley, an astrophysicist at the California Institute of Technology, used Hubble and other telescopes to clock the jet’s “superluminal motion,” meaning the trippy illusion of faster-than-light speed, in a study published on Wednesday in Nature.

“We have demonstrated in this work that precision astrometry with space-based optical and infrared telescopes is an excellent means of measuring the proper motions of jets in neutron-star mergers,” Mooley and his colleagues said in the study. “The James Webb Space Telescope (JWST) should be able to perform astrometry much better than that with the HST, owing to the larger collecting area and smaller pixel size.”

The crash between these neutron stars was so explosive that it created ripples in the very fabric of spacetime, known as gravitational waves. Even though the merger happened a whopping 140 million light years away, scientists were still able to detect these subtle waves when they passed through Earth in August 2017.  

The event, named gravitational wave (GW) 170817 after the date it was discovered, quickly earned a momentous place in space history. For starters, it was the first time that scientists had ever identified waves from a merger between two neutron stars. A handful of gravitational waves formed by mergers between black holes had been discovered at that point, but collisions between neutron stars had remained elusive.

The nature of the objects is important because black hole mergers do not produce visible light, and can only be spotted through the novel process of gravitational wave astronomy. In contrast, collisions between neutron stars, which are compact roiling objects formed by the explosive deaths of large stars, do produce luminous blasts of radiation.

The possibility of capturing two different signals of the same event—in this case with gravitational waves and a light signal—can produce a wealth of insights that are impossible to discern from only one observational technique.

For this reason, scientists hustled to get as many telescopes as possible pointed at the place in the sky where GW170817 originated to look for the radiant explosion from the mergers, including the jets that these events shoot out into space. Sure enough, the brilliant aftermath of the collision was spotted by dozens of telescopes, which followed the eruption as it faded. The achievement marked a major advance in the field of multi-messenger astronomy, which describes the observation of multiple types of signals from the same event.

Now, five years later, Mooley and his colleagues have added more detail to this astronomical mosaic with observations from Hubble, as well as from the European Space Agency’s Gaia observatory and several radio arrays on Earth involved with the field of very-long-baseline interferometry (VLBI). The team was able to see the jet slamming through a blob of material that had been blasted into space from the merger, which accelerated the mass to high speeds.

By measuring the motion of the blob, the researchers were able to show that the jet appears to be outpacing the speed of light sevenfold. As far as we know, nothing can travel faster than the speed of light, except for the expansion of the universe itself. The illusory effect of the superluminal motion stems from the ultra-relativistic speed of the jet, which is traveling just slightly slower than the light it emits.

The matter in the jet is just barely trailing its luminous light particles, known as photons, from our perspective on Earth. Because of this effect, photons that the jet emits in the early phases of its eruption can end up arriving at Earth around the same time as photons emitted at later stages, because the jet is more or less keeping pace with its own light output. This trippy phenomenon makes it seem as if the jet is moving faster than light-speed, a result that would shatter our understanding of physics, when in fact the jet is merely moving near light-speed, a result that is still pretty dang mind-boggling.

With this new study, Mooley and colleagues have presented a roadmap for discovering similar features in future unions of neutron stars. These efforts might unravel some of the mysteries of these explosive events, such as the potential link between neutron star mergers and highly luminous flashes known as short gamma-ray bursts.

“Our study represents, to our knowledge, the first proper motion constraint on the Lorentz factor”—which is a special measurement of moving objects—“of a gamma-ray-burst jet indicating ultra-relativistic motion,” the researchers said in the study.

“The combination of optical astrometry and radio VLBI measurements (with current observing facilities) may be even more powerful, and could deliver strong constraints on the viewing angles of neutron-star mergers located as far away as 150 megaparsecs,” equivalent to nearly 500 million light years, “as long as they have favorable inclination angles and occur in relatively dense environments compared with GW170817,” the team concluded.

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With the decriminalization of cannabis comes a list of questions and concerns over its medical and recreational use – including figuring out how long the drug's effects actually last for.

While society has had decades to question the relationship between alcohol consumption and intoxication, the duration of impairment from inhaling or ingesting weed has been more anecdotal than scientific.

A meta-analysis of 80 papers published last year narrowed down this timeframe. Depending on factors such as how the cannabis is consumed and how strong it is, the user can remain impaired for between three and 10 hours.

This information can help inform advisory information given to patients, help recreational users make better decisions about performing tasks such as driving after consuming cannabis, and help update the laws to better reflect the reality of cannabis impairment.

"THC can be detected in the body weeks after cannabis consumption, while it is clear that impairment lasts for a much shorter period of time," psychopharmacologist Iain McGregor from the University of Sydney (USYD) in Australia explained in 2021.

"Our legal frameworks probably need to catch up with that and, as with alcohol, focus on the interval when users are more of a risk to themselves and others. Prosecution solely on the basis of the presence of THC in blood or saliva is manifestly unjust."

A meta-analysis is what it sounds like: a review and analysis of the relevant scientific literature, cross-referencing the results to arrive at a finding based on a broader array of methodologies and subjects (in this case, people) than can be covered in a single study.

For this research, a team led by USYD nutritionist Danielle McCartney referenced 80 separate studies into impairment from tetrahydrocannabinol (THC), the intoxicating compound in cannabis, performing the first meta-analysis of its kind.

From those 80 papers, the team studied 1,534 "performance outcomes" from people who had taken cannabis; that is, how these people performed at driving or equivalent cognitive tasks at various stages after taking cannabis.

How long the impairment lasted depended on three main factors: how strong the dose of THC is; whether the cannabis was inhaled or taken orally in the form of food, capsules, or drops; and whether the person was an occasional or regular user of cannabis.

"Our analysis indicates that impairment may last up to 10 hours if high doses of THC are consumed orally. A more typical duration of impairment, however, is four hours, when lower doses of THC are consumed via smoking or vaporization and simpler tasks are undertaken," McCartney said.

"This impairment may extend up to six or seven hours if higher doses of THC are inhaled and complex tasks, such as driving, are assessed."

Interestingly, regular users of cannabis can build up a tolerance, and perform better at cognitive tasks than occasional users after consuming the same amount. It's therefore not easy to predict how much cannabis is going to impair a regular user, or for how long, since they may take higher doses to reach the same level of intoxication as an occasional user.

"We found that impairment is much more predictable in occasional cannabis users than regular cannabis users," explained USYD behavioral pharmacologist Thomas Arkell.

"Heavy users show significant tolerance to the effects of cannabis on driving and cognitive function, while typically displaying some impairment."

The findings suggest that most driving-related skills could return within five hours after inhaling cannabis, although this time may vary.

More research will need to be conducted into these time intervals for regular users, in order to better characterize the effects of THC across the board. Once this is done, though, the information can guide legislation, the researchers said.

"Laws should be about safety on the roads, not arbitrary punishment," McGregor said. Given that cannabis is legal in an increasing number of jurisdictions, we need an evidence-based approach to drug-driving laws."

The research was published in Neuroscience & Biobehavioral Reviews.

An earlier version of this article was published in April 2021.

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"While antibody immunity is not completely gone, BA.2.75.2 exhibited far more dramatic resistance than variants we've previously studied, largely driven by two mutations in the receptor binding domain of the spike protein," says the study's corresponding author Ben Murrell, assistant professor at the Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet.

The study shows that antibodies in random serum samples from 75 blood donors in Stockholm were approximately only one-sixth as effective at neutralizing BA.2.75.2 compared with the now-dominant variant BA.5. The serum samples were collected at three time points: In November last year before the emergence of omicron, in April after a large wave of infections in the country, and at the end of August to early September after the BA.5 variant became dominant.

Only one of the clinically available monoclonal antibody treatments that were tested, bebtelovimab, was able to potently neutralize the new variant, according to the study. Monoclonal antibodies are used as antiviral treatments for people at high risk of developing severe COVID-19.

BA.2.75.2 is a mutated version of another omicron variant, BA.2.75. Since it was first discovered earlier this fall, it has spread to several countries but so far represents only a minority of registered cases.

Risk of increased infections

"We now know that this is just one of a constellation of emerging variants with similar mutations that will likely come to dominate in the near future," Ben Murrell says, adding "we should expect infections to increase this winter."

Some questions remain. It is unclear whether these new variants will drive an increase in hospitalization rates. Also, while current vaccines have, in general, had a protective effect against severe disease for omicron infections, there is not yet data showing the degree to which the updated COVID vaccines provide protection from these new variants. "We expect them to be beneficial, but we don't yet know by how much," Ben Murrell says.

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Mind Fixers: Psychiatry’s Troubled Search for the Biology of Mental Illness
Anne Harrington
W. W. Norton, $17.95 (paper)

Desperate Remedies: Psychiatry’s Turbulent Quest to Cure Mental Illness
Andrew Scull
Harvard University Press, $35 (cloth)

In 1990 President George Bush announced that “a new era of discovery” was “dawning in brain research.” Over the next several decades the U.S. government poured billions of dollars into science that promised to revolutionize our understanding of psychiatric disorders, from depression and bipolar disorder to schizophrenia. Scientists imagined that mental illnesses in the future might be diagnosed with genetic tests, a simple blood draw, or perhaps a scan of your brain. New pharmaceuticals would target specific neurochemical imbalances, resulting in more effective treatments. The 1990s, Bush declared, would be remembered as “The Decade of the Brain.”

This brave new world of brain research also promised to free us of the stigma and discrimination attached to mental illness and addiction for centuries. Localizing psychiatric disorders in the brain would make them chronic medical diseases—like diabetes and high cholesterol—instead of individual moral failings or deficiencies in character. While it was impossible to predict exactly what the future would bring, there was an overwhelming sense that psychiatric science was going to crack the “mystery” and “wonder” of this “incredible organ,” as Bush called it.

The reality of psychiatric practice is far less glamorous than the optimistic visions I grew up with.

Looking back as a psychiatrist and historian today, I find that these hopes feel quaint. They remind me of other misplaced visions of technological futures from the twentieth century: flying cars, pills for a whole day’s nutrition. The reality of psychiatric practice is far less glamorous than the visions of its future that I grew up with. Thirty years later we still have no biological tests for psychiatric disorders, and none is in the pipeline. Instead our diagnoses are based on criteria in a book, the Diagnostic and Statistical Manual of Mental Disorders (often called, derisively, the “bible” of American psychiatry). It has gone through five editions in the last 70 years, and while the latest edition is almost 100 pages longer than the last, there is no evidence that it is any better than the version it replaced. None of the diagnoses is defined in terms of the brain.

We also have not had any significant breakthroughs in treatment. For decades the pharmaceutical industry has churned out dozens of antidepressants and antipsychotics, but there is no evidence that they are more effective than the drugs that emerged between 1950 and 1990. People with serious mental illness today are more likely to be homeless or die prematurely than at any point in the last 150 years, with lifespans that are 10 to 20 years less than the general population. Biological research has also failed to reveal why psychiatric drugs help some patients but not others. When a patient asks me how an antidepressant works, I have to shrug my shoulders. “We just don’t know, but we do have evidence that there’s about a 30 percent chance that it will help your mood.” Perplexed, one patient responded, “Doesn’t it have to do with neurotransmitters or something?” I sighed, “Yes, that was the theory for a while, but it didn’t pan out.”

And how about stigma? As anthropologist Helena Hansen has argued, the neuroscience of addiction has often reinforced stigma by reducing substance use to an individual problem, instead of the result of structural factors rooted in longer histories of racial violence. American psychiatrists also diagnose Black and Brown patients with disproportionate rates of schizophrenia compared to white patients—a disparity that psychiatrist-sociologist Jonathan Metzl traces to psychiatrists in the 1970s who pathologized Black activism as “psychosis.” Finally, Black patients experiencing mental health crises, including children, are more likely to experience the violence of being physically restrained, tied to their beds in ways that resemble the experiences of asylum patients over a century ago.

In 2015 the former director of the National Institute of Mental Health (NIMH), Thomas Insel, crystallized this disillusionment:

I spent 13 years at [NIMH] pushing on the neuroscience and genetics of mental disorders, and when I look back . . . I realize that while . . . I succeeded at getting lots of really cool papers published by cool scientists at fairly large costs—I think $20 billion—I don’t think we moved the needle in reducing suicide, reducing hospitalizations, improving recovery for the tens of millions of people who have mental illness.

It does not help that academic psychiatry today feels out of touch. Many people have underscored the profound importance of mental health amid the social isolation of the pandemic, racial violence in our society, and the increasingly hyper-competitive culture of schools, sports, and the market. But academic psychiatry’s almost singular focus on brain-based research has meant that the profession has been largely absent from these conversations. And for what? All the “cool papers” on neurobiology have won academic grants and helped professors get promoted, but they have not meaningfully impacted the diagnosis and care of the millions of people suffering psychic distress.

How did we end up here? If we have failed to understand psychiatric disorders biologically, what happens when we examine them historically? Two recent books by historians explore the crisis in biological psychiatry, tracing the political, economic, social, and professional factors that led psychiatrists to attempt to pin the reality of mental illness—and the legitimacy of the profession—on the brain. Written by leading historians in the field, these are big books, in heft and scope, that cover two hundred years of the profession’s failures. They reveal that U.S. psychiatry, across its history, has been dangerously susceptible to hype and “cool,” ranging from enthusiasm for brain dissection in the 1890s to the fanfare surrounding neurotransmitters and genetics a century later.

Understanding the undulating history of psychiatric hype and crisis is crucial today as the profession builds toward its next trend: psychedelics, already heralded as a “renaissance” and psychiatry’s “next frontier.” These two histories demonstrate that the academic and corporate pursuit of such hype has neglected the perspectives of communities most affected by psychiatric research and care, resulting in significant psychological and bodily harm. The strengths and limitations of these important books push academic psychiatrists to reexamine our priorities. They challenge us to envision a future world where the billions of dollars invested in biological research are instead redistributed to the communities who need it most—in order to provide the resources necessary for radically reimagined forms of care that center whole humans instead of just brains.

In Mind Fixers: Psychiatry’s Troubled Search for the Biology of Mental Illness, Anne Harrington argues that the current crisis is just the latest in a long line of failures to discover the biology of mental illness over the last two centuries. In this sweeping study, the history of psychiatry undulates like the boom and bust of a speculative market. First a wave builds with enthusiastic promises of revolutionary breakthroughs that will change psychiatry as we know it. Then the wave collapses, as psychiatrists fail to deliver on those bold promises. Crisis ensues, and after the requisite finger-pointing, the next wave of psychiatric revolution begins to build. Rinse and repeat.

Psychiatry, across its history, has been dangerously susceptible to hype.

