Nat Geo photographer Babak Tafreshi (BabakTafreshi) and NASA astronaut Don Pettit (astro Pettit) are photographing the same places from radically different POVs—the ground and the International Space Station—creating a new way of seeing the world: on.natgeo.com/4pFm8zQ

The research published in Nature Plants by a global team of tropical forest scientists shows that the average size of trees in Amazon forests has increased over recent decades. The team of almost a hundred researchers monitored the size of trees in 188 permanent plots and discovered that the increase has continued for at least 30 years.

The study is the result of an international partnership of more than 60 universities in South America, the UK and beyond—including the Universities of Birmingham, Bristol, and Leeds.

Co-author of the study, Professor Beatriz Marimon, from Universidade do Mato Grosso, who coordinated much of the Brazilian data collection in southern Amazonia, commented, "This is a good news story. We regularly hear how climate change and fragmentation is threatening Amazonian forests. But meanwhile, the trees in intact forests have grown bigger; even the largest trees have continued to thrive despite these threats."

The study found that both large and smaller trees have increased in size, consistent with benefiting from fertilization by increased atmospheric carbon dioxide.

Microplastics are now so ubiquitous we're drinking, eating, and inhaling them. As a result, they're showing up in our poop, placentas, reproductive organs, and brains.

Now these fossil-fuel-derived particles, less than 5 mm in size, have been found deep within our bones.

A new review of 62 studies suggests microplastics and smaller nanoplastics are impacting our skeletal health in multiple ways.

"A significant body of research suggests that microplastics can reach deep into bone tissue, such as bone marrow, and potentially cause disturbances in its metabolism," says medical scientist Rodrigo Bueno de Oliveira at the State University of Campinas in Brazil.

Some of the studies in humans found these plastic leftovers accumulating in bone tissues via the blood, following ingestion. There, animal studies show they can reduce bone growth.

What's more, disruptions in osteoclasts – cells that support bone growth and repair – can lead to weakened bone structures, making these compromised bones more susceptible to deformities and fractures.

"In vitro studies with bone tissue cells have shown that microplastics impair cell viability, accelerate cell aging, and alter cell differentiation, in addition to promoting inflammation," explains Bueno de Oliveira.

"The adverse effects observed culminated, worryingly, in the interruption of the animals' skeletal growth."

Are we alone in the universe? Help us figure that out!

Join this citizen science effort and help UCLA SETI to train AI tools to separate Earth-based interference from possible technosignatures across the Milky Way. Learn more: zooniverse.org/projects/ucla-…

Advances in AI technology have ushered in a new era of digital romance, where people are forming intimate emotional connections with chatbots. For many, these AI companions are a crucial lifeline, helping to combat feelings of loneliness. Yet, despite a rapidly evolving social trend that has attracted widespread interest, it has been largely understudied by researchers.

A new analysis of the popular Reddit community, r/MyBoyfriendIsAI, is addressing the gap by providing the first in-depth insights into how intimate human–AI relationships begin, evolve and affect users.

Researchers from the Massachusetts Institute of Technology (MIT) studied 1,506 of the most popular posts from this Reddit community, which has more than 27,000 members. First, they used AI tools to read all the conversations and sorted them into six main themes, such as coping with loss. Then they used custom-built AI classifiers to review the posts again and measure specific details within them.

This allowed the MIT team to put numbers on the experiences and count exactly how many users reported key outcomes (reduced loneliness, risk of emotional dependency) to show the overall impact of these digital relationships.

Benefits and risks
In their paper posted on the preprint server arXiv, the researchers reveal that these intimate relationships often start by accident. Most users did not join a chatbot app in search of love. Instead, it grew unintentionally out of simply using the technology for practical reasons. A little more than one-quarter of users (25.4%) reported clear benefits, including reduced loneliness and improvements in their mental health. Meanwhile, only 3% felt that their AI relationship had caused them more harm than good.

The study also identified some risks. Almost 10% of users reported being emotionally dependent on their digital partner, and 4.6% struggled to distinguish between AI and real life. Some users also treat their chatbot companions as significant others by engaging in real-world rituals, such as purchasing wedding rings. Avoidance of real relationships was a concern for 4.3% of users.

