Birds do it, all right.

And they're perfectly happy to fly solo.

New research suggests that we should welcome birds to the sweaty club of animals that masturbate, which is way less exclusive than we thought.

"Avian self-pleasure is usually a rather inelegant affair, in which a bird rubs their cloaca (a shared orifice for both excretion and reproduction) against an object, like a branch, twig or toy," the team behind the study writes in The Conversation.

"This is often accompanied by a lot of flapping and self-satisfied vocalization."

But it's not, as you might assume, just a way for bored birds to pass the time in cages.

It turns out that wild birds love a solo sesh too – perhaps even more than captive ones.

The finding raises some questions, though.

It's obvious what the individual is getting out of it. But from an evolutionary perspective, why has masturbation flourished in the animal kingdom?

At risk of sounding like a puritanical preacher, masturbation 'wastes' a lot of time, energy, and in males, sperm. And why bother seeking out a partner when you can take care of things yourself?

Altogether, solo sex should, in theory, reduce reproductive success, which is the cornerstone of natural selection.

So why then does evolution seem to turn a blind eye to so many animals out there jerking, cranking, rubbing, tapping, inserting, or otherwise pleasuring themselves?

Studying the self-mating habits of birds could satisfy this scientific curiosity.

For the new study, evolutionary biologists at the Universities of Lancashire, Swansea, and Oxford in the UK collected data on 120 bird species from 22 major bird groups.

That info included their age, sex, whether they were wild or captive, which other birds they shared an environment with, and whether their species was monogamous or promiscuous.

It turns out, this bawdy behavior was widespread across birds, but to different degrees.

Males were more likely than females to rub one out, with 55 percent of male records involving masturbation. But that's not to say lady birds weren't also enjoying some me time – it showed up in 36 percent of female records.

A species' breeding behaviors were linked to masturbation tendency too.

Socially monogamous birds and those that form long-term pair bonds were far less likely to engage in some self-exploration than species with multiple mates.

A bird's age, and whether it was kept alone or with other birds, didn't seem to affect whether a species masturbated.

But the most surprising finding was that wild birds were more likely to ruffle their own feathers than captive birds. That directly contradicts one of the main hypotheses for why birds might masturbate.

"Despite assumptions that masturbation among captive birds like parrots is a result of their often-solitary living, our study finds that it is natural, healthy, and widespread across diverse bird species, even in different environments," says Chloe Heys, a biologist at the University of Lancashire.

Understanding this means that pet owners don't need to worry if they catch their bird in the act. Generally, the advice from vets has been to discourage the behavior, which is seen as a marker of stress or poor health.

Instead, it seems that all the bird needs is a bit of privacy.

When the researchers examined the phylogenetic relationships between bird species that engaged in a bit of solo fun, they found that it was concentrated across specific branches of the family tree.

That suggests masturbation has an evolutionary link, and isn't just something that enterprising individuals from different species figured out on their own.

So why hasn't natural selection stamped out this behavior? There are a few hypotheses.

For males, it may be that it helps clear out old sperm, leaving more viable newcomers and making future reproduction more successful.

For females trying to sneak in a quick round with a neighbor, masturbation could get things over and done faster, before their main bonded partner catches them.

Or it may be even more simple.

"Our findings indicate that the proximate mechanism of masturbation may be to serve as a sexual outlet in response to a high sex drive," the researchers write in the study.

It's not just birds, of course. Autoeroticism is all over the animal kingdom.

Monkeys in Indonesia have been caught using rocks to get their rocks off. Dolphins do it with dead fish. Elephants enjoy a spot of self-care. Walruses wank with their flippers, and are surprisingly flexible enough to self-fellate.

Related: Sexual Activity Before Bed Can Help You Sleep Better

There's no shame in it – more and more research suggests getting down to business by oneself is good for you.

The new research was published in the journal Ecology and Evolution.

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The experimental drug combo dasatinib and quercetin (known for short as D+Q) is one of the most promising anti-aging therapies being developed right now.

It is not yet approved for human use, but some scientists think it has the potential to fight disease by improving how our systems clear out worn-down cells.

According to a new study, however, there might be a big problem with D+Q.

A team from the University of Connecticut tested D+Q on the brains of mice, and discovered it caused serious damage to the myelin insulation wrapped around nerve fibers.

The effects of D+Q on the central nervous system haven't been extensively tested before, which was part of the motivation behind this new study.

The findings raise questions about widespread clinical use.

Various clinical trials for D+Q are already underway, for conditions such as kidney disease and pulmonary fibrosis.

Because of the hype, the experimental drug combo is even taken by some people without a prescription, as part of an unofficial 'anti-aging' regime.

That is something medical professionals warn against, as the drug combos have not yet been properly tested for safety or efficacy in humans.

"When you administer this cocktail to an animal, young or old, the myelin is damaged, which makes it disappear – even worse in the young animals than in the aged ones," says immunologist Stephen Crocker.

There are similarities between the brain damage observed here and the effects of both multiple sclerosis and something called 'chemo brain', where chemotherapy treatments lead to problems with cognitive function.

Dasatinib, on its own, is an essential medicine used to treat cancer, sometimes alongside chemotherapy, which might help explain what's causing the myelin loss.

When myelin is degraded, nerves can't communicate as efficiently, and much of the damage observed in the brains of mice was focused around a major information highway called the corpus callosum.

Further lab tests analyzed the reaction between D+Q and oligodendrocyte brain cells, which help grow and maintain myelin.

Tests showed that the combo drug treatment apparently caused oligodendrocytes to shrink back to a smaller and younger mode of operation.

There were changes in the metabolism of the oligodendrocytes, too, preventing enough myelin from being produced, and leaving nerves exposed.

While these results are only from a small number of animals rather than humans, there's definitely enough here to be concerning.

Further analysis is now definitely warranted – in monitoring brain cells during clinical trials of D+Q, for example.

"We suspect the drugs are choking off energy the cells need, and the cells respond by reducing complexity, reverting to a younger state, but less functional," says Crocker.

What makes D+Q exciting for scientists is that they act as senolytics, which are drugs that deliberately clear out damaged or old cells.

These dysfunctional cells are known as senescent cells, and they build up as we get older. Their presence in the body triggers inflammation, which may be related to a host of different diseases, including multiple sclerosis and Alzheimer's disease.

If senolytics like D+Q can reduce the senescent cell burden, then the potential impact on anti-aging diseases is immense.

The aging process is related to so many aspects of health, which is why so much research is dedicated to trying to slow it down.

But there is still much work to be done before that reality is realized.

Based on these new findings, caution moving forward is warranted.

There is some positive news to take out of this research among mice, though.

The stressed-but-still-alive oligodendrocytes are similar to cells seen in patients with multiple sclerosis.

This means D+Q could be used in lab tests to figure out what treatments might work best for reversing some of the damage done by the autoimmune condition.

Related: These Popular Supplements Are Sold With Anti-Aging Claims. Here's What Science Says.

"If we can mimic this, we have an amazing opportunity to see if the cells can recover and repair the brain," says Crocker.

The research has been published in PNAS.

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Every year, more than 2 million people in the United States are diagnosed with treatment-resistant depression.

Desperate for solutions, some brave patients are now volunteering to undergo surgery to place experimental 'pacemakers' into their brains.

These implanted electrodes are part of a treatment known as deep brain stimulation, which is currently used to address some cases of Parkinson's disease and epilepsy.

Now, clinical trials are starting to test if the therapy can treat severe cases of major depressive disorder, too.

The initial results are promising, albeit inconsistent.

In 2021, a patient treated with one of these brain pacemakers said that after the surgical procedure, her depressive symptoms disappeared abruptly.

"I wasn't sure if it would last," she reported at the time. "But it has… "

Now, neuroscientists at the Icahn School of Medicine at Mount Sinai have used the brains of three monkeys to show how this therapy might exert such lasting effects.

It appears to restructure key brain regions involved in depression.

"What is exciting about our findings is that they change how we think about deep brain stimulation," says neuroscientist Peter Rudebeck.

"For the first time, we show that deep brain stimulation does not simply alter electrical activity in the brain in the short term; it can actually remodel white matter structure, essentially rewiring brain circuits associated with depression."

Whether deep brain stimulation can trigger similar white matter changes in human brains remains to be seen. But these signs in a close primate relative are telling.

White matter in the brain contains nerve fibers, the 'arms' of neurons, which are protected in a fatty sheath called myelin. This protective layer helps conduct electrical messages between brain cells more quickly and efficiently.

Patients with depression typically show a decay of white matter in their brains.

While it is unclear if this association between depression and white matter has anything to do with behavioral symptoms, the link keeps showing up in study after study.

In monkeys, researchers at Mount Sinai have found that deep brain stimulation increases myelination of brain cells in brain regions involved in mood regulation.

The therapy also changes the way that neurons interact across various other brain networks, "most notably the default mode network that has been implicated in depression," the authors write in their published paper.

An overactive default mode network is linked to depression.