The first “revolution” in American psychiatry that Harrington tracks arrived in the nineteenth century. At the time, large lunatic asylums dominated the psychiatric landscape, such as the Blackwell’s Island hospital on what today is called Roosevelt Island in New York City. These institutions were designed to cure patients with mental disorders by placing them in the hospitable environment of the asylum architectural space. However, a series of journalistic exposés revealed that these asylums were overcrowded and underfunded with patients living in deplorable, instead of therapeutic, conditions. For example, in 1887, journalist Elizabeth Seaman, who wrote under the pen name Nellie Bly, went undercover as a patient in Blackwell’s Island Hospital and exposed horrible acts of brutality in her best-seller Ten Days in a Mad-House. Asylum psychiatry faced a crisis of public trust.

As Harrington explains, European neuroanatomists came to the rescue. Unlike asylum physicians, anatomists were pessimistic about the potential for a cure. Building on eugenic theories, they believed that asylum patients were “degenerates” who were biologically unfit to cope with the stresses of modern life. But they also believed that the mentally ill could provide a service to society after their deaths by offering their brains to science. The dissection of their pathological brains, the anatomists hoped, could reveal the biological causes of mental suffering.

As the asylum transformed from a therapeutic institution into a site for research over the course of the late nineteenth century, thousands of dissections were performed on the bodies and brains of mostly poor patients without their consent. Harrington concludes that they revealed “more or less nothing.” The problem was that neuroanatomists had no idea what they were looking for. The psychiatrist Karl Jaspers summed up these anatomical efforts as a “brain mythology.” Neuroanatomical dissection was a bust.

Abandoning the therapeutic nihilism of neuroanatomists, the second push for biological psychiatry swung to the other extreme. The early twentieth century in the United States was a period of unbridled, desperate experimentation on patients’ bodies in the desperate search for a cure. Andrew Scull’s new book Desperate Remedies: Psychiatry’s Turbulent Quest to Cure Mental Illness gives a chilling account of a period characterized by an “orgy of experimentation.” While covering much of the same historical ground as Harrington’s study, Scull’s more vivid account demonstrates that the foundations of biological psychiatry were built on violence inflicted on the bodies of women, the poor, and people of color. During the period from 1910 to 1950 in the United States, Scull argues, researchers treated their vulnerable patients “as objects, not sentient beings.” With few legal rights at the time, patients had little recourse for protesting doctors’ invasive and haphazard experiments on their bodies.

Take the American psychiatrist Henry Cotton, who appears in both Harrington and Scull’s accounts. In the 1910s and ’20s, Cotton was convinced that all psychosis was septic in origin—a result of an infection—because it had been demonstrated that one condition, called “general paralysis of the insane,” was caused by the syphilis spirochete Treponema pallidum in the brain. Based on this unproven theory of septic psychosis, Cotton concluded that psychosis could be treated by the surgical removal of potential sources of infection from patients’ bodies. Cotton maimed and killed thousands of patients as he surgically removed teeth, appendices, ovaries, testes, colons and more in the name of curing psychosis. The death rate of Cotton’s colectomies was later determined to be more than 44 percent, with women representing a disproportionate number of his victims.

Another example Scull examines is the Viennese physician Julius Wagner-Jauregg, who thought that inducing high fever and convulsions might help psychiatric patients. He won the Nobel Prize of Medicine in 1927 for using malaria to induce high fever to treat patients with general paralysis of the insane. Harrington points out that at the famous St. Elizabeths Hospital in Washington, D.C., certain patients with chronic psychosis, who were among the most socially marginalized, were turned into “malaria reservoirs” who stored the parasite in their bodies so that it could be distributed to other patients.

Scull suggests that the most extreme experiment during this period was lobotomy. The procedure initially involved applying local anesthesia to the head, drilling through the skull, and cutting the frontal lobes of the brain with a blade. The surgeon stopped cutting the brain when the patient began to get “confused.” The innovation earned Portuguese neurologist Egan Moniz a Nobel Prize of Medicine in 1949. Walter Freeman, who popularized the procedure in the United States, later innovated an approach that required insertion of an ice pick through each eye socket into the brain. Lobotomies were performed by the tens of thousands in the 1940s and ’50s, again disproportionately on women. Freeman described the effects of the procedure as changing his patients into people who were more like “domestic invalid or household pet” so that their behavior was easier for families and institutions to control.

In Harrington’s study, the history of psychiatry undulates like the boom and bust of a speculative market.

Sterilization was another invasive procedure popularized in American psychiatry during this period. Based on older theories of degeneracy, sterilization was a eugenic rather than therapeutic tool: it was meant to keep people with mental illness from passing on their “bad stock.” The ethically fraught practice made its way to the Supreme Court in the infamous Buck v. Bell case in 1927, when Associate Justice Oliver Wendell Holmes, Jr., argued that society was justified in seeking to “prevent those who are manifestly unfit from continuing their kind.” In the decade that followed the decision, some 28,000 Americans diagnosed with “feeble-mindedness” were sterilized.

Scull and Harrington conclude that the only effective treatment that psychiatry today has inherited from this period of frenzied and dangerous experimentation is electroconvulsive therapy (ECT). Believing (falsely) that seizure disorders and schizophrenia were antagonistic diseases, the Hungarian psychiatrist Ladislav Meduna sought to induce seizures with the powerful stimulant Metrazol in schizophrenic patients in the 1930s. As a result of the sheer violence of the treatment, about 40 percent of patients suffered compression fractures of their spines. The practice was adapted over time to make it safer for patients, eventually evolving into ECT, which continues to be used in American psychiatry today. Current research demonstrates that ECT is safe and effective in the treatment of depression, but like researchers in the 1930s, we still do not know why or how it works.

Rejecting this violent experimentation on the body, the next crop of psychiatric revolutionaries turned, instead, to an approach that focused solely on the mind: psychoanalysis. Sigmund Freud arrived in the United States in 1909, but his ideas did not take hold in the profession until after World War II. Experiences treating traumatized soldiers taught psychiatrists that the war’s psychological wounds could be just as devastating as their physical injuries.

Psychoanalysis developed what Scull calls a “fragile hegemony” over the field in the postwar period. Harrington emphasizes that psychiatrists turned to Freud’s work because they believed it provided a distinctly medical approach to mental illness: an intervention, namely psychoanalysis, elucidated and treated the underlying cause of the patient’s symptoms in the unconscious. By the 1950s most psychiatry residency training programs in the United States were led by psychoanalysts, and many influential analysts consolidated their professional power by denigrating earlier somatic approaches. In 1948, for example, an influential group of analysts argued that lobotomy was not a therapy but rather a “man-made self-destructive procedure that specifically destroys” parts of the brain essential to humanity. Figures in popular culture also saw psychoanalysis as a solution to broader problems facing American society. At the annual conference of the American Psychiatric Association in 1948, President Harry Truman stated that “experts in the field of psychiatry” were essential for safeguarding American “sanity,” which was the “greatest prerequisite for peace.”

But like the boom and bust of revolutions before it, psychoanalysis failed to deliver on its overambition, and the almost exclusive focus on the mind did little to prevent psychiatric harm against vulnerable communities. In the 1970s gay activists vocally protested the pathologization of their sexuality in American psychiatry. These activists, including some gay psychiatrists, stormed the annual conferences of the American Psychiatry Association (APA) and successfully demanded the removal of homosexuality from the profession’s catalogue of disorders.

The problem for activists in gay, feminist, Black Power, and disability movements in the 1970s was that institutional psychoanalysis embraced and conformed individuals to white, ableist, heterosexual, and upper middle-class norms. For those whose identities challenged such norms, psychotherapy was more likely to harm than heal. As members of the Chicago Gay Liberation Front proclaimed in a 1970 leaflet written to the American Medical Association:

We homosexuals of gay liberation believe that the adjustment school of therapy is not a valid approach to society. . . . Mental health for women does not mean therapy for women—it means the elimination of male supremacy. Not therapy for blacks, but an end to racism. The poor don’t need psychiatrists (what a joke at 25 bucks a throw!)—they need democratic distribution of wealth. OFF THE COUCHES, INTO THE STREETS!

Their call to abandon the couch for the street was an indictment of an academic psychoanalytic profession, composed largely of white men, that had reified, instead of challenged, structures of oppression in American society. Many American analysts at mid-century held the belief, for example, that Black people did not possess the psychological sophistication required for psychoanalytic work on the couch. Furthermore, historian Martin Summers has shown that in institutions that treated Black patients, psychoanalysts reinforced older, racist stereotypes of a “distinctive black psyche,” even in the face of data and clinical experience that undermined such a notion.

To be sure, more radical visions of psychoanalysis emerged in the political fervor of 1960s and ’70s, but you have to look beyond Scull and Harrington’s accounts to find them. In the French colony of Algiers, for example, Martinique-Born psychiatrist Frantz Fanon famously critiqued the anti-Black violence of colonialism to imagine more liberatory forms of care. And in Latin America, my own work has shown how Marxist psychoanalysts in the early 1970s imagined a “psychotherapy of the oppressed” that tied mental health to social and political liberation from capitalism and U.S. imperialism. But these radical efforts in the Third World were far removed, geographically and politically, from the mainstream psychoanalysis discussed in these two books.

For Scull and Harrington, perhaps the most damning blow to the legitimacy of American psychiatry came from within the profession itself. In 1973 forensic psychiatrist David Rosenhan published an experiment, titled “On Being Sane in Insane Places,” in the journal Science. His famous study concluded that psychiatrists could not distinguish sanity from insanity. For the experiment, Rosenhan sent eight “pseudo-patients” who pretended to hear the words “empty,” “dull,” and “thud” for interviews at psychiatric hospitals. Rosenhan found that all eight were admitted to the hospital by psychiatrists; their average length of stay was nineteen days. All but one of the patients were given a diagnosis of schizophrenia on discharge. Journalist Susannah Cahalan has more recently shown that Rosenhan fabricated many of his results, but at the time the paper shook the foundations of the profession and broke psychoanalysis’ tenuous grip on the field.

The turn to biology has not meaningfully impacted treatment, but it has been wildly successful as a marketing strategy for psychopharmaceuticals.

Enter the biological psychiatrists of the 1980s, who laid the groundwork for the biological revolution we find ourselves in today. Partly in response to Rosenhan’s study, this new coalition of psychiatrists blamed the crisis in professional legitimacy on psychoanalysis. Its obscurantist theories, they argued, were more jargon than substance and had turned American psychiatry into a Tower of Babel, where psychiatrists could barely communicate meaningfully with each other. Research from as early as the 1960s showed that diagnosis among psychiatrists was not reliable statistically—that is, psychiatrists often disagreed on diagnosis even when assessing the same patient. The influential psychiatrist Robert Spitzer believed that the solution was to radically reform a book that most professionals had ignored: the DSM. Spitzer and the DSM-III Task Force gutted the psychoanalytic underpinnings of the manual and replaced it with what they believed were clear and objective criteria for each illness based on observable aspects of patient behavior that could guide treatment and research.

The publication of the third edition of the DSM in 1980 heralded the birth of what proponents explicitly called a “biological revolution” in psychiatry. For evidence of this revolution, Spitzer and others pointed to developments in psychopharmacology, especially the introduction of the first effective antipsychotic chlorpromazine in 1954 and biological research that examined the role of neurotransmitters and genetics on mental illness. Research on the brain and the body, they believed, would eventually connect the diseases described behaviorally in the DSM-III to their underlying biological causes.

We now know that this hoped-for science never arrived; psychiatry keeps waiting for its biological Godot. While the DSM-III and subsequent editions, including IV and 5, have improved diagnostic reliability, psychiatry continues to suffer from the problem of validity. In other words, the collection of symptoms that defined each condition in the DSM have still—after billions of dollars of investment—not been correlated with robust changes in our brains, blood, or genes.

The oft-cited claim, for example, that schizophrenia has a genetic basis has failed to pass scientific muster. As Scull discusses, after failing to find a Mendelian set of genes that could explain schizophrenia, researchers in the 2000s pinned their hopes on new genome-wide association studies (GWAS) that could investigate hundreds of thousands of base pairs in the search for genetic linkages to psychiatric disorders. But GWAS studies have not revealed a clear genetic basis for schizophrenia (or bipolar disorder, for that matter). While combining hundreds of genetic sites can help explain, at best, 8 percent of the observed variance of schizophrenia, it is still possible for an individual to have many of these genetic variations without developing the disease. Prominent psychiatrists Michael Rutter and Rudolf Uher have reflected on the disappointment: “Molecular genetic studies of psychiatric disorders have done a lot to find very little. In fact, in the era of genome-wide association studies, psychiatric disorders have distinguished themselves from most types of physical illness by the absence of strong genetic associations.”

While the turn to biology has not meaningfully impacted diagnosis or treatment, it has been wildly successful as a marketing strategy for psychopharmaceuticals. In fact, the most significant change in psychiatry over the last half-century might be the birth of Big Pharma, not any revolution in biology. Psychiatric markets were attractive to pharmaceutical companies for at least two reasons in the 1980s. First, psychotropics are taken over long periods of time: many patients are life-long consumers. Second, self-perception and subjective experience play major roles in the diagnosis of mental illness. This fact, pharma executives realized, means that demand can be influenced and manipulated by effective marketing that positions drugs as a solution to consumers’ dissatisfaction with their lives.

In the 1990s drug companies invested millions to create direct-to-consumer advertisements that capitalized on the biological fervor of academic psychiatrists. These ads claimed, misleadingly, that their drugs targeted “chemical imbalances” in the brain that cause everyday feelings of depression and anxiety in Americans. In addition to consumer demand, the industry also focused their considerable influence on prescribers. Pharma offered influential physicians at prestigious academic centers drug samples, lucrative consulting gigs, and other incentives to peddle their products.

Today the industry financially supports almost every journal and scientific meeting in psychiatry. Some 69 percent of the members of the Task Force of the current DSM-5 disclosed financial ties to the pharmaceutical industry—a 21 percent jump from disclosures reported by the Task Force for DSM-IV. Pharma’s influence on the DSM has contributed to an expansion of diagnostic categories so that the concept of “mental illness” itself has become more inclusive, increasing the size of potential drug markets.

Over the last half century, pharma has also influenced the federal approval of drugs by the Food and Drug Administration (FDA). Today, the FDA gets 46 percent of its budget from companies filing drug applications (so-called “industry user fees”), and companies conduct the safety and efficacy trials on the drugs that they produce. This obvious conflict of interest has led pharma to distort evidence of safety and efficacy, hide negative results and side effect data, and hire ghostwriters to pen academic articles. While a number of major civil and criminal rulings have punished companies for these offenses, the structural source of this unethical behavior—the fact that the industry evaluates the products that it profits from—remains today.

