❌

Normal view

Received — 22 August 2026 ⏭

I’d heard ringing in my ears before. This time, it didn’t stop

✇The Guardian
By: Miranda Luby
22 August 2026 at 23:00

Miranda Luby was only 36 years old when her tinnitus arrived in the middle of the night, without warning and for no clear reason

One night two years ago, I was lying in bed when I began to hear a high-pitched, electronic hum. The scene that followed would be comical if it wasn’t so traumatic. I roamed around the house in my PJs, frantically pressing my ears against various electrical appliances. It took half an hour to realise the sound was coming from inside my own head.

I’d heard ringing in my ears before, rising then falling, like a one-note crescendo of an orchestra. As a kid, I used to believe the myth it was the sound of dying ear cells, playing a swan song for a frequency I’d never hear again. This was different. This time, it didn’t stop.

Continue reading...

© Photograph: Carol Yepes/Getty Images

© Photograph: Carol Yepes/Getty Images

© Photograph: Carol Yepes/Getty Images

America’s murder rate hasn’t been this low in 70 years

✇Vox
By: Bryan Walsh
22 August 2026 at 15:30
Baltimore’s Safe Streets office.

A few things are certain in life: death, taxes, LeBron James playing professional basketball — and Americans’ belief that crime is getting worse. Since Gallup began asking about national crime in 1989, a majority of respondents said they thought crime in the US was higher than the year before in every survey year except 2000, 2001, and 2025. Even in that last year, 49 percent still said more crime was happening. It’s perhaps the archetypal example of negativity bias, the mental habit of giving more weight to bad news than good.

Last week, the FBI put some numbers on just how big that bias is. The American murder rate — which peaked in 1980 at 10.2 per 100,000 — fell to an estimated 4.1 per 100,000 people in 2025, matching the rates recorded in 1955 and 1956 for the lowest ever measured in the country. The violent crime rate (murder, rape, robbery and aggravated assault) fell 9.7 percent, the largest single drop since J. Edgar Hoover was running the bureau in 1936. 

That much is known. But what’s not known for sure about the crime drop is almost everything else. Adam Gelb, who runs the Council on Criminal Justice, says that there is no single or easy explanation for the historic lows, while Jeff Asher, the analyst who spotted this decline before nearly everyone else, agrees. For every leading candidate — federal pandemic spending, some normalization after the 2020 social collapse, better violence prevention, even the decline of drinking — there is a corresponding hole. 

But there is one American city where researchers can point to a specific program, measure what it did, and put real numbers on it. And it just happens to be the city that spent 50 years — and five award-winning seasons on HBO — as America’s shorthand for murder.   

What Baltimore did

Baltimore recorded more than 300 homicides a year for most of the last decade, and more than 200 for most of the past half-century. In one month, July 2015, 45 people were killed — an astounding figure for a city of just around 600,000 people at the time. 

But Baltimore finished 2025 with 133 homicides, the fewest since 1977 and about 60 percent fewer than in 2020. Through the first eight months of this year, the city has seen 60 murders, and the police commissioner’s target is to stay under 100. 

What caused this? Three things at once.

Baltimore Mayor Brandon Scott’s Group Violence Reduction Strategy identifies the few people most likely to shoot or be shot — two groups that heavily overlap — and sends people to their doors with two messages: you are on our radar, and here is housing and job training. Separately, the longer-running Safe Streets program puts outreach workers with real street credibility between disputes, aiming to interrupt them before they become shootings.

That’s the harm reduction element. There’s also a tough-on-crime component. The state’s attorney office says it has secured 2,129 convictions since 2023 across several gun-related violent-crime categories, with over 1,700 of those defendants incarcerated. 

Meanwhile, Baltimore’s homicide clearance rate reached 60 percent by mid-2026. Its nonfatal-shooting clearance rate was 54 percent, up more than 12 percentage points from a year earlier. Criminologists have long held that the certainty of being caught deters criminals more than the severity of the sentence, and more successful shooting investigations are a common thread where violence is falling around the country. 