Ultimately, the researchers hope that their work will lead to a change in how society views these new relationships. As they write in their paper:

"Our findings demand nuanced, nonjudgmental frameworks that move beyond assumptions that benefits and harms of human-AI interaction depend primarily on the technology alone, protecting vulnerable users while respecting their autonomy to form meaningful connections in ways that align with their individual needs and circumstances."

The MIT team argues that protecting vulnerable users and respecting their right to find meaning must be the guiding principles for the next era of digital relationships.

Until recently, it was thought that Homo sapiens and Neanderthals split off from their last common ancestor around 600,000 years ago, but a prehistoric skull from China has just shattered that narrative. Dated to a million years ago, the cranium belongs to an extinct human clade which encompasses the Denisovans, indicating that we had already branched off from our sister lineage prior to this point.

Discovered in Hubei Province in 1990, the so-called Yunxian 2 skull has been at the center of a taxonomic confusion for the past 35 years, largely because the specimen is badly crushed and therefore difficult to study. Due to its age and the shape of its braincase, though, some scholars had assumed that the cranium belonged to Homo erectus.

However, using CT scanning and digital reconstruction techniques, the authors of a new study have managed to correct the skull’s distortions and build a complete model of the specimen. In doing so, they revealed that Yunxian 2 possesses a mosaic of features, some of which are typical of more primitive hominins like H. erectus while others are more aligned with Homo sapiens.

Cross-referencing more than 500 of these morphological traits against 104 other human fossils, the researchers determined that Yunxian 2 belongs to the Homo longi clade, which includes a 145,000-year-old skull that was recently identified as a Denisovan. However, Yunxian 2 itself is not a Denisovan, but probably sits near the base of the lineage that gave rise to this enigmatic species. 

What’s more, while Denisovans and Neanderthals were previously thought to be sister lineages, the team’s analysis indicates that the Homo longi clade is in fact the sister group to the Homo sapiens clade.

“We really have to say we don't know where the common ancestor lived.”
— Professor Chris Stringer

“Because [Yunxian 2] is about a million years old, by definition, the Homo longi clade must be about a million years old at minimum,” said study author Professor Chris Stringer to IFLScience. “And that, in turn, implies that if sapiens and Neanderthals had already branched off, then their groups must be equally or even older in their origin.”

In other words, the Homo sapiens group must have emerged more than a million years ago, which is around 400,000 years earlier than certain genomic models suggest. Overall, the researchers estimate that our clade originated about 1.02 million years ago, while the Homo longi group dates back to 1.2 million years ago.

Ketogenic diets, usually shortened to keto, are promoted as a way of losing weight and improving your general health, but the long-term impacts of following such a diet are still being unraveled. A new study throws some concerning findings into the mix, suggesting that while the diet may be effective for weight loss, it could lead to complications like fatty liver disease. 

Keto diets are designed to get the body into a state of ketosis, where fat stores are used as an energy source rather than carbohydrates. To achieve this, these diet plans recommend strict limits on carbohydrate-rich foods, things like starchy vegetables, grains, and sugars. Instead, there’s a focus on protein- and fat-rich foods like meat, fish, unsweetened dairy, nuts, and seeds. 

For some people, a keto diet is an essential part of medical treatment for a chronic illness. For example, ketogenic diet therapy can help children with drug-resistant epilepsy experience fewer seizures. But as the British Dietetic Association points out, following such a strict diet plan comes with its own risks and should be closely monitored. So, what about people without a medical indication who simply choose to follow this diet for themselves?

Lots of people claim the diet has helped them lose weight and feel better, but the internet also abounds with anecdotes from people who claim it ruined their health. The “long-term effects [of ketogenic diets] on metabolic health remain understudied,” write the authors of a new study.

Shortly before his death in August 2025, A. James Hudspeth and his colleagues at The Rockefeller University’s Laboratory of Sensory Neuroscience accomplished a milestone that had never been reached before. They succeeded in keeping a small section of the cochlea alive and working outside the body, making it possible to study the organ’s function directly for the first time. Using a specially designed device, the team was able to track the cochlea’s extraordinary abilities in real time, including its fine-tuned sensitivity, precise frequency detection, and capacity to process a wide range of sound levels.