Big Pharma’s heavy influence on the profession has played a major role in shifting the identity of the American psychiatrist—from a psychoanalyst at mid-century to a prescriber of pharmaceuticals today. While research has shown that psychotherapy is just as, or more, effective than drugs for anxiety, depression, and other disorders, psychiatrists generally focus on the prescription of drugs and send patients to psychologists and social workers for therapy. And this shift has paid off handsomely. The psychotropic drug industry today is worth almost $60 billion, and one in six Americans took a psychiatric medication in the last year.

The real crisis in academic psychiatry is that there is no crisis.

But if the pharmaceutical industry has invested so heavily in psychiatry, why have there been no breakthroughs in drug treatment? A major reason is that the industry has spent billions of dollars more on advertising psychiatric medications than on research and development of novel drugs. As psychiatrist David Healy has shown, money earmarked for R&D is often not intended to produce genuine innovation. Almost all of the psychopharmaceuticals produced since 1990 have been “copycats” that mimic older, generic pharmaceuticals, with only minor chemical modifications. These (unfortunately named) “me-too” drugs work no better clinically than the drugs that came before them, but their slight biochemical novelty means that they can be patented, so that pharma can charge insurance companies’ top dollar.

Perhaps the worst news is that Big Pharma, having created and capitalized on psychiatric markets, is now jumping ship. Anthropologist Joe Dumit has shown that most psychiatric drugs will soon go off patent, so companies will be forced to charge less for them. With the market already saturated with pharmaceutical copycats and no significant scientific biological breakthroughs in sight, there is suddenly little room for growth. Almost all of the major pharmaceutical companies have decided to divest from psychiatric drug research and turn to more promising sectors, especially the development of “biologics” and other cancer drugs.

Does psychiatry, then, have a future? With the pharmaceutical well running dry, Harrington and Scull offer few solutions beyond vague statements about the need for humility in academic psychiatry and the message that psychiatrists should focus on psychosocial, not just biological, approaches to treatment.

Scull also wonders whether a return to psychotherapy might be the answer. Outpatient psychiatry in the United States today is often based on brief, fifteen- to thirty-minute visits that narrowly focus on medication management and symptom check lists. Scull laments the loss of connection that psychoanalysis represented for some (mostly privileged) American patients at mid-century—at least psychiatrists listened to patients in the 1950s, he emphasizes.

Unfortunately, psychotherapy in the last fifty years has become more pill-like itself: standardized, quick, corporate, and cheap. In the 1980s and ’90s, managed care magnified the critiques of some psychiatrists that the intensive and exploratory nature of long-term psychoanalysis was a large investment in time and money with modest gains. They advocated for faster and more affordable forms of care that included not only drugs but also new cognitive-behavioral therapy (CBT) techniques that, as historian Hannah Zeavin has argued, devalued the healing power of the therapist herself. Certain CBT approaches attempted to reduce therapists’ role to largely automated dialogue and manualized programs defined in workbooks and computer programs written for each disorder. In the CBT model, the patient’s thoughts and feelings were understood as scripts that could be reprogrammed, while the introspection and psychological insight—the “listening” valued by Scull—was denigrated by some practitioners as navel-gazing. As a result, traditional psychoanalysis has become almost impossible to come by today. While many therapists adopt an eclectic approach that borrows insights from CBT and various strands of psychoanalysis in practice, the kind of long-term, open-ended therapy that traditional psychoanalysis represented is extremely difficult to access now. Insurance refuses to cover it, and patients who want psychoanalysis are often forced to pay high fees out-of-pocket.

With the decline of psychoanalysis, therapy has continued to verge toward corporate automation. Psychologists and social workers today often search for “gig work” across growing digital platforms like Talkspace to earn around $25 an hour with little control over their hours, fees, or working conditions. Others engage in therapy with an artificially intelligent (and usually feminized) chatbot. Disturbingly, these digital apps are largely unregulated and have questionable standards of care. Given financial pressure from insurance companies and a health system that demands quick fixes, the future of psychotherapy frankly looks bleak—both for patients who desire human contact and for providers whose labor is being devalued to the point of automated erasure.

The only real source of excitement on psychiatry’s horizon seems to be psychedelics, which Harrington mentions very briefly in her conclusion. Non-profit organizations and academic researchers are currently conducting over fifty FDA trials of MDMA (ecstasy), psilocybin (magic mushrooms), LSD (acid), mescaline, ibogaine, and ayahuasca for a wide range of psychiatric disorders. Esketamine has already been approved for treatment-resistant depression. Researchers and journalists, such as Michael Pollan, have dubbed these developments a “psychedelic renaissance” that will revolutionize psychiatry, open new understandings of the connection between mind and brain, and provide benefit to thousands of patients.

But doesn’t this sound all too familiar? The “psychedelic renaissance” feels like the next Harringtonian revolution, with its bombastic claims, massive financial investment, and at this point, uncertain benefit for patients. The verdict is still out about efficacy, but what is already clear is that the pharmaceutical industry has taken notice. In 2020 London-based Compass Pathways, which received seed investment from Peter Thiel’s Thiel Capital, was the first psychedelic pharmaceutical company to go public, with a post-IPO run-up valuation of $1.1 billion.

A pill, however effective, cannot abolish the carceral and capitalist system that is the source of so much trauma.

Not to be left out, Big Pharma is also up to its usual tricks. As I have noted elsewhere, Johnson & Johnson was interested in ketamine’s benefit for depression but could not patent the drug, because it was already a cheap generic. J&J decided to make a copycat, chemically isolating one of the compound’s mirror images. They called this “me-too” compound “Spravato,” patented the drug, and now, charge almost one thousand dollars per dose. Companies are already using similar tactics to isolate patentable compounds from psychoactive botanicals that Indigenous communities have used for centuries, raising ethical concerns about how the burgeoning psychedelic industry perpetuates Euro-American exploitation of Indigenous knowledge, plants, and land in settler colonies.

This “psychedelic renaissance,” then, is likely just the next stage of the larger revolution in Big Pharma that started in the 1980s. And whatever clinical benefit psychedelics end up offering, drugs are not a solution for the structural problems that plague our mental health system. Big Pharma, and the academic psychiatrists who partner with industry, will continue to profit. And psychedelics can only help those who have access to them in our society: mostly white, upper middle-class people with private insurance.

While both of these impressive books cover significant historical ground, they also miss something critical about psychiatry’s past that limits their vision of its future: they fail to confront the profession’s role in the mass incarceration of the Black community over the last half-century. For Harrington and Scull, carceral approaches to psychiatry largely came to an end, at a population level, with the closure of large asylums and the rise of deinstitutionalization—a movement in the 1960s that attempted to transition care from psychiatric hospitals to communities. In this common narrative, the problem with deinstitutionalization was one of neoliberal neglect: patients were discharged en masse from institutions with few resources and little support, leading to high rates of homelessness among people with serious mental illness.

But this story overlooks the silent and subtle ways that incarceration has become further intertwined with psychiatry. As historian Anne Parsons has argued, “the asylum did not disappear” with deinstitutionalization. Instead “it returned in the form of the modern prison industrial complex.” Some of the largest mental health centers in the country currently operate in prisons, and today, there are more people with serious psychiatric illness in America’s prisons than in its remaining psychiatric hospitals. Around 40 percent of people diagnosed with serious mental illness will face incarceration in their lifetimes, in many cases, as a consequence of the racist policies that undergird the ongoing War on Drugs. This carceral mental health is highly segregated. While psychiatric hospitals tend to house white, middle-aged patients, prisons disproportionately confine people with psychiatric disorders who are Black and under the age of forty.

Moreover, sociologist Anthony Ryan Hatch has argued that the use of prison psychopharmaceuticals has allowed for incarceration at the level of the brain. Prison-policy strategists have framed psychopharmaceuticals not as medical treatments but rather, as an important component of technocorrections, that is, “the strategic application of new technologies in the effort to reduce the costs of mass incarceration and minimize the risks prisoners pose to society.” In 2000, some 95 percent of maximum or high-security state prisons were distributing psychiatric drugs to incarcerated people.

These facts are missing from these books because both Harrington and Scull are ultimately focused on elite academic psychiatrists—a community that tends to avoid work in prisons. As Hatch notes, almost all of our public knowledge about psychopharmaceuticals comes from their use among the unincarcerated, while knowledge about prison psychotropics tends to be as tightly guarded as inmates themselves. This silence is a form of oppression that covers up both the use of psychotropics as a technology of custodial control and the failure to provide people in prison—many of whom are traumatized by their incarceration—with the humane treatment that they deserve.

As a psychiatrist myself, I believe that an important part of this tragedy is the silence and lack of accountability among those who represent our field. Despite the decreasing life expectancy of people with mental illness, high rates of incarceration and homelessness, and the failure of the biological paradigm, the biopsychiatric research machine just keeps growing. In his own new book, Healing: Our Path from Mental Illness to Mental Health, Insel argues that the failures of biological psychiatry’s past indicate that we should “double down on brain research” instead of re-examining our priorities. Insel’s successor at the NIMH, Joshua Gordon, has maintained the organization’s focus on biopsychiatric research, narrowly construed. While both Harrington and Scull point to a “crisis” in the profession today, the scarier truth is that many in the academy are proceeding with business as usual. The real crisis in academic psychiatry, in other words, is that there is no crisis.

These books invite us to imagine a future where the billions invested in biological research are instead redistributed to the communities who need it most.

If these histories of elite academic practitioners do not show us the whole problem, they are also not going to produce imaginative solutions. Searching for answers requires de-centering the academy and looking to narratives that have largely been neglected in standard histories of psychiatry. The historical work of disability activist and scholar Liat Ben-Moshe, for example, turns to Mad communities who have embraced neurodivergence not as a medical problem that needs to be fixed but as an identity that should be celebrated. Mad activists and professional allies in the 1970s, such as the antipsychiatrist Thomas Szasz, successfully demanded the abolition of violent psychiatric hospitals and carceral practices in American society. While this movement to deinstitutionalize psychiatry did not result in wholesale liberation of people with disabilities in the United States, Ben-Moshe argues that it offers important lessons about how communities can successfully resist the structures that repress them in the name of care.

Ben-Moshe’s work not only provides a means for critically examining the psychiatric violence of the past but also offers what she calls “genealogies” for thinking about futures that seem otherwise unimaginable. Genealogies of resistance conceptualize “health” not in terms of access to individualized treatment provided by academic physicians but rather in terms of collective liberation from the structural conditions that produce the vast extent of psychological suffering and trauma. These genealogies undergird the work of communities and professionals fighting today to abolish the carceral system and to imagine non-violent forms of care through peer support, soteria houses, and political protest. In Los Angeles last year, for example, a vocal coalition of community organizers, academics, and officials successfully stopped the construction of a “psychiatric jail” and advocated for the reinvestment of those funds into initiatives for community-based mental health care. “Care first, jails last,” they are demanding.

There are also unexpected lessons here for more privileged communities. Material wealth does not completely insulate people from the psychological damage of capitalism, of course. Burnout and depression are endemic among upper middle-class physicians and medical students, to name only one example. Over a third of students at Yale, many of whom come from privileged backgrounds, seek mental health services for psychic distress. As psychotherapist Gary Greenberg has bluntly put it, “The fact is, if we didn’t have such a fucked-up society, I’d be out of a job.” Psychological suffering in the upper crust of society is not only evidence that we need increased access to care, whether through pharmaceuticals or psychotherapy. It is also a call to mobilize against the pathogenic features of our local social climates, from toxic training programs and high-pressure university cultures to dehumanizing factory floors. As historian Joanna Radin encouraged me to discuss in my undergraduate course on the History of Drugs, the question is not only, What is the right drug for me?, but also: What would the world have to look like for me not to need drugs at all?

Harrington and Scull surely did not intend for their books to be read this way, but we might understand them as a call to defund biological psychiatry in the United States—to refuse yet another promise of a “revolution” or “renaissance” that would save an academic project that has done little to help and lots to harm. We do not need to be neuroscientists to know that psychological and emotional suffering is “real” or “legitimate,” and that a pill, however effective, cannot abolish the carceral and capitalist system that is the source of so much trauma. As these books teach us, psychiatric paradigms are fragile, and perhaps biology’s tenuous grip on the profession is finally easing under the strain of recent critiques. The future of our profession, if it has one, does not lie in tired promises of biological breakthroughs. It depends on unearthing and embracing neglected histories and genealogies of solidarity with the communities that academic psychiatry claims to serve.

Marco Ramos

Marco Ramos, MD, PhD, is a historian of medicine and psychiatry resident at Yale University. His historical research focuses on mental health activism and ...

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Communities in three Australian states have been ordered to evacuate as torrential rain brings major flooding.

Parts of the country have received up to four times their average October rainfall in just 24 hours.

At least 500 homes have been flooded, one person has died and another is missing as the disaster unfolds.

Widespread flooding across Australia - driven by a La Niña weather pattern - has killed more than 20 people this year.

Victoria - Australia's second most populous state - has been worst hit this week. Several communities have been ordered to evacuate, including some in the state capital Melbourne.

Floods have swamped roads, forced school closures and cut power to 3,000 houses and businesses.

Premier Daniel Andrews said the number of inundated homes was "absolutely certain to grow", calling it one of the state's worst flood events in decades.

"This has only just started, and it's going to be with us for a while," he told the Australian Broadcasting Corporation.

Barry Webster, who lives in Melbourne's north-west, is one of those whose house has gone underwater.

"I always said I wanted riverfront views, but not like this," he told The Age.

"Going downstairs and seeing the lounge floating… it's a bit surreal, kind of like a movie."

Many areas received massive 24-hour rainfall totals, but the highest was in Strathbogie, north-east of Melbourne.

It received 220mm - more than double the town's average October rainfall, or about a third of London's annual average.

Several rivers have also flooded in Tasmania after up to 400mm of rain fell in some areas in 24 hours. It is unclear how many homes and business have been affected there.

In New South Wales, about 600 people were told to evacuate from the town of Forbes, where about 250 properties and business were expected to flood.

One man died in the state's west earlier this week after his car became submerged in floodwaters.

Rescuers have also been searching for man thought to have been swept away in similar circumstances on Tuesday.

More rain is forecast in the coming weeks, placing strain on already swollen rivers and saturated ground.

Experts say recent flooding in Australia has been worsened by climate change and a La Niña weather phenomenon. In Australia, a La Niña increases the likelihood of rain, cyclones and cooler daytime temperatures.

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"It was important to document the work that has been done. We really do want to raise the profile of the use of machine learning in nuclear physics to help people see the breadth of the activities," said Amber Boehnlein, lead author of the paper and the associate director for computational science and technology at the U.S. Department of Energy's Thomas Jefferson National Accelerator Facility.

Because the paper gathers and summarizes major work in the field thus far, Boehnlein hopes it can act as an educational resource for interested readers, as well as a roadmap for future endeavors.

"It provides a benchmark that people can use as they go forward into the next phase," she said.