"Overall," the team concludes, "our data indicate that white matter remodeling as well as selective changes in multiple brain networks may contribute to deep brain stimulation's therapeutic efficacy."

To this day, no one knows why depression arises, or why its symptoms vary so widely from person to person, though there are some known risk factors.

Many standard treatments for depression are based on hypotheses about what causes the mental health disorder, such as a lack of serotonin in the brain.

For up to a third of patients with major depressive disorder, however, standard treatments like antidepressants or therapy don't seem to work.

Until recently, electroconvulsive therapy has been one of the only available alternatives.

This treatment involves electrically stimulating the brain to trigger controlled seizures under anesthesia, and it seems to be very effective at treating episodes of mental illness. But it is not necessarily a long-term solution.

It also comes with risks and negative side effects, such as nausea, headache, fatigue, confusion, and temporary memory loss, and it doesn't work for everyone.

That's why some researchers are turning to deep brain stimulation.

A brain implant that works sort of like a neurological 'pacemaker' could be a more precise alternative to electroconvulsive therapy.

Once the device is implanted in the brain, it sends high-frequency electrical pulses, usually without the patient feeling the stimulation.

For cases of epilepsy or Parkinson's, deep brain stimulation targets gray matter, or the bodies of neurons, in parts of the brain involved with motor control.

But for depression, the best results in clinical trials so far tend to be when the implants target white matter.

One potential target has been white matter tracts adjacent to the subcallosal anterior cingulate cortex, an area implicated in mood regulation.

"Previously, it was not clear how deep brain stimulation affected brain structure and function," explains neurologist Helen Mayberg.

But research on monkeys is changing that.

"This study addresses a major gap in our understanding and points to an unappreciated mechanism contributing to sustained long-term recovery," adds Mayberg, "something we have observed in our deep brain stimulation depression clinical research over many years."

Related: A Common Arthritis Drug Appears to Work When Antidepressants Don't

Researchers at Mount Sinai were some of the first in the US to test how deep brain stimulation might treat depression.

Their follow-up research among monkeys is now digging deeper to figure out what may be driving these symptoms in the brain.

"Now that we know deep brain stimulation can drive structural plasticity in white matter, we can begin thinking about how to optimize stimulation approaches and potentially develop novel therapies that target these mechanisms through nonsurgical means," says Mayberg.

The study is published in Nature Neuroscience.

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Ötzi the Iceman is about as deceased as an organism can be.

He died 5,300 years ago, his body exquisitely mummified in Italy's glacial Ötztal Alps – one of the oldest and best-preserved human mummies ever discovered.

In the extreme cold of the alpine environment in which he died, microbial activity was suppressed – and, since microbes are the main driver of decomposition, Ötzi did not succumb to its ravages.

But the Iceman's corpse may not have been completely devoid of life.

A new study of the microbes all over his body suggests that some potentially active species may be nearly as old as the mummy himself – while others may have adapted to the conditions of the cold storage where he lies today.

"A mummy's microbiome is unique because we are dealing with microbes that are over 5,000 years old and, at the same time, with modern microbes that have been introduced since the discovery," says first author Mohamed Sarhan, a microbiologist at Eurac Research in Italy.

Ötzi (pronounced like 'curtsy' without the 'c') was discovered in 1991, when two hikers spotted what they thought was a recently deceased mountaineer protruding from the melting ice of a glacier, at an elevation of 3,210 meters (10,530 feet).

It was only once his body had been transported to a laboratory that scientists understood the true significance of the find – a Copper Age hunter who had lived and died around 3300 BCE, mummified so exceptionally well that he appeared far more recent.

Since then, scientists have discovered much about Ötzi.

He was around 46 years old when he died, was adorned with at least 61 hand-poked tattoos on his dark skin, wore clothing stitched from the skins of multiple animals, and ate a last meal rich in ibex fat, wild meat, and cereals.

Previous studies even examined his gut microbiome, finding it more consistent with that of ancient, non-industrialized human populations than with that of modern Western populations.

Researchers also recovered an ancient strain of Helicobacter pylori, the stomach bacterium associated today with ulcers and gastric cancer.

However, all these studies had one thing in common: They mostly treated those microbes as biological remains, rather than investigating whether any might still be active today.

And no one had undertaken the painstaking work of extricating Ötzi's native microbiome from environmental contaminants that may have moved in after he died, both on the glacier and afterward, when he was moved to cold storage to prevent decomposition.

Sarhan and his colleagues took swab samples from all over Ötzi's body, as well as meltwater inside him. They also used data on intestinal and stomach tissue from previous studies, and tested a sample of the soil from where he was found, collected at the same time as the Iceman himself.

They ran these samples through DNA and RNA sequencing, looking for patterns in the types of microbes therein.

Broadly, the microbes fell into two main groups. The first were ancient microbes that were part of Ötzi's living microbiome.

The second were cold-loving yeasts found on Ötzi's skin and in meltwater collected from inside the mummy. These yeasts were highly specialized species adapted to cold environments, genetically related to microbes found in gelid regions such as Antarctica.

This suggests that these microbes likely originated in the glacier environment that preserved Ötzi's body.

But there was something else a bit strange. Some of the samples were heavily degraded, showing that the microbes were ancient – but others were relatively fresh, implying ongoing activity.

"We see continuity here," says microbiologist Frank Maixner, director of the Institute for Mummy Studies at Eurac Research.

"These yeasts have accompanied Ötzi on his long journey through the millennia."

There's another piece of the strange puzzle. Some of the microbes may have benefited from the conservation techniques used on the body.

After he was found, Ötzi's body was treated with phenol, a toxic compound that prevents fungal growth. Three of the four yeasts were species capable of metabolizing phenol.

It is, to be clear, impossible to tell whether these active microbes are the descendants of a long, unbroken line quietly making their home on Ötzi's body for millennia, even in the ice-cold, or whether they were dormant and revived after the mummy was thawed.

Related: Artist Tattooed Himself to Solve Mystery of Ötzi The Iceman's Tattoos

But the evidence strongly indicates that, in some fashion, the Iceman's body supported their survival.

Samples taken in 2010 and 2019 showed that one cold-loving species increased over the decade – suggesting that at least some of the microbes are surviving and even slowly reproducing in the subzero conditions of Ötzi's storage chamber.

"The Iceman mummy is not a static artifact but a dynamic ecosystem of living archive where ancient glacier-derived microbes and modern contaminants coexist under museum conditions," the researchers write.

The findings have been published in Microbiome.

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Researchers have made a significant step forward in understanding how gut bacteria, and specifically a newly discovered virus, can contribute to one of the most common forms of cancer in the developed world.

Scientists from institutions in Denmark and Australia wanted to take a closer look at a previously identified association between colorectal cancer and a bacterium called Bacteroides fragilis.

B. fragilis often shows up in healthy people too.

"It has been a paradox that we repeatedly find the same bacterium in connection with colorectal cancer, while at the same time it is a completely normal part of the gut in healthy people," says microbiologist Flemming Damgaard, from Odense University Hospital in Denmark.

The team wanted to see if there was a crucial difference in the bacterium in individuals who develop cancer – and that's exactly what they found.

"We have discovered a virus that has not previously been described and which appears to be closely linked to the bacteria we find in patients with colorectal cancer," says Damgaard.

Using genetic sequencing, the researchers analyzed the gut bacteria of cancer patients in a large Danish population study.

They found that in these patients, B. fragilis often carried a bacteriophage.

Bacteriophages are viruses that live inside bacteria, hijacking these cells to duplicate and spread.

While the initial signal was discovered in a relatively small group of people, the findings were later verified in a larger cohort of 877 people with and without colorectal cancer – and point to a link that suggests viruses lurking in B. fragilis may tip the scales toward cancer.

People with colorectal cancer were twice as likely to have detectable levels of the bacteriophage in their gut bacteria, the data showed. What's more, it's not a virus that fits the description of anything recorded to date.

However, the researchers can't prove a direct cause-and-effect relationship yet. This is a notable association that will be useful for studying colorectal cancer and potential treatment targets, but there may be much more going on.

"It is not just the bacterium itself that seems interesting," says Damgaard.

"It is the bacterium in interaction with the virus it carries."

"We do not yet know whether the virus is a contributing cause, or whether it is simply a sign that something else in the gut has changed."

Around 80 percent of colorectal cancer risk has been assigned to environmental factors, including gut bacteria composition. That means a better understanding of these factors and how they influence one another could affect millions of cancer cases.

Studying the mix of bacteria in the gut is no easy task.

These incredibly complex microbiomes are both indicators of what else is going on in the body and influencers that can impact everything from sleep quality to weight loss.

Now there's an extra layer that future studies can examine: not just bacteria, but the viruses living inside them. One question the researchers are keen to look at next is exactly how B. fragilis might be affected by its bacteriophage lodgers.

This research is still very much in the early, experimental stage, but anything that helps experts understand how cancer starts could potentially also help develop targeted treatments – though that may take years.

"The number and diversity of bacteria in the gut is enormous," says Damgaard.