“We can now observe the first steps of the hearing process in a controlled way that was previously impossible,” says co-first author Francesco Gianoli, a postdoctoral fellow in the Hudspeth lab.

The achievement, detailed in two recent publications (in PNAS and Hearing Research, respectively), represents the culmination of Hudspeth’s fifty years of pioneering research into the cellular and neural basis of hearing. His work has continually pointed toward new possibilities for preventing and treating hearing loss.

Beyond its immediate applications, the advance also delivers long-sought experimental confirmation of a fundamental biophysical principle that underlies hearing across diverse species, a concept Hudspeth had pursued for more than twenty-five years.

“This study is a masterpiece,” says biophysicist Marcelo Magnasco, head of the Laboratory of Integrative Neuroscience at Rockefeller, who collaborated with Hudspeth on some of his seminal findings. “In the field of biophysics, it’s one of the most impressive experiments of the last five years.”

The mechanics of hearing
Though the cochlea is a marvel of evolutionary engineering, some of its fundamental mechanisms have long remained hidden. The organ’s fragility and inaccessibility—embedded as it is in the densest bone in the body—have made it difficult to study in action.

These challenges have long frustrated hearing researchers, because most hearing loss results from damage to sensory receptors called hair cells that line the cochlea. The organ has some 16,000 of these hair cells, so-called because each one is topped by a few hundred fine “feelers,” or stereocilia, that early microscopists likened to hair. Each bundle is a tuned machine that amplifies and converts sound vibrations into electrical responses that the brain can then interpret.

Sitting in the audience at a stand-up show; watching a comedy at the movies; at the office party when your boss breaks out their best knock-knock joke: these are all places where laughter is both encouraged and expected. During a quiet moment in church? Not so much. But wherever you are, if you hear someone else laughing, it’s likely you’ll get the urge to giggle too – however inappropriate that may be! Should we all just be able to control ourselves better, or is laughter really contagious?
The answer, in short, is yes.

“All emotions are contagious”
“Is laughter contagious? Well, actually, all emotions are contagious,” Dr Sandi Mann, chartered member of the British Psychological Society, told IFLScience. “We are designed to pick up other people’s emotions.”

It’s part of our evolution, and it’s something we share with other mammals. It’s been well established that apes – our closest relatives – laugh in a remarkably humanlike way. If you’re ever close enough to a bonobo to try tickling it (not something we’d necessarily recommend), you’ll find out.

Recent research even found that apes may have a sense of humor and love to tease each other. A 2021 review concluded that 65 different animal species show evidence of “play vocalizations” that mimic humans laughing when we’re having fun, mostly mammals but a few birds as well. 

In fact, laughter is such a fundamental part of what it means to be human that it transcends language and culture – there’s not a single community of people on Earth that we know of who don’t laugh. 

Why laughter is good for us
Part of the reason why a fit of the giggles spreads so easily, Dr Mann told us, is that shared emotions are integral to social bonding. A 2022 paper from University of Oxford Emeritus Professor of Evolutionary Psychology Robin Dunbar explored this further. 

“I suggest that, when hominins needed to increase the size of their groups beyond the limit that could be bonded by grooming, they co-opted laughter […] as a form of chorusing to fill the gap,” Dunbar wrote. 

Grooming – a social behavior we particularly associate with monkeys and apes, but which is seen throughout the animal world – boosts the production of endorphins in the brain. These chemical messengers relieve pain and generally make us feel good. Dunbar detailed some evidence that laughter has a similar effect, with the added benefit of being less intimate and time-consuming than grooming. Hence, humans laugh together all the time, but we’re rarely seen picking lice out of each other’s hair these days. 

A hit of endorphins also helps us de-stress. When a group of people are sharing a tense situation, Dr Mann told IFLScience, humor can help to alleviate that as well as strengthen the bond between them: “Sometimes we just need to smile, laugh, have fun to relieve the stress.”