A machine learning revolution

After attending a workshop exploring artificial intelligence at Jefferson Lab in March 2020 and publishing a follow-up report, Boehnlein and two of her co-authors, Witold Nazarewicz and Michelle Kuchera, were inspired to go a step further. Together with 15 colleagues representing all subfields of nuclear physics, they decided to conduct a survey of the state of machine learning projects in nuclear physics.

They started at the beginning. As the authors describe, the first significant work employing machine learning in nuclear physics used computer experiments to study nuclear properties, such as atomic masses, in 1992. Although this work hinted at machine learning's potential, its use in the field remained minimal for more than two decades. In the last several years, that changed.

Machine learning, which involves building models that can perform tasks without explicit instruction, requires computers to do specific things, including complicated calculations. With recent advances, computers can better meet these demands, which has allowed physicists to more readily incorporate machine learning into their work.

"This would have been a less interesting paper in 2019, because there wouldn't have been enough work to catalog. But now, there is significant work to cite due to the increased use of the techniques," Boehnlein said[.]

Today, machine learning spans all scales and energy ranges of research, from investigations of matter's building blocks to inquiries into the life cycles of stars. It is also found across the four subfields of nuclear physics: theory, experiment, accelerator science and operations, and data science.

"We made an effort to compile a comprehensive, collective resource that bridges the efforts in our subfields, which will hopefully spark rich discussions and innovation across nuclear physics," said co-author Kuchera, who is an associate professor of physics and computer science at Davidson College.

Machine learning models can be used to help both the design and execution of experiments in nuclear physics. They can also be used to aid in the analysis of those experiments' data, of which there is often in excess of petabytes.

"I expect machine learning to become embedded into our data collection and analysis," Kuchera said.

Machine learning will speed up these processes, which could mean less time and money is needed for beamtime, computer usage, and other experimental costs.

Connecting theory and experiment

So far, however, machine learning has developed the strongest foothold in nuclear theory. Nazarewicz, who is a nuclear theorist and chief scientist at the Facility for Rare Isotope Beams at Michigan State University, is especially interested in this subject. He says that machine learning can help theorists do advanced calculations faster, improve and simplify models, make predictions, and help theorists understand the uncertainties of their predictions. It can also be used to study phenomena that researchers cannot conduct experiments on, such as supernova explosions or neutron stars.

"Neutron stars are not very user friendly," said Nazarewicz.

He uses machine learning to study hyperheavy nuclei and elements, which have so many protons and neutrons in their nuclei that they can't be observed experimentally.

"I find the results to be the most impressive in the theory community, particularly the low-energy theory community that Witold is associated with," Boehnlein said. "They seem to be really embracing these techniques."

Boehnlein said theorists have also started to embrace these techniques at Jefferson Lab in their study of proton and neutron structures.

Specifically, machine learning can help extract information from complicated theories, such as quantum chromodynamics, the theory that describes the interactions between the quarks and gluons that make up protons and neutrons.

The authors predict that machine learning's involvement in both theory and experiment will speed up these subfields independently, and it will also better interconnect them to speed up the entire loop of the scientific process.

"Nuclear physics helps us make discoveries to better understand the nature of our universe, and it's also used for societal applications," said Nazarewicz. "The faster we can do the cycle between experiment and theory, the faster we will arrive at discoveries and applications."

As machine learning continues to grow in this field, the authors expect to see more developments and broader applications incorporating this tool.

"I think we're only in the infancy of the application of machine learning to nuclear physics," Boehnlein said.

And, along the way, this paper will act as a reference, even for its own authors.

"I hope the paper is used as a resource to understand the current state of machine learning research, allowing us to build from these efforts," Kuchera said. "My research is centered on machine learning methods, so I absolutely will utilize this paper as a window into the state of machine learning across nuclear physics right now."

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The damage to capital investment and R&D in the Western semiconductor industry will exceed Washington’s modest subsidies for the chip industry by a factor of five or more.

The US measures won’t affect China’s sensors, satellite surveillance, military guidance and other strategic systems because the vast majority of military applications use older chips that China can produce at home. But it may postpone autonomous driving, cloud computing and other efforts to digitize China’s economy.

It will also elicit an all-out Chinese effort to replace American chip-making and design technology. CapEx and R&D will shrink drastically in the US semiconductor industry while China allocates a massive budget to the sector.

On a five- or ten-year horizon, America’s technological edge in semiconductor design and fabrication is likely to vanish. As capital budgets collapse in the Western semiconductor industry, the damage to the US and other Western economies is likely to be greater than the harm inflicted on China.

US President Joe Biden wants more advanced semiconductors produced in America. Image: Twitter

The Biden administration meanwhile proposed a 14% budget cut for the Defense Advanced Research Projects Agency (DARPA), which is a much larger cut after inflation. Starving US high-tech industry of public as well as private funds is a strange way to conduct a strategic rivalry with China.

The incipient global recession turned the chip shortage of 2021 into a glut, reflected in a collapse of the Philadelphia index of semiconductor stocks (PHLX) by nearly half during 2022. NVIDIA, the leading US chip designer, has lost 68% of its market capitalization so far this year.

The industry had already cut capital investment plans from about US$200 billion to $160 billion for 2022. US restrictions on exports of semiconductor equipment, design tools and high-end chips to China will shrink revenues further, putting an air pocket into R&D and capital expansion. The world’s dominant chip fabricator, Taiwan’s TSMC, planned $44 billion in CapEx just six months ago but on Wednesday announced a cut to $36 billion.

The Biden administration’s $50 billion, five-year subsidy for onshore chip fabrication will help firms that use older technology to supply the US defense industry, which mainly buys chips five to seven generations behind the cutting-edge semiconductors targeted by the new round of US sanctions.

Smaller American fabricators like GlobalFoundries and SkyWater Technology, who make chips for the US military several generations behind the present state of the art, will benefit from the Biden subsidies. But companies with the most advanced technology have the most to lose, including American manufacturers of chipmaking equipment.

It’s still unclear what loopholes will be left in Washington’s chip bans, or how damaging they will ultimately be. Reuters headlined an October 12 report, “US scrambles to prevent export curbs on China chips from disrupting supply chain,” noting that the leading South Korean fabricators, Samsung and SK hynix obtained a 12-month reprieve for investment in their mainland chip plants, while TSMC obtained a one-year license to ship US chipmaking equipment to its expanding plants in China.

Few military applications of chip technology will be affected. According to a 2022 RAND Corporation study, the vast majority of chips used by the US military use so-called mature nodes with wider transistor gate width than the latest 3 to 7-nanometer (nm) chips that only TSMC and Samsung can produce. RAND published the chart below showing the node size of chips employed for key military applications:

The new US restrictions won’t stop China’s 2,000 surface-to-ship and surface-to-surface missiles from targeting US aircraft carriers in the Western Pacific, or US air bases in Guam and Okinawa, and they won’t prevent China’s more than 1,000 interceptors from aiming long-range air-to-air missiles at US planes. But they are likely to delay the rollout of key digital applications in China’s civilian economy, such as autonomous vehicles.

The US is “doing everything in our power to protect our national security and prevent sensitive technologies with military applications from being acquired by the People’s Republic of China’s military, intelligence, and security services,” US Commerce Department official Alan Estevez said in an October 7 release.

The best that might be said about the Biden policy is that it came ten years too late to make a dent in the military balance in the Pacific. But the Biden administration estimates that it will spend $30 billion a year in student loan forgiveness over the next ten years, but less than $10 billion a year in subsidies to the US semiconductor industry.

Federal subsidies will cover a small fraction of the reduction in CapEx and R&D due to the economic downturn and restrictions on semiconductor sales to China.

China is by far the world’s largest consumer of semiconductors, with 53% of the global total. The US manufactures just 12% of the world’s chips, but it leads in some areas of chip technology, including some chip-making equipment.

LAM Research, a top producer of etching and other hardware, earned 30% of its sales revenues from China in 2022. KLA, its top competitor, also sells to China. Cadence, a top producer of Electronic Design Automation (EDA) software, obtained 45% of its total revenue from China in the second quarter of 2022.

Two years ago, a Boston Consulting Group study warned that an all-out US ban on chip sales to China would eliminate 37% of the revenue of US semiconductor companies, lead to severe cuts in R&D and capital expenditures, and the loss of 15,000 to 40,000 highly skilled direct jobs in the US semiconductor industry.”

China can’t match American EDA tools yet. It would take China five to ten years to catch up, using software it already had purchased, or pirated copies without manufacturer support. It also can’t match the lithography machines that burn impossibly small transistors with a gate width of 7nm or less, with Extreme Ultraviolet (EUV) technology.

ASML introduced the first extreme ultraviolet (EUV) lithography machines for mass production in 2017, after decades spent mastering the technique. Credit: ASML

That’s available only from Holland’s ASML, and the US has banned sales of the newest machines to China because they contain a significant amount of US intellectual property.

Hardest to gauge is China’s ability to work around US technological restrictions. Mainland China has 20 of the world’s 50 highest-ranked engineering schools – and more if Hong Kong is counted – and graduates seven times the American count of engineers each year. China can’t buy some American technology, but it can hire anyone it wants.

At worst, the damage to China’s economy is likely to be temporary, and the impact on its military capacity is likely to be minimal. But the impact of the incipient depression in the Western semiconductor industry may well do permanent harm.

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If someone drives aggressively in an EV, how does that affect the battery life?

How much do variations in battery materials make a difference in how an EV performs in various conditions?

Researchers and manufacturers have partial answers to these questions based on the data they have collected. But they would know much more if they shared their data in formats they all could understand.

This is the premise behind the Battery Data Genome, a new initiative led by Argonne National Laboratory in Illinois and Idaho National Laboratory, among others. The name is a reference to the Human Genome Project, a monumental data-sharing project launched in 1990 that contributed to innovations in medical science.

“It’s going to take a lot of data, data from a lot of sources,” said George Crabtree, a distinguished fellow at Argonne and director of the Department of Energy’s Joint Center for Energy Storage Research.

Crabtree is one of more than two dozen co-authors of a paper published this month in the journal Joule announcing the project. Regular readers will recognize him as someone I often ask to help translate battery science into plain language.

The Battery Data Genome will collect information from every part of the battery life cycle, including basic data like how batteries respond to different types of charging and discharging, and additional variables like the effects of temperature, driving speed, and differences in the materials within the batteries.

The participants include national labs, like Argonne and Idaho, and anyone else who wants to join, which could include universities, automakers, and other businesses. The partners can choose how much they want to share.

“I think one of the things that everyone realizes is that some will be reluctant to join, because, you know, it compromises their secrets, trade secrets, and that’s OK,” Crabtree said. “It’s kind of an open decision for anyone who wishes to participate.”

The project is aiming to create a common set of standards for how battery data is formatted, so everyone is speaking the equivalent of the same language.

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People adore their sweet treats, as seen by the enormous range of sodas, candies, and baked goods that are sold globally. However, consuming artificial sweeteners or white table sugar in excess might have negative effects on your health. Researchers looking for a better sweetener have recently published findings in the Journal of Agricultural and Food Chemistry of the American Chemical Society (ACS). The low-calorie mixture is as sweet as table sugar and, in lab tests, feeds “good” gut microbes.

The popularity of artificial sweeteners has skyrocketed because they allow individuals to enjoy sweets without the accompanying calories. Although they are thought to be safe for intake by people, research on both humans and animals suggests that some of them may stimulate appetite, resulting in increased food consumption and weight gain as well as other negative health outcomes.

As a result, scientists have started looking for low-calorie or very sweet compounds derived from natural sources as potential substitutes. Galactooligosaccharides, for instance, are low-calorie sugars with prebiotic activity that may be a source of energy for beneficial gut microbes but aren’t quite sweet enough to replace table sugar. These sugars can be found in mammalian milk. Alternatively, mogrosides, which are 200–300 times sweeter than table sugar, are found in extracts from the luo han guo fruit. However, these extracts sometimes contain off-flavors which can be removed using enzymes.

So, F. Javier Moreno and colleagues wanted to take advantage of the best aspects of both natural substances, using enzymes to modify mogrosides while simultaneously producing galactooligosaccharides for a brand-new low-calorie sweetener.

The researchers started with lactose and mogroside V (the primary mogroside in luo han guo fruit). When they added β-galactosidase enzymes, the researchers obtained a mixture that contained mostly galactooligosaccharides and a small amount of modified mogrosides. A trained sensory panel reported that the new combination had a sweetness similar to that of sucrose (table sugar), suggesting it could be acceptable to consumers.

In test tube experiments, the new sweetener increased the levels of multiple human gut microbes that are beneficial, including Bifidobacterium and Lactobacillus bacterial species. In addition, increases in bacteria-produced metabolites, such as acetate, propionate, and butyrate, indicated that the mixture could potentially have a prebiotic effect on the gut microbiome. The researchers say that the new sweetener holds promise in these initial analyses, and their next step is to study the substance’s impact on human gut health more closely.

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MIT engineers are taking advantage of a phenomenon known as emergent behavior on the microscale. They have designed simple microparticles that can collectively generate complex behavior, much the same way that a colony of ants can work together to dig tunnels or collect food.

Working together, the microparticles can generate a beating clock that oscillates at a very low frequency. The researchers demonstrated how these oscillations can be harnessed to power tiny robotic devices.

“In addition to being interesting from a physics point of view, this behavior can also be translated into an on-board oscillatory electrical signal, which can be very powerful in microrobotic autonomy. There are a lot of electrical components that require such an oscillatory input,” says Jingfan Yang. He is one of the lead authors of the new study and a recent MIT PhD recipient.

A simple chemical reaction is performed by the particles used to create the new oscillator, which allows the particles to interact with each other through the formation and bursting of tiny gas bubbles. Under the right conditions, these interactions form an oscillator that behaves similar to a ticking clock, beating at intervals of a few seconds.

“We’re trying to look for very simple rules or features that you can encode into relatively simple microrobotic machines, to get them to collectively do very sophisticated tasks,” says Michael Strano. He is the senior author of the paper and the Carbon P. Dubbs Professor of Chemical Engineering at MIT.

Along with Yang, Thomas Berrueta, a Northwestern University graduate student advised by Professor Todd Murphey, is a lead author of the study, which will be published today (October 13, 2022) in the journal Nature Communications.

Collective behavior

Demonstrations of emergent behavior can be seen throughout the natural world, where colonies of insects such as ants and bees accomplish feats that a single member of the group would never be able to achieve.

“Ants have minuscule brains and they do very simple cognitive tasks, but collectively they can do amazing things. They can forage for food and build these elaborate tunnel structures,” Strano says. “Physicists and engineers like myself want to understand these rules because it means we can make tiny things that collectively do complex tasks.”