"Previously, it has been like looking for a needle in a haystack. Instead, we have investigated whether something inside the bacteria – namely viruses – might help explain the difference."

The team suggests that their findings might also be used for colorectal cancer screening. With further research, stool sample scans could be developed to look for this B. fragilis virus, for example.

Related: Colorectal Cancer Is Rising in Young People. Here's How to Lower Your Risk.

"In the short term, we can investigate whether the virus can be used to identify individuals at increased risk," says Damgaard.

The research has been published in Communications Medicine.

An earlier version of this article was published in February 2026.

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The human population is growing larger and older, which means cancer cases and deaths are increasing, too.

Based on the current trends, there will be 35.3 million cases of cancer diagnosed annually by 2050, and 18.5 million deaths.

For every 10 people diagnosed with cancer, seven will be in low- and middle-income countries, where survival rates are much lower.

This is way beyond the current capacity of global healthcare systems.

According to a new report commissioned by The Lancet Oncology, the cancer workforce will be running 100 million people short by 2050.

Most of those projected shortages are in nursing, and diagnostic roles such as radiologists and pathologists.

The research was led by radiologist Hedvig Hricak of the Memorial Sloan Kettering Cancer Center in the US, and oncologist Patrick Loehrer of Indiana University Melvin and Bren Simon Comprehensive Cancer Center.

"Our global initiative brings a clear warning: without urgent action to address critical workforce shortages, we risk a cancer crisis unlike anything we've seen before," says Hricak.

"We call for immediate, country-specific strategies, smarter workforce use, task-shifting and AI/digital health adoption, alongside future-ready education and strong, sustainable financing through public–private partnerships."

To get a sense of what lies ahead, the team created models of current and future scenarios based on 17 common types of cancer, and 18 types of cancer workforce personnel.

They expect diagnosed incidence rates of these cancer types to increase globally, particularly in low- and middle-income countries, due to aging populations, changing risk factors, and the increasing size of the human population overall.

And it looks like we're on track to have nowhere near enough healthcare staff to deal with it.

By 2050, the global cancer workforce will fall short by about 100 million staff needed to cope with these rising cancer rates, the report states.

It suggests we need to do something, fast, to fill the need for 65 million more nurses and 16 million more diagnostic specialists.

There's also expected to be a global gap of 10 million in demand for specialized medical doctors, with at least 10 years of training; a gap of 6 million in advanced clinical specialists with 6 to 10 years of training; and a shortage of 15 million technical and allied health professionals with 3 to 5 years of training.

These shortages are particularly concerning in Africa and Asia, which are predicted to have the lowest five-year net cancer survival rates globally in 2050. The report estimates those survival rates at just 34 percent in Africa and 39 percent in Asia.

"Crucially, we estimate that one in three cancers go undiagnosed worldwide, with more than 60 percent of cancers remaining undiagnosed in parts of Africa," Hricak and team report.

"Rather than cancer type or biological factors, the most important determinant of cancer survival for many patients is therefore the country in which they receive diagnosis and treatment."

By comparison, in high-income areas like North America and Oceania, survival rates are expected to reach 60 percent.

If the global community can somehow scale up the workforce – and ensure these workers are positioned where they're most needed – it could avert 170 million cancer deaths between 2030 and 2050, the report says.

They propose a suite of strategies to address the crisis. A global cancer workforce registry – which currently doesn't exist – would help inform training, hiring, and resource allocation.

Partnerships between workforce sectors and nations could aid in training, research, diagnostics, therapeutics, and equipment.

They also urge for more investment in digital and artificial intelligence solutions.

In economic terms, the team says these strategies could deliver US$120 trillion of benefits between 2030 and 2050. That's a $4 return on every dollar invested in addressing the problem.

Related: Almost 50% of Preventable Cancers Linked to Just Two Lifestyle Habits

"Make no mistake; this is a wake-up call, no matter where you are in the world," said Mark Lawler, co-author and oncologist at Queen's University Belfast in the UK, at the commission's launch event.

"What we've uncovered is shocking – how can we reconcile a 15 million increase in cancer cases diagnosed with a 100 million decrease in cancer staffing? The data unfortunately do not lie. We can't wait until 2050 to see if our projections are correct – we must act now."

The research was published in The Lancet Oncology.

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Reddit deep dives can involve anything from TV show fan theories to DIY advice.

A new AI-assisted analysis now suggests that the 'front page of the internet' could help researchers spot potential side effects of GLP-1drugs used to manage weight and diabetes, such as Ozempic, Wegovy, Mounjaro, and Zepbound.

A team from the University of Pennsylvania analyzed more than 410,000 Reddit posts across a six-year span, looking for mentions of two active ingredients in widely used GLP-1-based drugs: "semaglutide" or "tirzepatide", or their brand names.

" Clinical trials are the gold standard, but by design, they are slow," says computer and information scientist Sharath Chandra Guntuku.

"This is not a replacement for trials, but it can move much faster, and that speed matters when a drug goes from niche to mainstream almost overnight."

When it came to potential side effects that doctors may not know about, two groups of complaints stood out: reproductive health issues (including irregular menstrual cycles) and temperature-related problems (such as chills and hot flashes).

The way the body's metabolism burns energy is known to impact temperature balance, so there is a real mechanism that potentially links the side effect to the drug in a causative way. But there is less research on how these drugs affect the menstrual cycle.

It's worth noting that these previously "unrecognized potential effects" were far from the most commonly reported on Reddit, and the researchers emphasize that they don't see their new analysis as a replacement for trials or clinical assessments.

However, the findings suggest that online boards and peer-to-peer conversations may be places where people feel able to discuss certain symptoms, some of which they might not mention to a doctor.

"Some of the side effects we found, like nausea, are well known, and that shows that the method is picking up a real signal," says Guntuku.

"The underreported symptoms are leads that came from patients themselves, unprompted, and clinicians could potentially pay attention to them."

This kind of large-scale data capture and interrogation is made possible by the latest AI models. Here, the researchers used GPT models from OpenAI to crunch through Reddit posts and find patterns.

That's no easy task, given the volume of text and the variety of ways people might talk about GLP-1 drugs and their side effects. These scans can be completed rapidly, identifying potential sources for investigation in future clinical trials.

With little else known about the Reddit posters involved, the research can't be definitive about whether drugs like Ozempic or Mounjaro are actually causing these symptoms.

However, these self-reported side effects are worth further investigation.

"These drugs are thought to work by engaging part of the brain called the hypothalamus, which helps regulate a wide variety of hormones," says psychologist Jena Shaw Tronieri.

"That doesn't mean the medications are necessarily causing these symptoms, but it could suggest that reports of menstrual changes and body temperature fluctuations are worth studying more systematically."

GLP-1 drugs are named after glucagon-like peptide-1, a natural hormone that the medications mimic. Specifically, the drugs limit appetite, slow down digestion, and trigger the release of insulin from the pancreas in response to high blood sugar levels.

While these treatments are associated with significant benefits in weight loss and diabetes management, research is ongoing into other potential consequences of GLP-1 use.

Those consequences potentially include protection against Alzheimer's, better cardiovascular health, and a greater risk of acute or chronic pancreatitis – so, quite the mix. We also know that regaining most of the weight after GLP-1 treatments is common.

The kind of online analysis done here may highlight problems that might otherwise be missed.

"The whole point of this kind of approach is that it can move quickly, and that's exactly when it's most valuable," says Guntuku.

Reddit tends to skew towards younger, male, US adults – but that doesn't mean it can't be useful for flagging problems that researchers need to know about.

Related: Ozempic-Like Drugs Can Help You Lose Weight, But There's a Catch

"Clinical trials generally identify the most dangerous side effects of drugs, but they can fail to find what symptoms patients are most concerned about," says computer and information scientist Lyle Ungar.

"Even though social media is not necessarily representative, a large collection of posts may reflect additional concerns."

The research has been published in Nature Health.

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The hottest giant planets in the galaxy should, in theory, have the fastest winds.

The hotter a planet is, the stronger its atmospheric currents should be – and a category of exoplanets known as hot Jupiters contains the hottest worlds we've ever found.

They orbit so insanely close to their host stars that some of them are literally evaporating from the heat…

Yet a new analysis of seven hot Jupiters reveals wind speeds that are practically sluggish, compared to what astronomers expected.

The best explanation for this surprise, according to a team led by astronomer Julia Seidel of Côte d'Azur Observatory in France, is that something is holding the winds back.

And the mechanism that could best explain that powerful braking effect is a magnetic field.

If the team's findings are validated, these laggardly winds could be the best evidence we've seen yet of magnetic activity on a world outside the Solar System.

"This breakthrough opens a completely new window on exoplanet research," Seidel says.

"It's the first time we can compare the magnetic environments of other worlds – a key step toward ultimately understanding which planets can stay alive, keep their water, and perhaps even, one day, host life as we know it."

Hot Jupiters are already some of the most fascinating exoplanets in the Milky Way. These worlds are in such proximity to their stars that, in the most extreme cases, their orbits are less than a day.