How do you tell whether a program worked, or whether a city just got lucky? Drug trials get a control group; cities don’t. Baltimore got one almost by accident: the strategy launched in the city’s Western District in 2022 and nowhere else, which left the rest of the city as a comparison.

That’s what a team of economists and criminologists used. They measured the Western District against Baltimore neighborhoods that hadn’t started the program yet, and over 18 months the number of people shot there, fatally or not, ran about 30 percent below that stand-in. Killings alone fell by a similar share, but deaths are rare enough that chance couldn’t be ruled out. Police made no more arrests than before. Arrests for serious violent crime rose 81 percent.

A second, looser test set the whole city against a composite of other big American cities and put Baltimore’s murder rate about 25 percent below it. The authors are careful with that one: too much changed in Baltimore at once to say how much it the strategy was responsible for.

Murder is contagious

Baltimore’s success is built on two ideas, and they came from two very different places. 

The first came from a doctor named Gary Slutkin, who spent the 1980s and early 1990s fighting tuberculosis in San Francisco, cholera in Somali refugee camps, and AIDS across Africa. He came home to Chicago in 1995, a year the city recorded over 800 homicides. 

Key takeaways

  • Americans have told Gallup crime is getting worse in nearly every year since 1989. In 2025 the US murder rate fell to 4.1 per 100,000, tying 1955 and 1956 for the lowest ever measured, and violent crime dropped 9.3 percent — the largest single-year fall since the FBI began national estimates in 1936.
  • Nobody can say why. Federal pandemic spending, the unwinding of the 2020 collapse, violence prevention programs, Americans drinking less: every leading explanation has a hole in it.
  • Baltimore is an exception. Because its Group Violence Reduction Strategy launched in one police district first, researchers could measure it against the rest of the city. Shootings there ran about 30 percent lower — and police made no more arrests than before.

When Slutkin examined the city’s shooting maps, they looked familiar. Clustered in space, clustered in time, and spreading case to case — murder resembled the outbreaks he used to fight. Slutkin reasoned that the way to treat violence was to treat it like cholera: find the people most likely to transmit. Interrupt the transmission. Change the conditions that let it spread. Slutkin built the model into a program called CeaseFire, now Cure Violence Global, and its Baltimore descendant is Safe Streets.  

The second idea came from a criminologist. David Kennedy, working in Boston in the 1990s, found that 61 gangs with about 1,300 members — under 1 percent of the city’s young people — were tied to at least 60 percent of its youth homicides. Get those people in a room with police, prosecutors, and community elders, tell them plainly what comes next, and the shooting slows down.

That approach is called focused deterrence. Baltimore’s Group Violence Reduction Strategy is a version of it. To see how it works over a longer period of time, take a trip across the Atlantic to Glasgow in Scotland, which in the early 2000s was considered the murder capital of Europe.

In 2005, in the midst of that wave of violence, Glasgow’s Strathclyde Police established a Violence Reduction Unit that operated with a basic thesis: evidence shows that violence can be prevented. Among other interventions, the unit sent trauma surgeons into schools to describe what a blade does to a face and stationed outreach workers at hospital bedsides to reach victims in the vital hours after an attack, the moment when retaliation can still be stopped. 

In 2024-25, Scotland recorded 45 homicide victims, the fewest since comparable records began in 1976 and down from 96 two decades earlier. Every case was solved.

Pull the handle

So we have clues to why crime has dropped so much, but not clear conclusions. As successful as Baltimore’s group violence strategy has proved, a 2023 study of a similar street-outreach effort in Boston found no effect whatsoever. And the latest evaluation of Baltimore’s own Safe Streets — 11 sites, each measured against a stand-in version of the same neighborhood without the program — produced numbers that sound terrific but settle very little: youth homicides down 42 percent and youth shootings down 21 percent, but neither is strong enough to rule out chance. And while some sites saw youth homicide fall by as much as 100 percent, two sites saw it rise by 42 and 89 percent. 