In this study, the researchers wanted to design particles that could generate rhythmic movements, or oscillations, with a very low frequency. Until now, building low-frequency micro-oscillators has required sophisticated electronics that are expensive and difficult to design, or specialized materials with complex chemistries.

The simple particles that the researchers designed for this study are discs as small as 100 microns in diameter. The discs, made from a polymer called SU-8, have a platinum patch that can catalyze the breakdown of hydrogen peroxide into water and oxygen.

When the particles are placed at the surface of a droplet of hydrogen peroxide on a flat surface, they tend to travel to the top of the droplet. At this liquid-air interface, they interact with any other particles found there. Each particle produces its own tiny bubble of oxygen, and when two particles come close enough that their bubbles interact, the bubbles pop, propelling the particles away from each other. Then, they begin forming new bubbles, and the cycle repeats over and over.

“One particle by itself stays still and doesn’t do anything interesting, but through teamwork, they can do something pretty amazing and useful, which is actually a difficult thing to achieve at the microscale,” Yang says.

The researchers found that two particles could make a very reliable oscillator, but as more particles were added, the rhythm would get thrown off. However, if they added one particle that was slightly different from the others, that particle could act as a “leader” that reorganized the other particles back into a rhythmic oscillator.

This leader particle is the same size as the other particles but has a slightly larger platinum patch, which enables it to create a larger oxygen bubble. This allows this particle to move to the center of the group, where it coordinates the oscillations of all of the other particles. Using this approach, the researchers found they could create oscillators containing up to at least 11 particles.

Depending on the number of particles, this oscillator beats at a frequency of about 0.1 to 0.3 hertz, which is on the order of the low-frequency oscillators that govern biological functions such as walking and the beating of the heart.

Oscillating current

The engineers also demonstrated that they could use the rhythmic beating of these particles to generate an oscillating electric current. To do that, they swapped out the platinum catalyst for a fuel cell made of platinum and ruthenium or gold. The mechanical oscillation of the particles rhythmically alters the resistance from one end of the fuel cell to the other, which converts the voltage generated by the fuel cell to an oscillating current.

Generating an oscillating current instead of a constant one could be useful for applications such as powering tiny robots that can walk. The MIT scientists used this approach to show that they could power a microactuator, which was previously used as legs on a tiny walking robot developed by researchers at Cornell University. The original version was powered by a laser that had to be alternately pointed at each set of legs, to manually oscillate the current. The MIT team showed that the on-board oscillating current generated by their particles could drive the cyclic actuation of the microrobotic leg, using a wire to transfer the current from the particles to the actuator.

“It shows that this mechanical oscillation can become an electrical oscillation, and then that electrical oscillation can actually power activities that a robot would do,” Strano says.

One possible application for this kind of system would be to control swarms of tiny autonomous robots that could be used as sensors to monitor water pollution.

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Few studies have examined the impact that feast or famine has on the developing brain in isolation from other variables that contribute to adversity, despite the fact that food insecurity is an issue for a rising proportion of the American population, made much worse by the coronavirus pandemic.

University of California, Berkeley researchers have simulated the impacts of food insecurity on young mice and discovered long-lasting changes later in life.

“We show that irregular access to food in the late juvenile and early adolescent period affects learning, decision-making, and dopamine neurons in adulthood,” said Linda Wilbrecht, UC Berkeley professor of psychology and member of the Helen Wills Neuroscience Institute.

One key behavioral difference involved cognitive flexibility: the ability to generate new solutions when the world changes.

“Mice searching for rewards might be inflexible, sticking to only one strategy even when it no longer yields a reward, or they might be flexible and quickly try out new strategies. We found that the stability of the food supply mice had when they were young governed how flexible they were under different conditions when they were grown up,” she said.

Epidemiological studies have connected childhood and teenage food insecurity to later-life weight gain, as well as learning difficulties and worse math, reading, and vocabulary scores. However, other poverty-related factors, such as maternal depression and environmental stressors, confound these studies. The new research was designed to investigate the developmental and behavioral effects of food insecurity in a controlled environment that would not be achievable with human subjects.

The findings have ramifications for humans. Policymakers recognize the need for good nutrition from infancy through high school, with federally supported free or reduced-price breakfast and lunch programs offered in schools around the country. The federal Supplemental Nutrition Assistance Program (SNAP) also offers subsidies to help poor families supplement their food budgets. These meal programs have shown effects on low-income families, particularly improved academic performance and graduation rates.

But there may be times when kids cannot access food programs, such as during summer vacation. Programs may also inadvertently create a feast and famine cycle when benefits are distributed with weeks between payments, potentially leaving impoverished families unable to afford food at the end of each payment cycle. According to a recent report from the U.S. Department of Agriculture, 6.2% of households with children — 2.3 million households total — were food insecure in 2021.

“I think that we have to understand that even transient food insecurity matters, the brain doesn’t just catch up later. Food insecurity can have long-term impacts on how someone’s brain functions,” Wilbrecht said. “The ability to learn and make decisions is something that’s developing during childhood and adolescence, and we are seeing how these critical skills are impacted by access to food. Access to food is something that we can address in this county. Feeding and benefits programs exist, and we can make them better by making access to benefits or food more reliable and consistent. Supporting brain development is a good reason to support food programs.”

The research, conducted with UC Berkeley faculty members Helen Bateup, Stephan Lammel, and their lab colleagues, was recently published in the journal Current Biology.

Flexibility under changing rules

Wilbrecht and her colleagues, including Robert Wood Johnson Foundation Health and Society Scholar Ezequiel Galarce, mimicked human food insecurity in mice by delivering food on an irregular schedule while still allowing enough food to maintain a safe body weight. This food regimen began a week before puberty onset in mice, equivalent to late childhood in humans, and continued for 20 days through the equivalent of late teen ages in mice. Another group of mice was offered food whenever they wanted it.

They then tested cognition in adulthood using foraging tasks where mice searched a changing environment for rewards. For example, a behavior — in this case, learning which odor led to the Honey Nut Cheerios — might be successful for a short time, but not forever. A second odor now predicted where the reward was hidden.

The well-fed and food-insecure mice were tested as adults in both certain and uncertain settings, with noticeable differences in cognitive flexibility. Food-insecure mice were more flexible in uncertain situations than well-fed mice, while well-fed mice were more flexible in more stable situations.

“You would have to test in the field to see how these different flexibility profiles affect survival,” she said. “The findings are nuanced, but hopeful because we identify both gain and loss of function in learning and decision-making that are wrought by the experience of scarcity.”

While the effect of food insecurity on cognition in male mice was robust, female mice showed no effect on cognition.

“This is one of the most robust behavioral effects we’ve ever seen when we’ve been modeling adversity,” Wilbrecht said.

Food insecurity had other decidedly negative effects in female mice, however. Those females who were food insecure when growing up tended to become overweight when given unrestricted food in adulthood, something mirrored in humans who’ve grown up with food insecurity. Male mice showed no such effect.

Doctoral student Wan Chen Lin and researchers in the Bateup and Lammel labs also looked at the brain’s reward network, which is governed by the neurotransmitter dopamine, and found changes there, as well, in male mice.

“We found that the neurons in the dopamine system, which is critical for learning, decision- making and reward-related behaviors, like addiction, were significantly altered in both their inputs and their outputs,” Wilbrecht said. “It suggests there are more broadscale changes in the learning and decision-making systems in the brain.”

For example, the researchers saw changes in the synapses of dopamine neurons that project to the nucleus accumbens and also found changes in dopamine release in the dorsal striatum. These dopamine neurons have been shown to play a role in learning and decision-making in numerous other studies.

The researchers are continuing their studies of food-insecure mice to determine if they are more susceptible as adults to addictive behaviors, which are associated with the dopamine network.

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This breakthrough is important because plastic waste is a massive problem both globally and in the United States. In fact, only about 5% of used plastic is recycled in the U.S., according to NREL.

Packaging materials, containers, and other discarded items are filling up landfills and littering the environment at an incredibly rapid pace. According to NREL, scientists estimate that by 2050 the ocean will have more plastic by weight than fish.

A collaboration led by NREL’s Gregg Beckham and including Lucas Ellis, an OSU researcher who was an NREL postdoctoral fellow during the project, combined chemical and biological processes in a proof of concept to “valorize” mixed plastic waste.

Valorize means to enhance the value of something.

The research builds on the use of chemical oxidation to break down a variety of plastic types, a method pioneered a decade ago by chemical industry giant DuPont.

“We developed a technology that used oxygen and catalysts to break down plastics into smaller, biologically friendly chemical building blocks,” said Ellis, an assistant professor of chemical engineering. “From there we used a biologically engineered soil microbe capable of consuming and ‘funneling’ those building blocks into either a biopolymer or a component for advanced nylon production.”

Beckham, a senior research fellow at NREL and the head of the Bio-Optimized Technologies to keep Thermoplastics out of Landfills and the Environment Consortium – known as BOTTLE – said the work provides a “potential entry point into processing plastics that cannot be recycled at all today.”

Current recycling technologies can only operate effectively if the plastic inputs are clean and separated by type, Beckham explains.

Plastics can be made from different polymers, each with its own unique chemical building blocks. When polymer chemistries are mixed in a collection bin, or formulated together in certain products like multilayer packaging, recycling becomes expensive and nearly impossible because the polymers often have to be separated before they can be recycled.

“Our work has resulted in a process that can convert mixed plastics to a single chemical product,” Ellis said. “In other words, it is a technology that recyclers could use without the task of sorting plastics by type.”

Scientists applied the process to a mix of three common plastics: polystyrene, used in disposable coffee cups; polyethylene terephthalate, the basis for carpets, polyester clothing and single-use beverage bottles; and high-density polyethylene, used in milk jugs and many other consumer plastics.

The oxidation process broke down the plastics into a mixture of compounds including benzoic acid, terephthalic acid, and dicarboxylic acids that, in the absence of the engineered soil microbe, would require advanced and costly separations to yield pure products.

The researchers engineered the microbe, Pseudomonas putida, to biologically funnel the mixture into one of two products – polyhydroxyalkanoates, an emerging form of biodegradable bioplastics, and beta-ketoadipate, which can be used in the manufacture of performance-advantaged nylon.

Trying the process with other types of plastics including polypropylene and polyvinyl chloride will be the focus of upcoming work, the researchers said.

“The chemical catalysis process we have used is just a way of accelerating a process that occurs naturally, so instead of degrading over several hundred years, you can break down these plastics in hours or minutes,” said co-author Kevin Sullivan, a postdoctoral researcher at NREL.

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The cathode is a marvel of molecular choreography. How much power a battery holds, and how long it lasts, depends on its lattice of metallic atoms—how well it can catch and release lithium ions. For decades, engineers have fiddled with designs that help this movement along. And they’ve gotten pretty good, if the electrical vehicles and phones of today are any barometer. But the cathode is also the place where things inside the battery typically go wrong. This immaculate structure, so artfully arranged, starts to lose its integrity. Ions run loose, or clog up. Just like that, your battery life goes kaput.

But even as the structure fails, the atoms inside of the cathode haven’t changed. This is why, in theory, it should be possible to reuse them. “A metal atom is a metal atom,” says Alan Nelson, senior vice president for battery materials at Redwood Materials, a company that specializes in recycling. “That element doesn’t know if it was previously in a battery or if it was in a mine.” This is potentially a good thing, because many of those atoms, including metals like cobalt and nickel, are in short supply and only found in major volumes in places where mining them entails major ecological and human costs. Today, Nelson’s company released the results of tests at Argonne National Lab comparing recycled materials to virgin ones. These suggest it’s true that an atom is an atom; the performance of the two materials was almost exactly the same.

Redwood is one of a number of companies trying to turn a supply of old batteries into materials for new ones. That’s low-hanging fruit, in the sense that it involves using up waste and could ease some of the pressure on new mines. But last year, the company, which originally sold its recycled raw materials to other suppliers, took the unusual step of announcing plans to produce its own cathode materials, and later selected a site outside of Reno, Nevada, where it would spend $3.5 billion over 10 years on a new plant. The company says it plans to produce enough cathode material (as well as copper anode foil) for 100 GWh worth of battery cells by 2025—roughly equivalent to what CATL, the dominant battery maker in China, produced last year.

That’s something of a departure for the US battery industry. Despite a flurry of manufacturing announcements, bolstered in part by infrastructure spending and the climate provisions in the Inflation Reduction Act, most have been focused on the steps closest to automakers and consumers, like assembling battery cells and packs. The US has meanwhile struggled to build up industries that lie deeper in the supply chain—from the mining that digs up key minerals such as lithium and cobalt to the extensive processing that turns them into components like the cathode. Most of that is done elsewhere. According to Benchmark Mineral Intelligence, a group that studies the battery supply chain, China currently makes 78 percent of the world’s cathode materials, and that share is poised to grow to 90 percent by 2030, despite efforts in the US to invest in domestic battery supply chains.

One reason Chinese firms remain so dominant is that they have a closed loop of battery production, says Hans Eric Melin, founder of Circular Energy Storage, a consultancy that tracks battery recycling. Having battery cell production at home means it’s possible to break down scrap materials and quickly put the valuable metals back into production. The complex supply chain that refines the raw metals into that perfect crystalline cathode structure is also localized, centralizing expertise and reducing transportation costs.

Redwood is among the companies trying to pull the US manufacturing loop a little tighter. The tests, which were performed by independent researchers at Argonne National Lab, are an early step in a qualification process to reassure battery makers of the quality of these hand-me-down materials. The process begins by taking the battery apart and breaking its components down with heat and acids into metal sulfate compounds, composed of elements like cobalt, manganese, and nickel.

Once those metals have been separated, the next step is putting them together again. The design tested by the Argonne researchers is what’s known as NMC-811: 80 percent nickel, 10 percent manganese, and 10 percent cobalt. These nickel-rich cathodes have been prioritized by automakers like Tesla because they rely less on cobalt while retaining the driving range EV owners have come to expect from their new cars. The researchers took two sets of precursor materials—recycled metal sulfates provided by Redwood and sulfates made with raw material—and ran them through a series of steps that intimately mix the elements together and then layer in rows of lithium. The result is a cathode material that could be stuck into battery cells and run through a set of standard tests.

Those tests are meant to capture measures like capacity, cycle life, and rate capability, which relates to a battery’s power. The researchers found the two types of cathodes—recycled and virgin—to be nearly identical by these measures. (In some cases the recycled versions tested better, though the team cautioned that this couldn’t be tracked back to recycling.) “Honestly, it’s a pretty boring result,” says Jason Croy, a battery scientist at Argonne National Laboratory who led the research. But it wasn’t a given, he says. While an atom is an atom, there was no guarantee that recycling would produce a totally pure metal product, instead of one with irregularities or extra gunk that would mess up the final cathode design. Next, Redwood is working to scale up production and have its material tested by battery and EV makers.