This means that two things are usually true for hot Jupiters. The first is that they are tidally locked, with one side permanently in daylight facing the star, and the other in permanent darkness facing away.

This produces a temperature contrast that should create some absolutely demented weather.

The second is that these worlds are usually heated to equilibrium temperatures of several thousand degrees, helping drive even stronger atmospheric circulation.

Now, we can't directly measure magnetic fields on exoplanets, but previous studies of individual hot Jupiters have shown that, by tracing vaporized iron in the atmosphere, wind speeds can be established.

Because we know that magnetic fields can act as a brake on electrically charged gases, the researchers thought they might be able to use hot Jupiter wind speeds as a proxy for magnetic field activity.

They used the MAROON-X instrument on the Gemini North telescope and the ESPRESSO instrument on ESO's Very Large Telescope to measure wind speeds across seven hot Jupiters.

Now, wind speeds on these worlds are still far beyond anything we might see in the Solar System. The researchers recorded howling gales at speeds between 2 and 7 kilometers (1.2 to 4.3 miles) per second. Jupiter's wind speeds – the fastest in the Solar System – only get as high as about 0.4 kilometers per second.

However, what makes the hot Jupiters interesting is the clear relationship between wind speed and temperature.

The researchers found that the hotter the exoplanet, the slower its winds.

There are some other explanations for slower-than-expected winds on hot Jupiters; but, the researchers argue, the other possibilities would still show the opposite trend, with wind speed increasing with temperature.

"This is totally counterintuitive because, all things being equal, hot planets have more energy to accelerate the winds!" says astronomer Vivien Parmentier of Côte d'Azur Observatory. "Something must happen that slows down the wind speeds for hotter objects."

This something, the researchers argue, is most likely to be magnetic fields… and, based on the trend in their observations, they were even able to infer the strength of the field producing the effect.

The hot Jupiters, they found, should have magnetic fields of only a few gauss, roughly comparable to Jupiter's.

Because it's a proxy measurement, further observations may be required to confirm the team's findings.

Related: Ludicrous Lemon-Shaped World Is Like Nothing We've Ever Seen

However, it's still a lovely result – one that shows just how far we've come in understanding alien worlds, moving away from the characteristics of individual planets to statistical-level analyses that start to reveal patterns.

"Here on Earth, we know the beauty of the northern and southern lights, where particles from the Sun hit our magnetic field and are guided toward the poles, colliding with gases in the atmosphere to produce colorful displays of green, pink, and purple," says astronomer Bibiana Prinoth, formerly of Lund University, Sweden, now at the ESO.

"I like to imagine that some of these worlds have a sky filled not only with stars, but with vast curtains of colorful light dancing across a planet that's half in perpetual day and half in endless night."

The research has been published in Nature Astronomy.

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One of the hardest things to do in physics is to generate true, provably unpredictable randomness.

That's because it's impossible to determine randomness based on the output alone.

Dice may have nicks and flaws that influence how they roll.

Computer random-number generators are usually driven by algorithms.

Even coin flips are governed by physical forces that, in theory, could be predicted.

The difficulty lies not in generating numbers that appear random, but in showing that no one could have possibly predicted the outcome – that the system isn't secretly affected by subtle hidden rules or biases.

Now, a team of physicists at ETH Zurich in Switzerland has overcome that challenge by leveraging one of the strangest phenomena in quantum mechanics: entanglement.

"The resulting sequence of zeros and ones is now really perfectly random, and we can even certify that," says physicist Renato Renner of ETH Zurich.

Randomness is crucial to modern security.

It's the core feature that makes passwords, authentication codes, and encryption keys harder to guess.

It's the reason password generators will produce a string of meaninglessly jumbled characters rather than something like YourFirstPet123.

But the stakes extend far beyond a Flickr password to international security.

Recent examples of security weaknesses include the 2024 PuTTY vulnerability, in which one of the world's most widely used SSH clients had a flaw in its random-number generation for cryptographic signatures.

And don't forget the 2025 AMD Zen 5 RDSEED bug, in which a hardware random-number instruction would generate predictable values while falsely reporting success.

If a code is not perfectly random, it's easier for attackers to guess.

"Any conventional electronic device, like a phone or a computer, is completely deterministic," Renner told Adam Kovac at Scientific American, "so it's actually very difficult for a computer or any other electronic device to generate a random value."

To try to find a solution to this problem, the researchers turned to a quantum experiment known as the Bell test.

They created a pair of entangled quantum bits, or qubits, separated by 30 meters (98 feet) and cooled to temperatures close to absolute zero.

Entangled particles are those that, when measured, show similarities that cannot be explained by classical physics alone.

Measurements performed on the qubits produced correlations so strong that they could not be explained by ordinary hidden rules or pre-programmed behavior.

This achievement required major technical improvements to both the stability and speed of the experiment, allowing the team to perform more than a billion Bell-test trials over roughly nine hours.

Previous quantum random-number generators could produce highly random outputs, but they still relied on trusted hardware and perfectly random starting conditions.

The ETH Zurich team instead demonstrated something called randomness amplification, deliberately starting with imperfect randomness – taking randomness that may contain subtle flaws or biases and transforming it into randomness that can be certified as perfectly unpredictable.

"Crucially," they write in their paper, "randomness amplification has been proven to be impossible by purely classical means."

The result is a system capable of generating certifiably perfect randomness, even when starting with flawed or imperfect randomness.

Related: Crystals Have Been Used to Generate Truly Random Numbers For The Very First Time

And it's also device independent, which means the randomness does not depend on trusting the hardware itself, but on the quantum behavior observed in the experiment.

In the long term, the researchers say that their system could perform the same function atomic clocks perform for timekeeping – a physically certified source of randomness against which others can be measured and set.

"The technical improvements allowed us, for the first time, to create random numbers that will remain perfectly random for all eternity – no matter what analytical methods are used to assess their randomness," Renner says.

The research has been published in Nature.

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For millions of people, statins are a daily shield against heart disease.

But around 10 percent of those who take statins to lower cholesterol experience a mysterious, painful side effect that causes many to discontinue these potentially life-saving medicines.

Scientists have recently found one possible reason why.

Research from Columbia University and the University of Rochester in the US revealed a potential culprit: a tiny calcium gate inside muscle cells that statins may force open.

The resulting calcium leak can damage muscle tissue, offering a new explanation for at least some cases of statin-associated muscle symptoms (SAMS).

"I've had patients who've been prescribed statins, and they refused to take them because of the side effects," said lead author Andrew Marks, a cardiologist at the Columbia University Vagelos College of Physicians and Surgeons.

Statins work by blocking an enzyme that's required for the biosynthesis of cholesterol in the liver.

As a result, levels of 'bad' LDL cholesterol are reduced in the blood, helping to prevent one of America's top killers: cardiovascular diseases like atherosclerosis, the buildup of fatty deposits in blood vessels.

But statins also affect "off-target" molecules, including a protein called ryanodine receptor 1 (RyR1). RyR1 is a mushroom-shaped channel, or gate, located on the sarcoplasmic reticulum, a web-like structure that surrounds muscle fibers.

RyR1 acts like a bouncer at a club, opening or closing the door to let calcium ions flow into the muscles. This calcium flow is an essential process that mediates muscle contractions.

Using mice as models, the researchers observed the precise way statins bind to RyR1, using an imaging technique called cryo-electron microscopy (cryo-EM).

Cryo-EM involves flash-freezing biological samples and then blasting them with electron beams. The deflection pattern of the electrons reveals tiny structures, allowing scientists to create highly detailed 3D images of things like proteins and view their constituent molecules.

Yet cholesterol-lowering drugs like simvastatin may keep these gates open, allowing calcium ions to leak into muscle cells, which can either directly damage muscles or trigger enzymes that degrade them.

As a result, statin users may experience persistent pain, weakness, tenderness, and cramps.

The issue is exacerbated in individuals with RyR1 mutations, who may also experience episodes of malignant hyperthermia (a severe overheating triggered by medication) or weakness in the diaphragm that leads to reduced lung function and respiratory disorders.

In rare but potentially life-threatening cases, the side effects of statins can induce rhabdomyolysis, a serious syndrome in which muscle tissues rupture and leak into the bloodstream, culminating in kidney failure.

The equally gruesome autoimmune-mediated necrotizing myositis may also rarely occur, a condition in which the immune system turns against its own tissues and kills muscle tissue.

The leaky calcium gate explanation may not apply to all cases of SAMS, but now that we understand this mechanism, it could help identify people at risk of statin intolerance.

Around 40 million adults take statins in the US alone, and approximately 10 percent of treated individuals experience SAMS.

"It's the most common reason patients quit statins, and it's a very real problem that needs a solution," said Marks.

Related: US Cardiologists Have Published New Guidelines For Managing Cholesterol

The researchers highlight two promising options. The first is to redesign statins so they don't bind to RyR1 but still inhibit cholesterol production in the liver.