Some experts, like the UC Irvine criminologist Emily Owens, argue the crime decline has been so widespread and similar — big cities and small, red and blue governments — that the true cause is some larger social change rather than what any one city is doing. Nor can we be sure the fall will continue. Billions in federal pandemic relief money has supported many of the programs that have worked well in places like Baltimore, and that money is already running out. But we can identify one reason why it happened, and learn from that success. 

As it happens, Gary Slutkin was not the first doctor to look at a map of the dead and see a pattern in it. In September 1854, a cholera outbreak was killing hundreds of people in London’s Soho district. A doctor named John Snow had mapped the outbreak and saw the dead were clustered disproportionately close to the district’s Broad Street water pump. Snow had a theory that water was connected to the disease and convinced a Soho parish board to remove the handle of the pump. 

Nobody in Soho at that moment could have told you what caused cholera. It would only be 29 years later that someone would definitely identify the responsible pathogen, and in doing so, explain why Snow’s intervention worked. But the explanation could wait. The dying stopped that month in Soho, just as it is stopping in Baltimore and around the US today. And that’s what counts.

A version of this story originally appeared in the Good News newsletter. Sign up here!

Michael Polansky is training an AI model on skin that’s still alive

✇TechCrunch
By: Connie Loizos
22 August 2026 at 04:31
Michael Polansky — better known publicly as Lady Gaga's partner and a former top deputy to Sean Parker — has quietly spent years building an AI-driven startup that keeps living human skin tissue alive for weeks outside the body to discover new skincare compounds, and is only now going public about it.

Which Anti-Aging Ideas Actually Work? XPrize Healthspan Is Testing The Best Longevity Innovations

✇TIME
By: Alice Park
21 August 2026 at 23:03
XPrize Healthspan is testing the best ideas for slowing aging. —Elena Noviello—Getty

Jamie Justice admits she has no poker face. As executive director of XPrize Healthspan, a philanthropic and corporate sponsored competition, Justice oversees one of the most buzz-worthy science competitions today. The contest, launched in 2023, attracted nearly 200 applicants from groups around the world who think they can help people to live not just longer lives, but healthier ones.

When the 15-member judging panel met in early summer to pick the top 10 teams who would continue on in the seven-year competition, Justice excused herself. “I couldn’t be in the room because my face shows everything,” she says, since she became familiar with each of the teams and their various approaches to extending human life.

Read more: TIME's 2026 Longevity Leaders

Both in the scientific community and the commercial market, there is no shortage of ideas—from legitimate, rigorously developed approaches to more fantastical schemes—for a fountain of youth. XPrize Healthspan exists to bring some order to that chaos, and legitimacy to the process of developing and, most importantly, testing ideas in longevity. Applicants for the prize, which has a total purse of $101 million, allocated in segments throughout the seven-year competition, included teams from academic research institutes as well as biotech and startup groups. All had to follow a few basic rules; they had to show early promise in human studies that their approach could improve health in three critical areas: muscle function, brain function, and immune function. All teams were judged based on standard measurements of these three functions that XPrize committees of experts had specified, to ensure that all projects were evaluated using the same metrics. The judges announced the top 10 projects on Aug. 11.

“This is where I get the most excited, when things get really sort of dirty and ugly,” says Justice, who spent time researching geroscience at Wake Forest University before coming to XPrize. “You’ve got biohackers selling you this, and you have a bro guy over here that wants you to take so much protein that you’re going to die. What we need to do is have a strainer, a filter where everybody is held to the same standard. There may be something really worthwhile and useful out of some of these things that seem harebrained. What XPrize does well is invite everyone in, teach them how to do the science to get to a level of super credibility. It’s an alliance that comes together to set the frameworks for the start line, a finish line, and how to get there.”

The projects are as varied as you might expect approaches to longevity to be—ranging from the latest anti-aging trends in Asia involving extracellular vesicles, to stem cells and more traditional, well-established programs that include exercise and supplements. Two of the teams are from Japan, one from South Korea, one from China and six from the U.S. Two of the groups are studying repurposed drugs for their potential in extending life, while the Korean team is investigating a novel longevity drug. Four projects involve supplements and five rely on biologic compounds including extracellular vesicles, peptides, and antibodies.