What’s likely to be even trickier for Redwood is obtaining enough recycled atoms to reduce demands for mined ones. Few electric vehicles are old enough to be recycled—and those that are getting up there in years are lasting longer on the road than analysts expected. In the meantime, Redwood and other recycling startups are competing to secure a diverse array of battery sources, including from hybrid cars (a good source of nickel), power tools (which commonly use lithium manganese oxide batteries), and small devices like phones that, despite their tiny batteries, often contain a high ratio of cobalt. “We still feel very comfortable that, based on our feedstock, we’ll be able to source 30 percent recycled nickel and 30 percent recycled lithium,” Nelson says. Due to declining demand for cobalt in newer battery designs, he expects recycling to cover all of Redwood’s needs for the metal.

Still, the company will also need to source plenty of new material for its cathodes, just like battery makers everywhere. “I think it’s important to look at Redwood more as a materials company than as a recycler,” says Melin. He points out that the company currently sources about half of its material from scrap discarded by battery makers—which, while good to reuse locally, isn’t actually material that’s getting its second run in a battery cell. That’s likely to remain the case for some time, he says, as the flow of dying batteries remains a trickle relative to demand for new ones. In the meantime, he adds, the world will need many more mines.

Recycled Battery Materials Can Work as Well as New Ones

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Black hole “burps” at half the speed of light, years after devouring star

At the end of September, a spot of good news: Relyvrio, a new drug for treating amyotrophic lateral sclerosis—or ALS, a neurological disorder without a cure—was approved in the United States. The ALS community rejoiced; the drug’s authorization was described as a “long-sought victory for patients.” 

But the next day, the price of the medicine was revealed: $158,000 a year. This was far higher than what the Institute for Clinical and Economic Review, an independent nonprofit that analyzes health care costs, had estimated would be a reasonable price, which it deemed to be between $9,100 and $30,700. 

Americans, though, probably weren’t shocked. Prescription drugs in the US cost about 2.5 times what they do in other countries, and a quarter of Americans find it difficult to afford them. Almost every new cancer drug starts at over $100,000 a year. And a 2022 study found that every year, the average price of newly released drugs is 20 percent higher. 

How drug prices are set in the US is a mysterious black box. When rationalizing their lofty price tags, one of the most common reasons pharmaceutical companies will cite is that a high price is needed to make good on the money invested in research and development. 

But is that true? “You hear it so much,” says Olivier Wouters, an assistant professor of health policy at the London School of Economics and Political Science. “That’s why I was like, well, let’s get some data, because I don’t believe it. I don’t think anyone believes it.”

So Wouters did just that. In September 2022, he and his colleagues published a new paper in JAMA that took this simple argument and put it to the test. In the study, they looked at the 60 drugs that had been approved by the US Food and Drug Administration (FDA) between 2009 and 2018 for which there was publicly available information about both R&D spending and pricing. And then they matched up the figures. “Essentially, it was like investigative journalism—check all the receipts, trace back in time on what they spend,” he says. If it were the case that R&D spending was the reason behind high drug prices, you’d expect to see a high correlation between the two. Instead, they found no correlation. 

Wouters acknowledges that the sample size in the research is small, but this is because pharmaceutical companies keep most of their financial data under lock and key. If the industry wants to refute the conclusion reached in his paper, then pharmaceutical companies need to make more data available, he says. 

To anybody in the field, the response to the paper’s finding is: Well, duh. We know what drives drug pricing, says Ezekiel Emanuel, chair of the Department of Medical Ethics and Health Policy at the University of Pennsylvania. “It’s, ‘How far can I go? What will the market bear?’” Still, Emanuel says, it’s important to have empirical data like this study to refute the industry’s claim.

Intuitively, it feels plausible that a drug’s price would be linked to its R&D costs—the risky biz of innovation is super expensive, right? It turns out even this is highly contested. In 2020, Wouters published another paper in JAMA that dug into how much it actually costs to bring a new medicine to market, something experts have been trying to work out for decades. The number thrown around the most comes from one paper, which relied on confidential data provided by pharmaceutical companies, estimating that it takes around $2.8 billion. “These estimates are sort of shrouded in secrecy. There’s a lot of controversy around them,” says Wouters. He and his colleagues instead found the number shook out at closer to $1.3 billion, less than half the commonly held estimate. Substantially lower R&D costs would suggest that this spending shouldn’t have such a big bearing on drug pricing.

Every so often, there are small glimpses behind the curtains into how pharmaceutical companies actually decide on a drug price. An example of this is the hepatitis C drug Sovaldi, which was put on the market in 2013 for a steep $84,000 per 12-week course. In 2015, an 18-month-long US government investigation that reviewed some 20,000 pages of internal company documents revealed that Gilead, the company who owned the drug, had set the high price as a way “to ensure its drugs had the greatest share of the market, for the highest price, for the longest period of time”—in essence, that it was prioritizing profit. In response Gilead said it “stand(s) behind the pricing of our therapies because of the benefit they bring to patients and the significant value they represent to payers, providers, and our entire healthcare system by reducing the long-term costs associated with managing chronic [hepatitis C virus].” 

In other countries, the price paid for a drug is decided by bodies that look at the value the drug provides. In the United Kingdom, for example, the National Institute for Health and Care Excellence (NICE) lands on the value of a new medicine by working out how much it costs to give a patient an extra year of “quality life” in comparison to current treatments on offer. If the drug offers too little value, NICE won’t recommend it to the National Health Service. Countries like France and Germany negotiate with pharmaceutical companies to land on a price determined by the clinical benefits a drug provides compared to others on the market. 

In the US, things may be beginning to slowly move in this direction. Under the new Inflation Reduction Act, Medicare will be allowed to negotiate prices for a small selection of drugs. However, Emanuel is skeptical it will actually have a big impact on drug price regulation, given the way that law was designed—too many loopholes, he says.

As for holding pharmaceutical companies to account, it shouldn’t fall to academics to do this, says Tahir Amin, founder and executive director of the Initiative for Medicines, Access & Knowledge (I-MAK), a nonprofit that addresses inequities in how medicines are developed and distributed. “We need the government authorities and bodies to be doing this work,” he says of the analysis by Wouters’ team. “How are they setting policy when they do not have this information?”

Wouters doesn’t see his paper as a game changer, but it's another weapon in the arsenal of those with power to refute excuses made by pharmaceutical companies. “I never thought this was a gotcha,” he says. “No, we always expected this to be the case. But I’m a firm believer that we need some evidence to point to.”

Big Pharma Says Drug Prices Reflect R&D Cost. Researchers Call BS

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Celine halioua drops into a crouch and greets Bocce, a Chihuahua-dachshund mix with soulful brown eyes, like a long-lost friend. “Oh my God, you’re so beautiful!” she chirps. The two have just met in an upstairs room at Muttville Senior Dog Rescue in San Francisco, where light streams in through the open windows and urine occasionally streams onto the floor. About a dozen elderly dogs, none taller than a kneecap, putter around on the gray linoleum or nap on blankets. When Halioua kneels, her dark hair tumbling over her shoulder, Bocce rests his head blissfully in her lap.

A tragedy of human-canine relations is that a 10-year-old dog such as Bocce is old, while a 28-year-old person such as Halioua is in the prime of life. Bocce is one of the lucky ones. Many dogs can only dream of living as long as he likely will, because dog lifespan is inversely correlated with body size. It’s the opposite of the wider pattern in the animal kingdom, where elephants easily outlast mice, which in turn outlive mosquitoes. A Chihuahua can expect roughly 15 years of life; an Irish wolfhound or Great Dane around seven or eight.

Halioua hopes that the startup whose name is emblazoned on her slim black T-shirt—Loyal—can start to fix this bug in humanity’s 14,000-year-plus wolf bioengineering project. The company, which she founded in 2019 and leads as CEO, is developing drugs to delay aging in dogs and extend their healthy lifespan. She has raised around $58 million and has two drugs in development. In a few years, she hopes to have the first commercial drug—for any species—to state on the label that it delays aging or extends lifespan. That alone would be a triumph, but Halioua sees it as a springboard to a still greater feat: creating similar drugs for humans.

The search for an antiaging elixir goes back at least to the Epic of Gilgamesh, and even today the most far-out ideas for thwarting death—freezing people for eventual revival, reincarnating them digitally—sound an awful lot like technological fairy tales. But in the world of lab animals, life extension is already here, with studies boosting or even doubling the lifespans of worms, flies, and mice. Regulators such as the US Food and Drug Administration, though, have not yet recognized aging as a condition that can be treated.

Celine, human. Age: 28. Lifespan: 79.

 Photograph: Joe Pugliese

Halioua, a fast talker who speaks in a confident, sometimes bewildering mix of Silicon Valley and biotech jargon, believes that starting with dogs puts her on the best and cutest path to the first aging treatments for people. There’s no escaping the poor odds of any treatment succeeding—about 90 percent of new drugs crash out of clinical trials as failures. But running a doggie clinical trial is cheap compared to a human one, and the animals’ shorter lives mean it won’t take decades to know whether a pill boosts longevity. Plus, the lifespan and lifestyle of a pet dog are more humanlike than a lab mouse’s is, so Halioua argues she’ll be in a good position to leap from pups to people.

For Halioua, who survived a toxic stint in academia before founding her company, Loyal is a way to work against aging on her own terms. That it happens to involve dogs—animals she has loved since her upbringing in suburban Texas—is canine kismet. It gives her an excuse to hang out at Muttville, for one, where Loyal has worked with the staff to recruit owners and their dogs into two studies of aging.

Sitting cross-legged on the floor, Halioua can imagine Muttville caring for a more diverse crowd if Loyal’s drugs work. “In that world, the age of dogs here would maybe go out from 10 to 12 or 14,” she says, as a glossy black spaniel mix with a grizzled muzzle named Snoop Dawg methodically licks her right arm.

For many dogs lucky enough to have homes, life has never been better. Pet parents invest more cash and emotion in them than ever and grant them a social standing that creates what sociologist Andrea Laurent-Simpson calls multispecies families. A drug to lengthen their time together would seem to be an easy sell. And should dogs end up delivering more years to humans? You couldn’t ask a best buddy for more.

halioua was a sophomore majoring in neuroscience at the University of Texas at Austin when she discovered aging research. In a departmental newsletter, she spotted an ad for summer internships at leading labs working on age-related diseases, decided to apply, and got a position at a prestigious independent stem cell lab in La Jolla, California. She’d never heard of the internship’s sponsor—a Silicon Valley-based nonprofit called the SENS Research Foundation, whose mission was to “help build the industry that will cure the diseases of aging.” Its cofounder and scientific mastermind was a Merlin-bearded computer scientist turned aging researcher named Aubrey de Grey. He was a fringe but high-profile voice in a corner of biology that itself was not fully established.

In 1993, shortly before Halioua was born, a team of molecular biologists at UC San Francisco, led by Cynthia Kenyon, showed that partially disabling a single gene in the millimeter-long nematode worm Caenorhabditis elegans could double its lifespan. For the worms in Kenyon’s lab, that equated to an additional 24 days spent eating E. coli bacteria, but the title of the group’s report in a nematode newsletter drew a provocative analogy to humans: “A Mutation Which Doubles C. elegans Life Span (Imagine Being 140).” The study helped ignite a new field dedicated to unpicking, and wresting control of, the biological mechanisms of aging.

Kenyon and other researchers tracked down genes linked to longevity and traced the biochemical pathways they controlled. Intriguingly, some of the same mechanisms they identified in worms could extend life in flies and mice. In labs around the world, evidence began to mount that aging was not just inevitable degradation. It was another biological process with genetic controls and components that might one day be hacked. The long lives of some wild animals hinted at the possibilities. DNA repair mechanisms help one of the longest-lived mammals, bowhead whales, live to 200 or more. Naked mole rats and some tortoises appear to slow biological time, making them remarkably resistant to age-related disease.

De Grey was inspired by the science but irritated by what he saw as society’s indifference to the prospect of slowing or even reversing aging in humans. In 2003, he drew interest to his cause by celebrating a dwarf mouse known as GHR-KO 11C, who died at Southern Illinois University a week short of his fifth birthday—roughly double his expected lifespan—thanks to a tweak similar to what Kenyon had done to extend worm longevity. De Grey announced that 11C’s creator had won the first payout from the Methuselah Mouse Prize, a fund of about $33,000 for scientists who set new records for mouse longevity. When speaking about 11C’s achievement, de Grey took the opportunity to promote a program he had drawn up called Strategies for Engineered Negligible Senescence that he claimed could eventually defeat aging, allowing a person who was 50 in 2030 to enjoy another 80 healthy years of life.

De Grey’s pronouncements charmed journalists but rankled many biologists, and in 2005, 28 distinguished researchers wrote a paper declaring his strategies—using genetic engineering, targeted toxins, and tweaks to the human immune system—a farrago in “the realm of fantasy rather than science.” This did little to hinder their target, whose eloquent but wild predictions continued to win media attention and who made headway with tech industry freethinkers. The next year, he received $3.5 million from Peter Thiel, a cofounder of PayPal. In 2009, de Grey cofounded the SENS Research Foundation, headquartered in Mountain View, California, across the 101 highway from Google.

By the time Halioua started her internship in La Jolla, the foundation was providing small grants to researchers around the world and had labs of its own in Mountain View, directed by de Grey. The summer fellowship program was intended to incubate a new generation of scientists who would dedicate themselves to the organization’s vision.

As much by accident as by design, Halioua’s summer in California primed her to think more deeply about aging than most teens. She spent her days gazing through a microscope at cells harvested from patients who had died from aggressive brain tumors, which, as with most forms of cancer, become more likely with age as changes accumulate in a person’s DNA. In the evenings, she returned to a room rented from an elderly but lively veteran with a goofy smile and a hill-running habit. The vet befriended the nervous intern, showing her around La Jolla and inviting her along on dates with his girlfriend. It was her first personal connection with an elder outside her own family. “He helped me realize, ‘Oh, I will be this old one day,’” Halioua says.

At the end of the summer, Halioua flew to the SENS Research Foundation’s annual conference in San Francisco, where she met de Grey and received a full-immersion baptism in the antiaging Kool-Aid. The crowd mixed respected academic scientists with tech investors, a science adviser to Obama’s secretary of state, and, in Halioua’s words, “immortalists” hoping to see de Grey’s most far-out predictions come true.

The idea that aging might one day be treatable, like a disease, was gaining ground in the world of medical research, and among Silicon Valley’s richest men. Shortly after turning 40, Google cofounder and CEO Larry Page announced that his company was backing a new venture called Calico that would work on aging treatments. It hired Cynthia Kenyon, the creator of the long-lived worms and just one of many academics changing the conception of aging. The US National Institutes of Health, the world’s largest public backer of medical research, created a “geroscience” initiative to investigate how the aging process contributed to chronic diseases traditionally seen as separate, such as Alzheimer’s and cancer, and how scientists might tinker with underlying processes common to them all.