Alternatively, when the researchers treated statin-intolerant mice with Rycal, an experimental class of drug used to treat patients with rare muscle diseases, they were able to close the leaky RyR1 calcium gates and prevent simvastatin-induced muscle weakness.

"It is unlikely that this explanation applies to everyone who experiences muscular side effects with statins," Marks explained.

"But even if it explains a small subset, that's a lot of people we could help if we can resolve the issue."

This research was published in the Journal of Clinical Investigation.

An earlier version of this article was published in February 2026.

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A life that leads to dementia can take many paths, but there are some common risk factors that make a diagnosis more likely.

An extensive new study shows, however, that among older adults, the effect of those risk factors differs.

Some risk factors seem to hit women's cognition harder than men's, and accruing multiple risk factors over a lifetime seems to worsen women's brain function more so than men's.

In other words, certain risk factors may not mean the same thing in a woman's brain as it does in a man's, which has implications for dementia research and treatments.

It's well known that dementia is more common in women than in men, and longer life expectancy does not fully explain the gap.

There's something else going on that these findings could also help us understand.

"Our study suggests that women may be at greater risk of dementia because they experience a greater number of risk factors, and because these risk factors reduce cognition to a greater degree than [in] men," the researchers write.

Study co-authors Megan Fitzhugh and Judy Pa, two neuroscientists from the University of California, San Diego, say their results provide further evidence that dementia risk needs to be assessed and managed in a personalized way.

"Looking beyond which risk factors are most common, we found that some have a disproportionately larger impact on women's cognition," says Fitzhugh.

"This suggests that prevention efforts may be more effective if they are tailored not just to risk factor prevalence, but to how strongly each factor affects cognition in women versus men."

The researchers analyzed health data from 17,182 individuals aged 40 or older, examining 13 risk factors linked to dementia.

Depression, physical inactivity, and sleep problems were more common in women, compared to men.

Higher rates of hearing loss, diabetes, and heavy alcohol use, on the other hand, were more often reported by men.

Some risk factors were linked to greater reductions in cognitive scores in women – an indication that they affect women's brains more negatively than men's.

These factors included high blood pressure, hearing loss, and diabetes.

Higher BMI was also associated with poorer cognitive performance in women in their 50s and 60s, but not at older ages.

Amid that picture of cognitive decline, there were some positive trends suggesting that certain factors might help preserve cognitive function in women compared to men.

"Two risk factors, years of education and total cholesterol, showed positive associations with cognition, such that higher levels were correlated with greater cognition," write the researchers in their published paper.

Given their links to cognitive performance, it's possible these factors may be especially important to investigate in women's dementia risk.

However, this observational study can't prove cause and effect. A longer-term analysis could provide stronger evidence that these risk factors were contributing to the cognitive test scores.

While 'women' and 'men' are recognized as gender categories, this study uses these terms to refer to individuals' self-reported biological sex.

"It is important to distinguish between sex differences in the prevalence of risk factors and their impact on cognition, because prevalence and impact may not correspond," writes the team.

"Targeting only the most prevalent risk factors within each sex may overlook certain risk factors that more markedly influence cognitive decline."

The new findings fit with previous research suggesting that dementia risk factors may affect men and women in different ways, though these studies have tended to look at only one risk factor at a time.

Alzheimer's disease now affects an estimated one in nine US adults aged 65 and older, and two-thirds of those affected are women.

While the figures for dementia may be bleak, there are real and practical ways to reduce risk, while work on treatments continues.

The researchers emphasize that all these risk factors are potentially modifiable. That means they're real targets that people and their doctors can try to address, whether it's drinking less, moving more, or seeking help for depression.

Next steps here could include research to determine why women's cognition may be more vulnerable to certain factors.

Hormonal changes around menopause may be involved, but the mechanisms remain unclear.

Related: One Vital Bodily Function Could Link Many Dementia Risk Factors

"These differences highlight the importance of considering sex as a key variable in dementia research," says Pa.

The research has been published in Biology of Sex Differences.

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Night shift work is not for the weak.

Staying awake from dusk through to dawn, as many nurses, doctors, and emergency responders do, seems to take a toll on the body and mind.

But does it have an impact on the brain?

Neuroscientists in Singapore have now found evidence that shift work is tied to brain volume losses in key parts of the brain.

If shift work is stopped, however, those reductions are partially recovered within two and a half years, on average.

What those losses and gains actually mean for human health or behavior is unclear.

A secondary analysis revealed a negative correlation between volume loss and cognitive performance: Increasing volume loss was associated with poorer performance on some, but not all, cognitive tests.

But the effect size is "very small", the authors warn, so the results "should be interpreted cautiously."

That said, there's an important clue in the details. The brain regions that showed significant volume losses also help govern our sleep cycles.

What's more, they are involved in many of the symptoms of shift work, like poorer emotional regulation and memory performance.

The study is the largest of its kind and finds a change in brain volume where most previous analyses of shift work have not.

It analyzed MRI and long-term health data from 14,198 middle- to older-age adults with no medical issues who took part in the UK BioBank.

Among 2,122 shift workers, the researchers noticed a symmetrical pattern of modest volume loss in the right thalamus, which is part of the brain's information relay 'hub' and is closely involved in memory retrieval.

They also noticed modest volume loss in the left amygdala, which regulates emotional responses.

This was after accounting for age, sex, chronotype, and skull volume, among other factors, in their analysis.

"The selective thalamic and amygdalar volume loss observed in healthy shift workers may represent an early, subclinical marker of neural vulnerability linked to chronic circadian disruption," the team concludes, led by neuroscientist Thomas Welton.

"These regions are central to sleep-wake regulation, emotion, and attention, functions that are commonly affected in shift work-related fatigue and mood disturbance."

Challenges with regulating emotions are often tied to poor sleep, and shift workers are known to face higher risks of both sleep disorders and mental health problems.

Researchers have long speculated that a disrupted circadian rhythm is to blame.

Other factors that may contribute include a lack of sunlight or changes to eating times.

But just because some parts of the brain are shrinking does not mean they are necessarily dying. The brain is a flexible organ that can rewire itself to meet the challenges of the time.

Perhaps that is what it is doing for shift workers; maybe their brains are somehow compensating in a way that allows them to work through the night.

"It is possible," the authors note, "that individuals who fail to acquire these brain changes are unable to tolerate shift work and are therefore biased toward non-shift working roles."

The study took place only among older adults, which means it's not clear how the brains of younger workers may cope with the demands of shift work.

Further studies are needed to fully understand how different people respond and are affected.

Today, full-time shift workers make up about 10 to 17 percent of the US population, but by some estimates, roughly a quarter of the adult workforce currently labors during non-traditional hours.

Related: Sleepless Nights Could Drive Half a Million Cases of Dementia in The US Each Year

If this work repeatedly disrupts the body's natural circadian rhythm, it could have a long-term and measurable impact on the brain, but we won't know until those changes are studied further.

"In the "era of longevity", it is critical to understand the relationship between shift work and structure of the middle-older aged brain," Welton and colleagues write.

"The apparent reversibility of these [observed] structural effects within two years of ceasing shift work highlights a potential therapeutic window for prevention and recovery," they add.

The study is published in NeuroImage.

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Just a few years ago, a strange signal was received from the plane of the Milky Way.

It was something astronomers had never seen before, pulsing with a radio beat too slow to fit any known astronomical object.

It may have just come and gone as a one-off anomaly.

But then they found another one.

And another.

To date, around a dozen of these long-period radio transients (LPTs) have been detected from diverse corners of the galaxy, leaving scientists baffled.

Now, a team led by astronomer Kovi Rose of the University of Sydney in Australia thinks they may finally have found their Rosetta Stone, the object that could help them interpret at least some of these weird, pulsating objects.

In the direction of the galaxy's inner regions, the researchers traced an LPT signal directly to a magnetic cataclysmic variable star – a strongly magnetized white dwarf cannibalizing its companion and belching periodic radiation.

"Long-period radio transients have puzzled astronomers for years," Rose says.

"We've only found about a dozen, and their origins have been unclear. Now, we've been able to show that the source for one of these transients comes from a white dwarf actively pulling material from a companion star."

The mystery of the LPTs, first detailed in a 2022 paper, reared its head again after astronomers found something in the plane of the Milky Way pulsing in a weird way.

Every 18.18 minutes, the brightness of an object named GLEAM-X J162759.5−523504.3 increased for 30 to 60 seconds, temporarily making it one of the brightest objects in the low-frequency radio sky.

Then it stopped.

But it wasn't long before astronomers found more – showing that, whatever this strange object was, it wasn't just a one-off weirdness.

As the population grew, astronomers began to piece together possible explanations.

Some observations pointed to highly magnetized white dwarfs, while others hinted that at least some LPTs might arise in binary systems, where a white dwarf interacts with a companion star.

A major breakthrough came in 2025, when one LPT signal, named ILT J1101+5521, was traced to a binary star consisting of a red dwarf and a white dwarf, orbiting so closely together that their magnetic fields repeatedly clashed, sending out periodic bursts of radio waves.