Both teams from Japan are working with the vesicles, which carry a wide menu of molecules in the body, from enzymes to peptides, fats and genetic material. But the teams are taking very different approaches to optimizing what these vesicles can do to improve health.

Time Traveler Corp., a biotech startup launched in 2024 by Rieko Akiyama to bring ideas from her father's research in tumor biology and cancer research at University of Tokyo to longevity is one of the teams focusing on this approach. Tomoatsu Hayashi, a project assistant professor at the University of Tokyo and co-CEO, started by studying human cells to find ways to make the vesicles at scale. Smaller versions of these vesicles, called exosomes, which are made when cell membranes fold inward, and pinch off tiny bubbles, are an increasingly popular component of anti-aging beauty products in Japan and Asia, but they remain untested from a longevity perspective, and Hayashi and his team were eager to study them in a more rigorous fashion.

Akiyama gave the team what turned out to be its XPrize-leading idea. She noted that during the COVID pandemic, there were more discussions about turning away from animal-derived materials in science, which are heavily regulated to ensure safety before they develop into products used in people, to plant-based sources, including for food products like mayonnaise. “I wondered whether human-derived exosomes could also be replaced by plant-derived exosomes, which might offer advantages in terms of safety, scalability, and ethical considerations,” she says through a digital translator during a recent interview near Hayashi’s labs at the University of Tokyo. “I brought this idea to my father and asked whether plant-derived extracellular vesicles could become a new approach for promoting healthy longevity. That conversation became the starting point of our plant-derived exosome business.”

Hayashi and his team started with edible plants and algae, assuming that those would have the strongest safety profile for eventual human use, and screened more than 140 species, including 95% of those that grow in Japan. While human exosomes were widely studied, those from plants were still a mystery, and “we didn’t know if plant exosomes would have the same effect in human cells,” he says. But starting first with mice and then with human cells, they showed that in fact, plant exosomes worked in very similar ways to human-derived exosomes, proving Rieko’s initial hunch correct. And of the species, it turned out exosomes from parsley showed the strongest effects.

In mice, the parsley-derived exosomes lowered inflammatory factors that are responsible for many aging processes in cells. Animals who were fed the exosomes in their water were able to maintain muscle strength, as measured by the longer time that these mice could hang from a wire cage compared to similarly-aged mice that didn’t get the supplement.

The team saw similar benefits in lowering inflammation in a small group of 40 people who started taking the supplement pill once a day. Anecdotally, the people reported sleeping more consistently and deeply and feeling more energy during the day. The animal and human data were enough to give the team a chance at testing their product further in more people in the next phase of the XPrize competition. That trial will evaluate volunteers on muscle function, walking, leg presses, cognitive tests, and tests looking at inflammatory markers in their blood.

The other Japanese team, also from University of Tokyo, is likewise banking on exosomes. But to address supply issues, instead of plants, they turned to stem cells. Keisuke Goda, professor of chemistry at University of Tokyo, decided to tackle the problem of getting exosomes to the cells where they are needed most. Relying on his chemistry and engineering background, he designed so-called super exosomes with specific molecules on their surface that can draw them to aging cells like a magnet. Because they are revved up to target aging cells, they can deliver the lipids, genetic material, and other compounds cells need to keep them acting like younger versions of themselves. “We knew from previous studies that exosomes secrete a range of molecules including growth factors, metabolic enzymes, lipids, and DNA and RNA, and previous reports showed that injecting young exosomes into aged mice rejuvenated the aged mice,” says Goda. “But there is a delivery problem.”

As part of the XPrize, Goda and his team will start testing the super exosomes in more than 100 people in a formal trial see how they affect muscle, brain, and immune cells.

He is confident that they will see similarly encouraging results as they saw in their mouse and human cells studies, which showed that older human cells in the lab treated with the exosomes had reduced markers of aging and appeared rejuvenated. “We know they work,” says Goda. “It’s exciting. When we saw the results, we doubted it was true. But the cells were rejuvenated, they were not dying.” About 25 months after they started studying the super exosomes in mice, the untreated animals are starting to die, he says, but the treated ones are not. “We of course want to see the actual effect in humans, assuming it’s safe,” he says.