One after another, studies in lab animals were showing that certain drugs could extend lifespan and stave off age-related diseases, a tantalizing glimpse of what people might one day enjoy. Some of them appeared to do so by boosting cellular signals that ramp up when food is scarce, mimicking the effects of a restricted-calorie diet. One of those drugs is rapamycin, taken by humans receiving an organ donation. In mice, it could extend their lives by up to 25 percent and also delay or reverse heart disease, cancer, and cognitive decline—results that were “absolutely astonishing,” says Steven Austad, codirector of an NIH aging research center at the University of Alabama at Birmingham. Austad was a coauthor on the 2005 paper slamming de Grey’s scientific ideas, but he agreed with the agitator of aging on one high-level point: It was worth seriously investigating how aging might be treated in humans.

in 2016, halioua returned to La Jolla for a second internship, renting the same room from her elderly friend. She found him diminished and dying from pancreatic cancer. He was still running but was easily winded, and he was struggling to pay the health insurance premiums underwriting his chemotherapy. Halioua smuggled him extra cash by intentionally overpaying her rent out of her modest fellowship stipend.

De Grey’s argument that it was imperative to devote more scientific effort to slowing or halting the processes underlying cancer and other age-related diseases began to feel more convincing. “It just made so much sense,” Halioua says. “I very quickly knew that this was a hundred percent where I was going to spend my life.” At the end of that summer she gave a presentation on her project, impressing an Oxford researcher involved with de Grey’s nonprofit. When he suggested she join him in the UK as a grad student, with SENS Research Foundation funding, she accepted. That fall, her La Jolla landlord died. In 2017, she flew to England with a new mission in life.

Halioua fell in love with Oxford. Her thesis examined how health systems might cover treatments that only paid off far in the future, a potential challenge for antiaging drugs. She had a part-time job consulting on science with a biotech startup that was also backed by the foundation. But her new life began to fracture.

Halioua’s relationship with her supervisor broke down. She felt he bullied her and was controlling, requiring her to do work related to a company he worked for and restricting whom she could talk with. (Halioua has spoken publicly about her experience without naming her supervisor. He did not respond to a request for comment.)

She also became uncomfortable with the SENS Research Foundation and its animating spirit, de Grey. She initially admired the foundation, she says: “They had a lot of glitz and glam for me.” She was impressed by the organization’s formal dinners, where rich and distinguished men were encouraged to donate to the war on aging. But she started to suspect she was only being invited “because I was a cute young girl,” she says. “Also smart, but that wasn’t what they cared about.” At one dinner, she says, de Grey plied her with alcohol and told her that as a “glorious woman” she had a duty to have sex with potential donors to encourage contributions. (After Halioua went public with her allegations several years later, de Grey denied making the statements.)

By 2018, Halioua was looking for an escape route. “I really snapped because of all of that stuff Aubrey and my professor did,” she says. “It created this desire to create my own sphere of influence, where I control the rules.” She turned to one of the only prominent women in the small circles working on aging treatments, Laura Deming. Deming was a wunderkind who had started working at age 12 in Cynthia Kenyon’s lab, enrolled at MIT at 14, dropped out after receiving a fellowship from Peter Thiel, and now ran a venture capital fund in San Francisco to bring aging-related startups into the Silicon Valley mainstream. (One of her latest projects involves developing technology to freeze organs without damaging them.) Halioua had once been introduced to Deming through de Grey, and now she emailed in pursuit of an internship.

Deming arranged a brief phone interview. Halioua was “very intense,” Deming recalls. “I asked her a question about Markov models”—a math trick to analyze processes that change over time—“and could tell that she didn’t have the exact answer but was determined to figure it out on the call” by wringing every possible clue from what Deming said. “That was really cool.” The internship was only two weeks long, but for Halioua it was enough—a refuge and perhaps a new beginning. In early 2018, she flew to California.

Halioua joined deming at a WeWork in the Tenderloin, a San Francisco neighborhood abutting City Hall and the headquarters of Twitter that is also rife with human misery and crime. Stepping out of the office at night felt risky in a way it never had in Oxford or Austin. Working in venture capital felt unfamiliar too. At Oxford, grad students and researchers left the lab at 5 pm and went home or to the pub. Important emails were long and formal. In San Francisco, entrepreneurs and investors worked late and then spent hours more, over fine dinners, debating the intellectual foundations of their theories about the future.

At the end of Halioua’s brief internship, Deming offered her a job. She found a way to accept but also complete her PhD in Oxford, and began flying back and forth. Halioua felt the arrangement was working at first, but relations with her supervisor worsened, and in the fall of 2018 she filed a formal complaint under Oxford’s bullying and harassment policy. He left the university soon after, but Halioua found her department’s investigation to be painfully slow. (The head of her former department, Georg Holländer, declined to comment on the case, but said "all complaints will always be considered carefully and rigorously under our procedures.") While she waited for its official assessment, she began to have panic attacks. “You kind of feel like you’re crazy,” she says. “Everybody tells you you’re being sensitive or misinterpreting what this person said to you.” Working for Deming began to soak up more of Halioua’s time and enthusiasm, and she left Oxford for good.

Halioua knew next to nothing about venture capital or Silicon Valley, but she poured herself into reading pitch decks, networking with founders, and drafting investment memos. She started to tweet, blasting out news of pharma deals, photos of San Francisco beaches, her Fitbit stats, and appreciations of Elon Musk. She helped bring about investments in Fauna, a startup exploring the age-defying biology of hibernation, and Gordian Biotechnology, which aims to fight diseases of aging by modifying a patient’s DNA. By the time news came from Oxford that it had upheld the majority of her complaints, almost a year after she had filed them, Halioua knew her future lay in biotech, not academia.

Halioua’s own company, Loyal, emerged from one of her early projects for Deming, a dense, roughly 50-page memo on the investment potential of the biochemical pathway Cynthia Kenyon had used to double the lifespan of worms. In many species—including humans—it involved a hormone called insulin-like growth factor 1, which adjusts an animal’s growth and metabolic response to food. Tinkering with this pathway could extend the lifespan of flies, worms, and mice.

Unfortunately for Halioua, the literature seemed less rich in clues for how to turn this knowledge into a drug for people. The role of IGF-1 in human aging was unclear, and although the pathway was clearly implicated in certain eye diseases unrelated to aging, Halioua couldn’t get excited about working on them.

In the summer of 2019, Halioua was drunk on a camping trip among strangers when a factoid she had omitted from the report came back to her. Organized by the founders of an autonomous trucking startup, the trip had brought together a group of young entrepreneurs and investors. Around the campfire, she joked—purely as an icebreaker—that she knew how to extend dog lifespan, because IGF-1 was implicated in dog body size and longevity.

Her quip took on a life of its own and became lodged in the collective consciousness of Silicon Valley. One investor on the trip mentioned Halioua’s idea to a founder he knew, who in turn told it to Greg Rosen, a venture capitalist. Inspired by the South Korean scientists who had produced the first cloned dog, an Afghan named Snuppy, Rosen was looking for an entrepreneur to start a US company to clone dogs for bereaved owners. When Rosen and Halioua met for coffee in downtown San Francisco, he realized she had a better solution for the same underlying problem—that a dog never lives long enough.

Halioua began 2020 with $5.1 million in funding. By way of thanks she sent all of her investors, including Rosen, fluffy toy puppies wearing company bandanas. She secured an office on the edge of downtown San Francisco, but the lease began in March, the same month the Bay Area became the first part of the US to enter pandemic lockdown. Her company’s formative months, and first hires, took place via Zoom, Slack, and eventually socially distanced meetups. Halioua raised another $6 million and hired scientists, veterinarians, and an expert in getting new animal drugs past the FDA.

She embraced the role of dog company CEO—painting a mural of a giant German shepherd in Loyal’s office and ordering shirts with the slogan “Save the dogs, save the world.” She adopted a fluffy white husky named Wolfie, whom she has described as her cofounder and Loyal’s chief evangelist. Her management style, she says, was informed by her bad experiences at Oxford. When she talks to her team about her goals or beliefs, she tries to pair her statements with evidence to convince her workers that the boss is being straight with them. “Even if you don’t trust me, you still know this is true,” she says.

Halioua’s new science team, including a scientist who previously led aging research at pharma giant Regeneron, helped refine her original idea. They identified a compound they believed could be given to young dogs of the largest breeds, such as French mastiffs, to delay their accelerated aging process. They found a second compound they thought could target processes that cause cognitive decline and kidney problems in older dogs of all sizes.

As her company gained traction, Halioua noticed certain patterns in her business interactions. She tried to recruit women investors but found it difficult because there weren’t many to ask. When she met with investors who were men, some would try to flip a business meeting into a date, and others would confidently explain science to her that she knew inside out. Mostly she brushed off such moments—her time at Oxford had lowered her expectations of those with more power and prestige than her.

She often felt different. Describing herself as an “Oxford dropout” helped convince people to take her seriously—never mind that she had left her PhD in part due to dissatisfaction with a harassment investigation, a circumstance missing from the dropout tales of archetypal boy geniuses like Mark Zuckerberg. She listened to hundreds of Silicon Valley podcasts to try to learn the industry’s patois. She trained herself to smile less and wrote in a blog post aimed at women entrepreneurs: “I come off as more of a grump now, but I am a grump who has the money she needs to build her company.”

In the spring of 2021, Halioua published a blog post about her Oxford PhD supervisor titled “The Gifts of My Harasser,” leaving him nameless. She described the paradox of one of her worst experiences laying a foundation stone for her later successes by teaching her to be skeptical of social hierarchies and institutional power. “It’s been two years since I left. I am not broken anymore, but I still feel the cracks,” she wrote. “His abuse shattered my preconceived notions of how the world worked and cleared a path I otherwise never would have found.”

Halioua also still felt the burden of her experience with de Grey, the aging guru of the SENS Research Foundation. Deming, too, had endured an uncomfortable experience with de Grey, whom she had known since she was 14. Days before her 18th birthday, Deming had emailed de Grey, then 48, asking him to introduce her to someone. In his reply he suggested he was interested in Deming sexually. “I have a fairly adventurous love life, and I’m not coy in talking about it, but I’ve always taken care to avoid letting conversations stray in that direction with someone so young as you,” de Grey wrote. “That has always felt quite jarring given that I could treat you as an equal on every other level. Maybe those days are over … Ahem - back to business 🙂 Yes, I’ll e-introduce you.” (De Grey later said the email was “an error in judgment.”)

Now, in June 2021, Deming and Halioua heard that de Grey might be mentoring another underage girl. The two women decided to formally report their experiences to the foundation, in the hope that doing so might protect this girl and others. The organization quickly retained a law firm to investigate the allegations and placed de Grey on leave. But in the weeks afterward, the nonprofit promoted social media posts featuring de Grey discussing a cryptocurrency fundraising campaign that would net the organization $25 million.

By August, Halioua says she and Deming became worried that the nonprofit was too conflicted to properly investigate itself, and they decided to go public. Late one Tuesday afternoon, the two women simultaneously posted detailed statements to their personal websites. Word spread fast, as did Halioua’s accompanying Twitter thread, prompting an outpouring of sympathy online, a round of media coverage about the allegations, and denials from de Grey.

Just over a week later, the SENS Research Foundation said its board learned that de Grey had attempted to undercut the ongoing investigation—by sending emails intended to pressure a participant in the inquiry, according to the official report of the investigation—and decided to “separate” from him immediately. The foundation’s law firm would later uphold Halioua’s and Deming’s accounts of these events. De Grey says that the women were tricked by people aiming to eject him from his nonprofit and that he has “never said anything to Laura or Celine verbally or otherwise that had improper intent.”

Halioua felt sure she had done the right thing, and she reasoned that Loyal had progressed enough that her career was not in danger. She was also too busy to dwell on the uproar. In late August her team announced that the NIH’s National Institute on Aging would collaborate with Loyal to test two of the company’s compounds, as part of a program on extending the longevity or healthy lifespan of mice. Three weeks later she turned 27. She rounded out the month by disclosing that Loyal had raised an additional $27 million in investment funding. Half of her new investors were women.

in 2022, halioua and her team, approaching 70 strong, began to flex the scientific muscles needed to upend conventional wisdom about aging. They analyzed and published data collected the previous year from nearly 500 dogs who were brought to a vet clinic for a health assessment. For a second study, they recruited some 2,000 owners—Halioua usually calls them “pet parents”—to receive Loyal-branded doggy DNA swab kits that might help them understand the markers of aging. Dog lovers on social media quickly picked up the scent; both studies filled up fast, and Halioua’s inbox was flooded with unsolicited dog pics. (Halioua says she has nothing against cats—and has even hired a few cat fanciers—but that their long lives, dislike of medicine, and not-very-humanlike physiology make them a less appealing target. “They’re like little biological aliens,” Halioua says.)

Less publicly, Loyal is preparing for the clinical trials of its two products. Halioua isn’t giving away many details about Loyal’s drugs, but she does say that both medicines have performed well when given to lab dogs. One is a pill that might delay the onset of age-related diseases such as dementia and kidney failure, two common reasons for owners to have an animal put down. Halioua says it uses some pathways seen in caloric restriction. Now the company is testing the drug in pet dogs, and she anticipates she’ll launch a full clinical trial designed to win regulatory approval next year. The second drug, released slowly by an implant, might dampen the cellular processes that are believed to condemn the largest dog breeds to short lives.

As is standard in the drug industry, the company will seek the FDA’s sign-off on its study designs first. That step is a big deal for Loyal, because the agency would be backing the notion that drugs can be tested and proven to boost longevity. That is, not to prevent a disease or slow one down, but to hit a whole suite of ailments by tackling aging at its root.

To navigate the scientific and regulatory hurdles, human longevity startups—Loyal’s nominal competitors—have taken to focusing on drugs that tick two boxes: They are effective enough to get first approved as a conventional treatment for a single disease, and they hold broad antiaging effects. The hope is that once the drug is benefiting patients, data will pile up that helps prove its general preventive powers against age-related disease.

James Peyer, a former venture capitalist who is CEO and cofounder of antiaging startup Cambrian Biopharma, has raised more than $160 million with that tack. He says that establishing a rich portfolio of nearly 20 potential drugs for humans helped win investors over. But he admits his two-step approach isn’t the only way to go, and it’s possible that Halioua, whom he has known for years, might have hit on a faster way to get an antiaging drug for humans. “Part of Celine and Loyal’s brilliance is that they found a completely different path,” he says, one that lets her focus solely on the drugs’ antiaging properties right from the start. If the mechanisms that Halioua’s team finds in dogs align with human biology—a considerable unknown—the company could be well positioned to jump species, Peyer says.