The picture grew even more complicated when astronomers discovered that one LPT, ASKAP J1832-0911, also emitted X-rays, suggesting energetic processes beyond radio emission alone.

But no single object seemed capable of tying all the clues together.

And that's what makes this new discovery so intriguing. Its name is ASKAP J1745-5051, and it's the first object to unite many of the puzzle pieces previously observed in other LPTs.

That includes both radio and X-ray emission, a white dwarf and a binary companion, strong magnetic activity, orbital motion, and accretion – the gravitational transfer of material onto the white dwarf.

"Some similar objects had been linked to binary systems before, but this is the first one where we can clearly see both stars and the accretion process in action," says astrophysicist Tara Murphy of the University of Sydney and the ARC Center of Excellence for Gravitational Wave Discovery (OzGrav).

The discovery was made using CSIRO's ASKAP radio telescope in Wajarri Yamaji Country in Western Australia – one of the world's most sensitive facilities.

Because the system is such a chaos gremlin, it's impossible to tell exactly how far away it is. The best estimates place it between around 1,300 and 30,000 light-years away.

But the data were detailed enough that the researchers could figure out what kind of object it is.

ASKAP observations show a system that flares in radio waves every 81 minutes (1.35 hours), accompanied by matching periodic X-ray emission detected by NASA's Swift observatory and the Einstein Probe X-ray Telescope.

Optical observations obtained using the Southern Astrophysical Research (SOAR) Telescope showed a white dwarf binary at the emission's location in the sky, with spectra revealing a clear orbital period of about 81 minutes – closely matching the period of the radio and X-ray bursts.

These observations reveal that the object is a magnetic cataclysmic variable. Every orbit, the white dwarf pulls material from its red dwarf companion star, which is funneled by the white dwarf's magnetic field onto its surface.

As the material crashes onto the white dwarf, it heats to millions of degrees and emits high-energy radiation – that's the source of the X-ray signal.

Related: Mystery Signals May Be Coming From One of The Rarest Stars in The Galaxy

Meanwhile, gas accelerated by the two stars' clashing magnetic fields appears to produce the radio signal, similar to the mechanism proposed for ILT J1101+5521.

It's such a beautiful convergence of characteristics that it could help explain other LPTs that only show some of these traits.

And it's genuinely exciting to be able to observe our understanding of LPTs evolve in real time.

"Each new discovery is helping us piece together the bigger picture," Rose says.

"We're only just beginning to understand this new class of cosmic events."

The research has been published in Nature Astronomy.

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The oceans are home to many of Earth's longest living creatures.

Glass sponges can survive for more than 10,000 years, and an individual quahog clam can thrive for more than 500.

A few jellyfish, jellies, and hydra are so good at regenerating themselves that they can theoretically live forever.

But the humble sea cucumber has a truly unique longevity trick.

Scientists in Canada have now discovered a sea cucumber species with tissue that may live 'indefinitely'.

When scientists amputated bits of a scarlet sea cucumber (Psolus fabricii), the tissues refused to die.

For three years and counting, the isolated tube feet and tentacles have sat all on their own in a tank of natural running seawater, without decaying away.

Not only are they not dead, but these tissues are biologically active and changing.

Many of their immune, metabolic, and cellular processes are still intact.

That's never been seen before – not from the tissue of any known animal on Earth.

"We haven't grown a new, complete sea cucumber yet, but we are seeing pretty stunning growth and diversification of cells literally years after this tissue was removed," explains marine biogeochemist Rachel Sipler from the Bigelow Laboratory for Ocean Science, a nonprofit research institute in the US.

"It's like a lizard that loses its tail. We know some lizards can grow new tails; we're talking about whether the tail can grow a new lizard."

Like many lizards on land, the sea cucumber species, P. fabricii, is a bit of a klutz in the ocean. It regularly loses or injures its tube feet and tentacles, which means it has a potentially great capacity for regeneration.

To test that idea in the lab, Sipler and her colleagues at Memorial University of Newfoundland watched and waited to see what happened to excised bits of this wild-looking sea cucumber.

Soon enough, the tissue samples began showing signs of wound repair. Their immune cells appeared to spring into action, and any dead cells were removed.

Repair was then followed by regeneration. Over time, the tissues began to absorb dissolved nutrients from the seawater, growing and restructuring themselves.

Years on, the isolated tentacles can still respond to tactile stimuli, indicating the preservation of a neural network.

This is the first known case of a tissue 'explant' surviving and growing long-term in a natural setting, write Sipler and her colleagues.

"Our findings," they add, "challenge conventional perceptions of tissue immortality."

They also raise the question: What does it mean for tissue to be alive?

For centuries now, scientists have tried to keep the cells and tissues of living animals functional, even when they are removed from the rest of the body.

While researchers have managed to engineer immortal cell lines from animal and human stem cells, these self-proliferating units must be kept in highly controlled environments, where they are carefully guarded against pathogens.

Keeping a whole bunch of cells alive within a section of tissue is much harder to manage.

Animal tissue is a flexible yet delicate structure; it requires a complex scaffold of communicating cells and a robust nutrient delivery system to keep everything plump.

Even when animal tissue is kept in a special solution to extend its longevity, it typically survives about 9 weeks in the laboratory.

But a bit of P. fabricii could live "indefinitely" in natural seawater, researchers speculate. In fact, it seems to thrive in the natural 'dirtiness'.

"Natural seawater is just about the most microbially diverse, least clean approach we could take experimentally," says Sipler.

"Yet, that rich environment full of bacteria and all this organic matter was actually feeding them and allowing this tissue to heal and grow."

The only other tissue culture that scientists have described as 'indefinite' was taken from a chicken embryo, and it did not show the same capacity for healing or survival as the scarlet sea cucumber.

In fact, P. fabricii may be unique even among sea cucumbers.

Sipler and her colleagues tested several other sea cucumbers, but none of their tissue explants survived more than 3.5 months.

"Here is this species that has this groundbreaking ability, and we had no idea," says Sipler.

"It's a reminder how much is yet to be discovered in the marine environment."

Related: Mammals May Have a Hidden Limb Regeneration Ability We Never Knew About

Andrea Bodnar, science director at the Gloucester Marine Genomics Institute, was not involved in the study, but she agrees with the paper's conclusions.

"The fact that tissue explants from a sea cucumber can heal, reorganize, and survive independently for years in natural seawater suggests an entirely new model for biological resilience and tissue regeneration," she says.

The study is published in Science Advances.

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Humans are not yet done cooking. We're continuing to evolve and adjust to the world around us, the records of our adaptations written in our bodies.

We know that some environments can make us unwell. Mountain climbers often experience altitude sickness – the body's reaction to a significant drop in atmospheric pressure, which means less oxygen is taken in with each breath.

And yet, at high altitudes on the Tibetan Plateau, where oxygen levels in the air people breathe are notably low, human communities thrive.

Over more than 10,000 years of settlement in the region, the bodies of those living there have changed.

They've changed in ways that allow the inhabitants to make the most of an atmosphere that, for most humans, would result in insufficient oxygen being delivered to the body's tissues via blood cells, a condition known as hypoxia.

Watch the video below for a summary of the research:

"Adaptation to high-altitude hypoxia is fascinating because the stress is severe, experienced equally by everyone at a given altitude, and quantifiable," anthropologist Cynthia Beall of Case Western Reserve University in the US told ScienceAlert.

"It is a beautiful example of how and why our species has so much biological variation."

Beall has been studying the human response to hypoxic living conditions for years. In research published in October 2024, she and her team revealed some of the specific adaptations in Tibetan communities: traits that improve the blood's ability to deliver oxygen.

To unlock this discovery, the researchers looked into one of the markers of what we call evolutionary fitness: reproductive success.

Women who deliver live babies are those who pass on their traits to the next generation.

The traits that maximize an individual's success in a given environment are most likely to be found in women who are able to survive the stresses of pregnancy and childbirth.

These women are more likely to give birth to more babies.

Those offspring, having inherited survivability traits from their mothers, are also more likely to survive, reproduce, and carry those same traits forward.

That's natural selection at work.

Natural selection can be a bit strange and counterintuitive; in places where malaria is common, for example, the incidence of sickle cell anemia is high, because it involves a gene that protects against malaria.

Beall and her team studied 417 women aged 46 to 86 who had lived their entire lives in Nepal at altitudes above 3,500 meters (11,480 feet).

The researchers recorded the number of live births – ranging from 0 to 14 per woman, with an average of 5.2 – along with physical and health measurements.

Among the things they measured were levels of hemoglobin, the protein in red blood cells responsible for delivering oxygen to tissues.

They also measured how much oxygen was being carried by the hemoglobin.

Interestingly, the women who demonstrated the highest rate of live births had hemoglobin levels that were neither high nor low, but average for the testing group.

But the oxygen saturation of their hemoglobin was high.

The results suggest that the adaptations are able to maximize oxygen delivery to cells and tissues without thickening the blood – an outcome that would increase stress on the heart as it struggles to pump a higher-viscosity fluid more resistant to flow.