Not all of the top 10 teams involve innovative or cutting edge scientific approaches. The group from Mount Sinai earned its spot by combining three, more familiar strategies: exercise and two supplements, one that’s been bandied about the aging community for a few decades now—rapamycin—and another, spermidine, that came out of work from one of the Mount Sinai scientists as a factor to control inflammation associated with aging. During the COVID pandemic, Dr. Miriam Merad, director of the precision immunology institute at the Icahn School of Medicine at Mount Sinai, and her team noticed a strong connection between age and inflammation that made older people more susceptible to the effects of a COVID infection. That led to a hypotheses about the role that inflammation might play in a range of age-related diseases, including heart disease, respiratory conditions, and muscle loss. “What we realized was that the inflammatory response was contributing to age associated diseases,” she says. “It’s very established what happens with age when organs decline—they acquire somatic mutations from the exposures we have, and at the same time as all of our organs age, our immune system is also declining, and producing more inflammatory molecules. Age-associated diseases are aggravated, or precipitated by chronic inflammation.”

Addressing inflammation, then, might be a powerful way to control the aging process, and in further studies in mice and with human cells in the lab, Merad and her team zeroed-in on a compound that older cells weren’t making as robustly as younger ones—a polyamine called spermidine. By giving older mice the supplement spermidine, they saw improvements in the animals’ immune responses that tipped the balance away from the chronic state of inflammation associated with accelerated aging. “Once we saw the data in the lab, we all started taking it ourselves because [the data] looked so good,” says Dr. Thomas Marron, professor of immunology and immunotherapy at the Icahn School of Medicine at Mount Sinai and the principal investigator of the team’s study of the compound.

The researchers also included rapamycin, a drug approved by the U.S. Food and Drug Administration to treat rejection in kidney transplants, as well as certain types of cancer, in the study as well. Because some, but not all, studies showed rapamycin extended the life of animals, it’s been a controversial product in the longevity field, with some in the health community using the drug off-label in the hopes of a longer and healthier life, despite the lack of solid evidence in human studies that it can have this effect.

That’s one of the reasons the Mount Sinai team is eager to put it to the test, in combination with an exercise regimen and spermidine. Their rationale in combining the two supplements and physical activity lies in the fact that aging isn’t likely directed by a single compound or process, but the net result of a multitude of body processes, so slowing aging will likewise require a multi-pronged strategy. Marron also expects that given the biological differences among people, some may respond more to one supplement, while others respond to the other, and still others may respond best to the exercise regimen. Studying them together could provide the first hints about which components are contributing to slowing aging, and by how much. The researchers will be taking blood samples throughout the coming year, and looking at certain markers of inflammation and as well as conducting tests of hand grip and leg strength, respiratory function and evaluations of changes in fat composition with MRI images. The participants will also take standard cognitive tests to monitor changes in their processing speed and executive function skills such as planning, memory, attention, and impulse control.

“The goal of XPrize is to improve health span by 10 years, and ultimately by 20 years,” says Marron. “But that’s hard because there is no validated way to measure health span, or aging. So the real goal is to inject more science into this process.”

The top 10 teams earned $1 million each to test their ideas in a larger group of people over the next year, and hopefully show improvements in the three areas targeted by the XPrize: muscle, brain, and immune function. “I love to have a front seat and watch the next phase of this go from hype cycle to durable evidence if there is any,” says Justice. But she also acknowledges that aging is a varied process, and no single, uniform solution that applies to the widely diverse human species will likely emerge. “We age at different rates, we have different constellations of diseases and functional decline, so a one-size-fits-all is probably unlikely,” she says. “I expect a lot of failure, but the question is whether you can take that failure and make something useful out of it. Does it become compost to build something better? There needs to be a lot more work from the field within geroscience to really lean on learnings. This is what gets me excited.”

❌