Loyal is not the only outfit trying to understand canine longevity. The Dog Aging Project, led by the University of Washington and Texas A&M College of Veterinary Medicine and Biomedical Sciences, has completed two small studies in which owners were given rapamycin or placebo pills without being told which. People who dosed their dogs with the drug reported that their pets became more active, says Matt Kaeberlein, a University of Washington professor who is codirector of the project and an adviser to Loyal. He suspects that rapamycin worked by soothing arthritis or other aches and pains, and he hopes to gather firm proof in a larger trial of about 600 dogs.

Kaeberlein has studied life-extending genes and treatments in yeast, worms, and mice and is convinced some aging mechanisms are shared across the animal kingdom. “Obviously I don’t know whether rapamycin is going to have a big effect on lifespan and health span in dogs, but I am as certain as I can be that something will,” he says. He declines to say whether he gives rapamycin to his own dog, Dobby, an 11-year-old German shepherd, saying it wouldn’t be proper to comment on such a use while running a trial investigating the same. But Kaeberlein will say that he takes the drug himself and believes it helped resolve an attack of frozen shoulder, a mysterious condition in which the joint becomes stiff and painful.

Like other veterans of academic aging science—and Halioua—Kaeberlein exudes levelheaded excitement but also impatience when asked about the future of aging treatments. Piles of evidence suggest it is possible to slow down the processes of aging in humans, or any other animal. You want that pill to exist? Just give scientists the time and money—and regulatory support—to figure it out, says Nir Barzilai, director of the Institute of Aging at Albert Einstein College of Medicine, in New York.

“Right now we need to start making progress with drugs that maybe wouldn’t make us live 150 years but will make us healthier for much longer,” Barzilai says, by delaying the onset of diseases such as cancer or Alzheimer’s. He has spent years trying to secure funding for a six-year human clinical trial to investigate whether a common diabetes drug can delay aging. He is less sure of Loyal’s approach, but he figures longer-lived and more active dogs could produce other effects in humans: more active, longer-lived owners, and more support for aging research.

Sitting cross-legged on an easy chair in Loyal’s San Francisco office, Halioua argues that Loyal can break the psychological barriers holding back the war on aging. “Many people don’t know that we’ve extended lifespan in mice many times, and even if they do, well, it’s a mouse,” she says, as Wolfie lolls nearby on a sunny cushion next to a floor-to-ceiling window. What would kick the field into a higher gear, she says, is a proof of concept that’s more persuasive and lovable than a wizened lab rodent.

She imagines appearing onstage one day with a healthy Great Dane that is 15 years old, almost twice the breed’s usual age—and thus persuading people to see aging science not as a realm of weird ideas and thinkers but as a conventional branch of biotech. Silicon Valley founders are often celebrated for creating products that cause jaws to drop and heads to explode. Halioua may make her greatest mark by killing hype rather than creating it, transforming the notion that drugs can extend life into an everyday comfort—like a faithful friend’s tail wagging when you walk through the door. 

Updated 10-13-2022, 1:00 pm ET: This story was updated to correct Aubrey de Grey's age. 

The Search for a Pill That Can Help Dogs—and Humans—Live Longer

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And while the cotton swab is the most common instrument, surprisingly, people use other everyday items such as combs, hairpins, pens, pencils, straws and toothpicks, to do the job as well.

Not only do cotton swabs—and those other aforementioned instruments—not remove ear wax, but they can pose a risk of hearing loss. Using small items of any kind puts us at an increased risk of puncturing the ear drum, which can cause pain, infection and even long-term hearing loss.

"For a lot of people, the feeling of cleaning the ears can be reassuring or satisfying. Some may never experience any issues for years," said Jason A. Brant, MD, assistant professor of Otorhinolaryngology: Head and Neck Surgery in the Perelman School of Medicine at the University of Pennsylvania. "There are also many people who feel that they need to clean their ears to be healthy and to stay clean, which is not the case."

According to the American Academy of Otolaryngology Head and Neck Surgery Foundation, as long as the ears are functioning properly, people should not be trying to remove ear wax, and should leave it alone.

For the vast majority, ear wax does not cause any problems and there isn't a need to remove it. There are actually benefits to having ear wax including a self-cleaning mechanism and some antimicrobial properties.

"Having ear wax does not mean that the ears are 'dirty,' it is a normal part of how the ear canals function," said Brant. While earwax may seem gross, a certain amount is helpful and can protect and prevent dust or other harmful objects from getting into the ear.

Using cotton swabs and other similar tools does not actually remove ear wax. Instead, these items push ear wax further down into the canal and can even get stuck, which can cause discomfort and potential damage to the eardrum, even after one use.

Ear, nose and throat (ENT) specialists, called otolaryngologists, like Brant treat patients with ear, nose, and throat disorders, and see many patients with ear drum perforations that are most often caused by ear infections or trauma associated with pushing of ear wax.

Brant also warns people to be wary of at-home ear wax removal systems and devices, as they too can end up pushing ear wax deeper, which can cause problems. Some people under a doctor's care may require regular cleanings, but this is not the case for everyone. More damage can be created by trying to clean or remove ear wax versus just leaving it alone.

"The skin in the ear is very thin and even slight trauma from such a device can cause injury," Brant noted.

But if you feel that there is too much water remaining in your ears after a bath or visit to the beach, it's okay to use a towel or wash cloth to wipe the outside of the ears. That should be enough, Brant says. There are some over-the counter drops a doctor or pharmacist can recommend too.

Of course, if one is experiencing pain, hearing loss, or seeing any concerning discharge, they should seek medical attention. A person whose ear wax "appears to be oozing out of the ear, seems to have a flaky or sticky consistency, is bleeding or expelling yellowish-pus, should seek medical attention for further evaluation," Brant says.

For people who have had previous ear infections, tubes, surgery, or any perforation in the ear drum, they'll need medical guidance before putting anything in their ears including over-the-counter drops.

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NASA says the Artemis I mission will be ready to launch in one month

The nasal version of the Oxford/AstraZeneca COVID-19 vaccine failed an early-stage clinical trial, dashing hopes for better infection prevention and forcing researchers to re-think the design.

Many experts have hyped the potential of nasal COVID-19 vaccines. They argue that snorting the shots could encrust the nasal mucous membranes with snotty antibodies—namely IgA—and other immune defenses that could blow away SARS-CoV-2 virus particles before they have the chance to cause an infection. Currently, the shots given intramuscularly in arms provide robust systemic immune responses that prevent severe disease and death but spur relatively weak antibody levels on mucous membranes and, relatedly, don't always prevent infection.

Researchers at the University of Oxford hoped to easily adapt their existing COVID-19 vaccine for such an infection-blasting schnoz spritz. The Oxford/AstraZeneca vaccine is a viral vector-based design, using a weakened, benign virus to carry the genetic code of the SARS-CoV-2 spike protein to human cells. The benign virus, in this case, is an adenovirus, a type best known for causing mild cold-like illnesses in humans, though the specific virus used in the vaccine was isolated from chimpanzees. (This vaccine has not been authorized in the US but is used in dozens of countries worldwide.)

Researchers got a whiff of success in pre-clinical trials involving non-human primates, which developed strong mucosal antibody responses after nasal administration. But their hopes were snuffed out in the early clinical trial, the results of which were published this week in the journal eBioMedicine.

Disappointing data

In the 42-person, phase I trial, nasal administration of the vaccine produced only modest mucosal antibody responses in just a few participants and also spurred weaker systemic responses than the intramuscular shots. The trial included 30 people who had not been vaccinated previously and 12 vaccinated people who tested the nasal vaccine as a booster. The nasal administration blew it on both accounts. The only good news was that no safety issues were found.

But, in yet more disappointing findings, the vaccine also appeared ineffective at preventing COVID-19. The small, early-stage trial was not designed to assess effectiveness, but the researchers note that 7 of the 42 participants reported SARS-CoV-2 infections after the nasal vaccination. This is "discouraging for the prospect of robust and durable protection," the Oxford researchers concluded in the published study.

In a press release, the trial's lead researcher, Sandy Douglas, at the Jenner Institute, University of Oxford, put it softly, saying, "The nasal spray did not perform as well in this study as we had hoped."

Douglas noted that data from researchers in China suggests more success with a similar vaccine administered with a nebulizer device, though the Oxford researchers noted they wanted to aim for the more practical administration of a nose squirt.

Douglas also noted that an intranasal vaccine had earned approval in India, but clinical trial data on that vaccine has not yet been published.

Overall, Douglas suggested that his research team will go back to the design stage, such as coming up with new formulations that may help the vaccine better glom onto the nares and respiratory tract to avoid slipping down into the stomach. The researchers also wondered if the adenovirus vector, originally wiped from chimpanzees, may simply be bad at infecting human snouts. They also pondered trying larger doses.

While the trial results are a setback to the cause, outside experts urged researchers to not give up. The outcome is "disappointing," infectious disease expert Andrew Freedman of Cardiff University said in a statement. "It should not, however, deter further work to develop more effective intranasal vaccines to protect against COVID-19 and other respiratory infections."

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No, really. That's not a joke, and there isn't a punchline. Instead, there's a real actual answer, thanks to a neural network system called DishBrain.

If that game is Pong, the number of brain cells is around 800,000.

While their slow-moving, one-sided strategy for digital table tennis won't see them win any e-sports championships in the near future, it does reflect the potential in fusing living tissues with silicon technology.

This is the first synthetic biological intelligence experiment that shows neurons can adjust their activity to perform a specific task – and, when provided with feedback, can learn to perform that task better. It's pretty amazing stuff, with potential applications in computing, as well as studying all sorts of brain stuff, from how drugs and medication impact brain activity to how intelligence develops in the first place.

"We have shown we can interact with living biological neurons in such a way that compels them to modify their activity, leading to something that resembles intelligence," says neuroscientist Brett Kagan of biotech startup Cortical Labs in Australia.

DishBrain is a heady mix of neurons extracted from embryonic mice and human neurons grown from stem cells. These cells were grown on arrays of microelectrodes that could be activated to stimulate the neurons, thus providing sensory input.

Under the microscope, tagged with fluorescent markers, the neurons, axons and dendrites glow purple, red and green. (Cortical Labs)

For a game of Pong, microelectrodes on either side of the dish indicated whether the ball was to the left or right of the paddle, while the frequency of signals relayed the ball's distance.

With just this set-up, DishBrain is capable of moving the paddle to meet the ball, but performs pretty poorly overall. In order to play the game well, the neurons need feedback.

The team developed a software to deliver critique via electrodes whenever DishBrain missed the ball. This allowed the system to improve at playing Pong, with learning observed by the researchers in as little as five minutes.

"The beautiful and pioneering aspect of this work rests on equipping the neurons with sensations – the feedback – and crucially the ability to act on their world," says theoretical neuroscientist Karl Friston of University College London in the UK.

"Remarkably, the cultures learned how to make their world more predictable by acting upon it. This is remarkable because you cannot teach this kind of self-organization; simply because – unlike a pet – these mini brains have no sense of reward and punishment."

A few years ago, Friston developed a theory called the free energy principle, which proposes all biological systems behave in ways that reduce the gap between what is expected and what is experienced – in other words, to make the world more predictable.

By adjusting its actions to make the world more predictable, Friston says, DishBrain is simply doing what biology does best.

"We chose Pong due to its simplicity and familiarity, but, also, it was one of the first games used in machine learning, so we wanted to recognize that," Kagan says.

"An unpredictable stimulus was applied to the cells, and the system as a whole would reorganize its activity to better play the game and to minimize having a random response. You can also think that just playing the game, hitting the ball and getting predictable stimulation, is inherently creating more predictable environments."

This has some really intriguing possibilities, especially in artificial intelligence and computing. The human brain, containing around 80 to 100 billion neurons, is way more powerful than any computer, and our best computers struggle to replicate it. Our best effort yet required 82,944 processors, a petabyte of main memory and 40 minutes to replicate just one second of the activity of one percent of the human brain.

If the architecture is more like that of an actual brain – perhaps even a synthetic biological system like the one developed by Kagan and colleagues – this goal may not be quite so far out of reach.

But there are other, perhaps more immediate implications.

For example, DishBrain might be able to help chemists understand the effects of various medications on the brain, to a cellular level. It might, one day, even help tailor medications to a patient's specific biology, using neurons cultured from stem cells reverse engineered from that patient's skin.

"The translational potential of this work is truly exciting: it means we don't have to worry about creating 'digital twins' to test therapeutic interventions," says Friston. "We now have, in principle, the ultimate biomimetic 'sandbox' in which to test the effects of drugs and genetic variants – a sandbox constituted by exactly the same computing (neuronal) elements found in your brain and mine."

For now, the next step is to figure out how DishBrain's ability to play Pong is affected by drugs and alcohol. "We're trying to create a dose response curve with ethanol – basically get them 'drunk' and see if they play the game more poorly, just as when people drink," Kagan says.

In other words, a dish of brain cells rolls into a bar…

The team's research has been published in Neuron.

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A trial run at planetary defense has proven successful. NASA released data yesterday showing that the DART mission was able to change the trajectory of a 160-m-wide asteroid, causing a 4% shift in the object’s orbital motion. “For the first time ever, humanity has changed the orbit of a planetary body,” said director of NASA’s Planetary Science Division Lori Glaze in a press conference at which the results were announced.

On September 26, the refrigerator-sized DART spacecraft intentionally collided with the asteroid Dimorphos at a speed of 14,000 mph (22,000 km/h). Since then, astronomers have kept a close watch on the asteroid to spot any change in its orbit around a nearby asteroid. The newly released data shows that Dimorphos’ orbital period has slowed by 32 minutes—with the asteroid now taking 11 hours and 23 minutes to complete a revolution. This slowdown is 25 times greater than the minimum bar that NASA scientists set for themselves as a successful deflection (see Research News: Countdown to DART Impact). “This is a watershed moment for planetary defense and a watershed moment for humanity,” said NASA Administrator Bill Nelson.

The scientists at the press conference all shared their excitement that the orbit shift was successful, but they note that more work lies ahead. “This result is one important step toward understanding the full effect of DART’s impact with its target asteroid,” Glaze said. Ongoing studies will better determine the shape and mass of Dimorphos, as well as reveal details of its new orbit. Scientists hope to eventually know the amount of momentum transferred to the asteroid during the collision. “As new data come in each day, astronomers will be able to better assess whether, and how, a mission like DART could be used in the future to help protect Earth from a collision with an asteroid if we ever discover one headed our way,” Glaze said.

–Michael Schirber

Michael Schirber is a Corresponding Editor for Physics Magazine based in Lyon, France.

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