"Previously we knew that lower hemoglobin was beneficial; now we understand that an intermediate value has the highest benefit," Beall said.

"We knew that higher oxygen saturation of hemoglobin was beneficial; now we understand that the higher the saturation, the more beneficial. The number of live births quantifies the benefits.

"It was unexpected to find that women can have many live births with low values of some oxygen transport traits if they have favorable values of other oxygen transport traits."

The women with the highest reproductive success rate also had a high rate of blood flow into the lungs, and their hearts had wider-than-average left ventricles, the chamber of the heart responsible for pumping oxygenated blood into the body.

Taken all together, these traits increase the rate of oxygen transport and delivery, enabling the human body to make the most of the low oxygen in the air respired.

It's important to note that cultural factors can play a role, too. Women who start reproducing young and have long marriages seem to have a longer exposure to the possibility of pregnancy, which also increases the number of live births, the researchers found.

Even taking that into account, however, the physical traits played a role. Nepalese women with physiologies most similar to women in unstressed, low-altitude environments tended to have the highest rate of reproductive success.

Related: Humans in The Andes Appear to Have Evolved a Strange Genetic Ability

"This is a case of ongoing natural selection," Beall said.

"Understanding how populations like these adapt gives us a better grasp of the processes of human evolution."

The research was published in the Proceedings of the National Academy of Sciences.

An earlier version of this article was published in October 2024.

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People have been consuming tobacco for millennia, though it wasn't until the late 1820s that nicotine was first extracted from tobacco plants.

Now, 200 years later, scientists have finally discovered how the tobacco plant makes those nicotine molecules.

The discovery could potentially transform products made from or using tobacco species, a practice known as 'plant molecular farming'.

Scientists have been engineering tobacco plants to produce therapeutic compounds and even vaccines, but the nicotine is problematic: it's highly addictive.

Understanding how nicotine is made could mean researchers could devise ways to prevent its production in plants.

"It is a big moment in plant science and biochemistry that we now have the answer we have been chasing for more than 200 years," says biologist Benjamin Lichman, from the University of York.

Lichman and colleagues at the University of Copenhagen in Denmark identified in their new study the genes and enzymes that help produce nicotine.

"With this new knowledge we can remove or repurpose the nicotine that is produced naturally by the plant and create better biotechnology tools," says Lichman.

"There is also exciting potential for the future to adapt tobacco's nicotine forming system to make useful pharmaceutical compounds."

Through a genetic analysis of tobacco (Nicotiana tabacum), the researchers flagged genes that sit close together in tobacco DNA, and activate at the same time as genes already known to be involved in nicotine production.

They then isolated the enzymes produced by these genes.

In both test tubes and living plants, the researchers demonstrated that these enzymes combined to form nicotine.

It turns out the enzymes work through a clever process that goes some way to explaining why they've remained hidden for so long.

Initially, a glucose molecule is attached to the building blocks of nicotine, putting them in the reactive state that's needed for nicotine assembly. That same molecule then snaps off after the process has finished – so the sugar does its essential job, then disappears.

The researchers also identified the two enzymes, NaGR and NicGS, that help assemble the nicotine molecule from its raw materials. Those materials are an amino acid linked to protein building and a vitamin-like compound.

"It is exciting because it has real-world applications," says Lichman.

"A close relative of tobacco, Nicotiana benthamiana, is already used in 'molecular farming' to produce life-saving drugs and vaccines."

"It opens up new ways to use tobacco plants for good: not in cigarettes, but for medicines and other valuable products."

Another recently published study backs up the findings: nicotine is created by glucose, helped by a chain of enzymes, before the glucose disappears.

That complete vanishing act, together with the unusual way glucose is used here compared to other plant processes, is what made the nicotine production process so elusive for so long, the researchers say.

There are still some questions about nicotine production in tobacco, but we now have the main steps and key ingredients sorted.

The researchers suggest the process could be tweaked to produce different chemical substances and tobacco with low levels of nicotine; however, previous attempts have stunted plant growth.

Related: Plants Stopped Thriving When Earth Warmed 56 Million Years Ago

Ultimately, these researchers have not only solved a 200-year-old mystery but also laid the groundwork for more advanced and precise bioengineering.

"Tobacco plants can be used in biotechnology as platforms for producing vaccines or other pharmaceutical products, but it is plagued by the presence of nicotine, which contaminates the products and requires processing to remove it," says Lichman.

The research has been published in Nature Communications.

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In 2019, astronomers recorded a distant star doing something unexpected.

For about an hour, its brightness gently flared before settling back down to baseline levels.

Its behavior matched no obvious stellar phenomenon – too long for a stellar flare, too brief for a supernova, and too smooth for most known kinds of stellar variability.

Now, after a careful probe into the event's properties, astronomers say it could be a signal from one of the most elusive objects in the Universe: a tiny primordial black hole weighing only about as much as three of Earth's Moons.

A black hole of that mass would have an event horizon about the same size as the period at the end of this sentence.

A team of astronomers led by Renee Key of Swinburne University of Technology in Australia say that no other explanation fits the event's statistics quite so well, and so they've named the candidate black hole Phoebe.

"Phoebe suggests a population of compact, lunar-mass objects associated with the dark matter distribution of the Milky Way, and potentially opens a new window to the physics of inflation," the team writes in a preprint posted to arXiv.

We tend to think of black holes as really weighty, large objects – with masses starting at at least a few Suns, and ranging all the way up to tens of billions of Suns.

This is because of the way they form, starting with the death of a massive star whose giant core then collapses under gravity, giving birth to one of the densest known objects in the Universe.

Just after the Big Bang, however, conditions may have been just right to create much, much smaller black holes. Quantum fluctuations in space-time could have created overdensities in the expanding Universe that collapsed much as a stellar core can today.

These black holes are known as primordial black holes, and currently, they are only known to exist in the world of theory.

This could be because they are hard to detect. A primordial black hole the mass of Earth would be just 1.8 centimeters (0.7 inches) across.

Even if such a black hole did manage to have an accretion event, the light screaming from the material caught in its gravitational grasp would be barely a pinprick – not detectable from Earth with our current instruments.

But that's not the only way we could detect a primordial black hole.

Even at very tiny diameters, the gravity around these objects would be extreme enough to bend space-time outside the event horizon.

This region of strongly curved space-time can act as a cosmic lens, and any background light passing through it would be magnified, producing a brief, gentle brightening before returning to normal levels – what is known as a microlensing event.

That's exactly the kind of signal the Dark Energy Camera (DECam) recorded in 2019 when it turned its gaze in the direction of the Large Magellanic Cloud, about 163,000 light-years away from Earth.

The event took place on December 18, when DECam ran for five consecutive nights as part of the Asteroid-Mass Primordial black hole Microlensing (AMPM) survey.

For about 60 minutes, the light of a star in the Large Magellanic Cloud grew in brightness when its neighboring light sources did not.

Microlensing events are rare, but not unknown. Previous microlensing events have been attributed to stellar-mass black holes, tiny, dim stars and their attendant worlds, or rogue exoplanets drifting through space untethered from a star.

To find whether Phoebe could be a black hole, the researchers had to first rule out glitches in the instrument, stellar flares, contamination from other stars, and stellar fluctuations.

Then, they had to model different microlensing scenarios: a free-floating exoplanet in the Milky Way; a free-floating exoplanet in the Large Magellanic Cloud; and a primordial black hole in the Milky Way's extended dark matter halo, away from the concentration of matter in the galactic plane.

According to their calculations, the lensing body, Phoebe – whatever it is – is five orders of magnitude more likely to belong to the Milky Way's dark matter halo than to known stellar populations in either galaxy.

The preferred explanation is that Phoebe is a primordial black hole, about three times the mass of the Moon, located around 59,630 light-years away.

That doesn't rule out a rogue exoplanet in the Milky Way's halo. In fact, the rogue exoplanet is still firmly on the table, given that, observationally at least, rogue exoplanets are far more likely to exist and be detected.

But, in the Milky Way's halo, which is only sparsely populated at best, a black hole is far more likely than a rogue exoplanet, which are generally thought to be more populous in regions of space that have a lot of stars.

The discovery lands smack-bang amid another debate.

In February 2026, astronomers in the US and Japan, analyzing data from the Subaru Telescope, identified 12 microlensing candidates toward Andromeda that, they said, could be due to primordial black holes.

Then, a different team from the University of Warsaw, Poland, reanalyzed the same data and uploaded their rebuttal in March, finding that every one of the events could be attributed to normal, known stars.

Related: LIGO May Have Detected The First Primordial Black Hole, Scientists Say

This new discovery is grist for this debate.

Key and her colleagues say their finding supports the original interpretation of the Subaru data that the events are consistent with primordial black holes.

Which means only one thing. We're going to need a more sensitive telescope.

"Our detection motivates the Roman and Vera C. Rubin Observatory microlensing programs to support high cadence, sit-and-stare observations to boost the sensitivity to low-mass microlenses," the team writes in their paper.

We can't wait.

The preprint is available on arXiv.

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The key to heart health isn't cutting down on pasta or potatoes, new evidence suggests; it's not even a low-fat diet.

The research suggests the focus of healthy eating shouldn't necessarily be on what's being excluded from your diet (for example, reduced carbs or lowered calories).

Instead, the emphasis should be on what you're actually putting into your body, and the quality of those ingredients.

A study that tracked nearly 200,000 men and women in the US for around 30 years found that some low-fat and low-carb diets are better for heart health than others.

What separates them?

The key was the quality of the food itself, not the quantity of carbs or fats.

The research, led by public health researchers at Harvard University, suggests that if a diet contains too many processed foods and animal proteins or fats, or if it otherwise lacks in adequate vegetables, fruits, whole grains, healthy fats, or essential macronutrients, it may not benefit cardiovascular health as much in the long run, even if it is low carb or low fat by definition.

"Our findings highlighted that it's not simply about cutting carbs or fat, but it's about the quality of foods people choose to construct those diets," concluded Harvard epidemiologist Zhiyuan Wu, who led the research, published in February.

"Focusing only on nutrient compositions but not food quality may not lead to health benefits."

Participants in the study who ate healthy, varied diets with adequate macronutrients showed higher levels of 'good' cholesterol in their blood, as well as lower levels of fats and inflammatory markers compared to those who ate diets lacking in those essentials.

They also had a significantly lower risk of developing coronary heart disease, the most common cause of heart attacks.

"These results suggest that healthy low-carbohydrate and low-fat diets may share common biological pathways that improve cardiovascular health," explained Wu.

"Focusing on overall diet quality may offer flexibility for individuals to choose eating patterns that align with their preferences while still supporting heart health."

The findings are based on the self-reported diets of participants, who were all health professionals, so they may have had higher health awareness and better access to health care than the general population.

Related: This Diet Change Cuts Over 300 Calories a Day, Without Decreasing Meal Size

That's somewhat limiting; however, the length of follow-up in the study is impressive, amounting to more than 5.2 million person-years.

The findings join growing evidence suggesting that eating fewer processed foods and more whole grains and vegetables is generally best for a wide range of health outcomes.

Strict diets that count calories, carbs, or fats may not be necessary.

"This study helps move the conversation beyond the long-standing debate over low-carbohydrate versus low-fat diets," said Yale University cardiologist Harlan Krumholz, editor-in-chief of the Journal of the American College of Cardiology.

"The findings show that what matters most for heart health is the quality of the foods people eat. Whether a diet is lower in carbohydrates or fat, emphasizing plant-based foods, whole grains, and healthy fats is associated with better cardiovascular outcomes."

The study was published in the Journal of the American College of Cardiology.

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A diet designed for weight loss could offer a different bonus benefit, according to a new review.

Researchers from the University of Coimbra in Portugal looked at dozens of previous studies analyzing this diet and its relationship to neurodegenerative diseases, such as Alzheimer's, Parkinson's, and Huntington's disease.

If you're on the ketogenic (or keto) diet, you'll be prioritizing fats and proteins, while cutting down on carbohydrates – and it turns out, at the same time you could be protecting your brain from disease.

The team also looked at research relating to the keto diet more generally, trying to pin down the effects of the high-fat, dairy-rich diet on the body's metabolism – how it stores and uses energy in the form of glucose (sugar).

Problems with processing glucose underpin several brain diseases, and the team concluded that the keto diet has real potential as a way of targeting these conditions.

They also acknowledge there are several challenges with using the diet as a treatment method.

"The ketogenic diet has emerged as a metabolically oriented strategy with potential preventive and therapeutic relevance in neurodegenerative diseases," write the researchers in their published paper.

"While preclinical studies have demonstrated encouraging results, significant gaps remain in understanding long-term effects, safety, and practicality of [the ketogenic diet] in clinical settings."

The keto diet works by getting the body to burn fat for energy rather than glucose (which we get mainly from carbohydrates). Biologically, this is known as a metabolic state called ketosis, where fat molecules called ketones are used instead of glucose.

It means weight can rapidly be lost, and the keto diet is actually prescribed for treating epilepsy in some cases.

As the researchers here summarize, there are multiple mechanisms through which it might protect against neurodegenerative conditions too.

Brains running on empty could use ketones as an alternative, emergency energy source, for example, as has been demonstrated in studies of Alzheimer's – thus going some way to restoring neuron stability and functionality.

Ketones have also been shown to reduce inflammation in mice models of Parkinson's and multiple sclerosis, boost an important cellular clean-up process called autophagy, and promote gut bacteria associated with better brain function.

Add all of that up, and there's plenty of evidence that the keto diet – and the metabolic changes that it brings about – can target some of the processes thought to contribute to several devastating brain diseases.

"The ketogenic diet may serve as a complementary metabolic intervention that supports disease-specific treatments by enhancing metabolic resilience and contributing to symptom management," write the researchers.

It's not quite as simple as using the keto diet with people at high risk of neurodegenerative problems, however. Most of the reviewed studies involved animals rather than people, so further investigation is required in terms of clinical trials.

The keto diet is also one of the most difficult to stick to, so getting patients to follow it might be a problem. It also tends to come with a variety of unpleasant side effects: it's been linked to constipation, insomnia, and high cholesterol in some people, for instance.

Past studies have found that the keto diet might cause harm in the longer term, and increase the risk of type 2 diabetes and heart disease. These downsides need to be weighed against any benefits that come along with the keto diet.

What this new review does is give us a 'state of play' in terms of scientific understanding right now. The multiple studies that were looked at offer solid evidence that following a keto diet and having better brain health are connected – though their results shouldn't be considered in isolation.

Related: Keto Diet May Have a Surprising Bonus Benefit, Mouse Study Suggests

"This review underscores the potential of [the ketogenic diet] for treating neurodegeneration on the basis of current scientific evidence while highlighting the need for further research to optimize its application and address existing gaps," write the researchers.

The research has been published in Translational Neurodegeneration.

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A diagnosis of multiple sclerosis (MS) comes with a wave of uncertainty about how the condition will progress.

Now, new research points to a potential mechanism and treatment target for those who are most severely affected.

MS damages nerve cells, stripping away their protective covering that keeps nerve signals firing.

The new study, from researchers in the Netherlands, suggests that in the most severe cases of MS, an immune cell usually in charge of repairing damaged tissue and clearing away waste becomes overloaded with fat droplets.

Known as "foamy microglia", these cells have been spotted in MS patients before, but it wasn't clear exactly what they were doing.

According to the findings from this latest study, they could be key drivers of MS at its worst.

MS is an autoimmune disease in which the body's immune system becomes overactive, mistakes its own cells as foreign, and starts causing damage through inflammation. But these foamy microglia suggest there's also more to the story.

"We found that patients with large numbers of these foamy microglia had a more severe disease course more frequently," says molecular physiologist Daan van der Vliet, from Leiden University in the Netherlands.

"It does not appear to be simply about the inflammatory response alone."

The team analyzed post-mortem brain tissue from 28 people with secondary progressive MS, where the disease has progressed to the point where cognitive and physical function are declining.

This tissue was compared against samples from 10 donated brains from people without the disease.

Using a combination of profiling techniques, the researcher created a map of proteins, fats, and active genes for the brain regions affected by MS lesions.

These lesions form when the fatty, protective coating around nerve fibers, known as myelin, is attacked by immune cells that have become too aggressive.

Not only was there a link between more foamy microglia and MS progression, but the researchers also found that the microglia were changing the mode of inflammation around the lesions – they had a different molecular signature in terms of proteins and enzymes.

The researchers suggest that as microglia arrive to try and repair the damage done to neurons, they get clogged up with fats (beginning with myelin) and become overwhelmed, which in turn, makes the inflammation worse.

"These cells are probably trying to do something good: clearing up damage," says van der Vliet.

"But they become overloaded, so to speak. As a result, they can no longer effectively contribute to repair."

The researchers also used a mouse model of MS, blocking one of the enzymes most active in foamy microglia. Tissue healing improved in these mice, further emphasizing the connection between these immune cells and worse MS progression.

We're still in the early stages of this research, and clinical trials with MS patients will be needed to see if the foamy microglia link holds up.

Researchers will also need to look at how these lesions that aren't repaired continue to develop over time.

However, these are promising findings in terms of figuring out why some people with MS live relatively normal lives for decades, while others become paralyzed sooner or develop more severe symptoms at a young age.

The study team is hopeful that the findings could help develop new MS treatments that target fat metabolism in cells.

There's also the potential, along with other lines of research, to identify more severe cases of MS at an earlier stage.

The researchers found signs of fats associated with foamy microglia floating around in cerebrospinal fluid, which they say could be measured as a marker of the disease.

Related: Scientists Identify Specific Bacteria Linked to Multiple Sclerosis

"That opens the possibility of developing biomarkers in the future that could help doctors identify earlier which patients are at risk of rapid decline – and which treatment would suit them best," says van der Vliet.

The research has been published in Nature Neuroscience.

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