What drives a person to keep drinking alcohol despite the harm it causes to their health, relationships, and overall well-being? New research from Scripps Research points to a possible answer: a small midline brain region helps shape how animals learn to drink in order to relieve the stress and discomfort of withdrawal.

In a study recently published in Biological Psychiatry: Global Open Science, the Scripps Research team examined brain activity in the paraventricular nucleus of the thalamus (PVT) in rats. They discovered that when rats linked environmental cues with alcohol’s ability to ease withdrawal symptoms, activity in this brain region increased, reinforcing relapse behaviors.

By uncovering this pathway, the study highlights one of addiction’s most persistent aspects—using alcohol not for enjoyment but to avoid suffering—and may pave the way for new therapies for substance use disorders (SUDs) and related conditions such as anxiety.

“What makes addiction so hard to break is that people aren’t simply chasing a high,” says Friedbert Weiss, professor of neuroscience at Scripps Research and senior author of the study. “They’re also trying to get rid of powerful negative states, like the stress and anxiety of withdrawal. This work shows us which brain systems are responsible for locking in that kind of learning, and why it can make relapse so persistent.”

“This brain region just lit up in every rat that had gone through withdrawal-related learning,” says co-senior author Hermina Nedelescu of Scripps Research. “It shows us which circuits are recruited when the brain links alcohol with relief from stress—and that could be a game-changer in how we think about relapse.”

Most people know sloths as slow-moving, bear-like creatures that dangle from trees, take nearly a month to digest a single meal, and defecate only once a week. Their closest relatives are anteaters and armadillos, which may sound like an unusual connection, but evolutionary history explains the link. Today only two sloth species exist, but in the past there were dozens, including one with a bottle-shaped snout specialized for eating ants and another that closely resembled early armadillos.

Many of these ancient sloths were far too large to live in trees. The giants of the group, belonging to the genus Megatherium, grew to the size of Asian bull elephants and weighed around 8,000 pounds [~3629kg].

“They looked like grizzly bears but five times larger,” said Rachel Narducci, collection manager of vertebrate paleontology at the Florida Museum of Natural History.

Narducci co-authored a study published in Science in which researchers examined ancient DNA and analyzed more than 400 fossils from 17 natural history museums to understand how and why some sloths reached such massive proportions.

Ground-dwelling sloths displayed an extraordinary range of body sizes. At one extreme was the enormous Megatherium, capable of stripping leaves from tall trees with its long, flexible tongue, serving as an ecological counterpart to giraffes. At the other was the comparatively smaller Shasta ground sloth, which thrived in the deserts of North America by feeding on cacti.

Tree-dwelling sloths, however, followed a different evolutionary path. Those that lived exclusively in the forest canopy have always been small, averaging about 14 pounds [~6.35kg]. Species that split their time between the ground and the trees were somewhat larger, weighing an average of 174 pounds [~79kg].

You don’t have to be a scientist to puzzle out why trees enforce a strict weight limit. It’s the same reason why modern tree sloths have a strange elastic quality to them: Branches break when put under too much strain, and sloths are not generally known for their ability to swiftly avert sudden disaster. Tree sloths have reportedly survived falls of up to 100 feet [~30m]. However, given that falls from even moderate heights can cause severe damage and some trees in the Amazon Rainforest top out at just under 300 feet [~91m], it makes evolutionary sense to be as small as possible when going out on a limb.

Why Did Ground Sloths Get So Big?
What’s less clear is why some ground sloths grew to such excessive sizes while others seemed content with being merely large. There may have been several reasons, which is why it’s been so hard for scientists to answer the question with confidence.

Larger sizes might have been advantageous for finding food or avoiding predators, for example. Ground sloths had a special fondness for caves, and their size undoubtedly played a role in their ability to find and make shelters. The moderately sized Shasta ground sloth favored small, natural caves bored by wind and water into the cliffsides of the Grand Canyon, like the alveoli of a gigantic, geologic lung. These also doubled as convenient latrines; in 1936, paleontologists discovered a mound of fossilized sloth poop, bat guano, and packrat middens more than 20 feet [~6m] thick in Rampart Cave, near Lake Mead.
Scientists analyzed ancient DNA and compared more than 400 fossils from 17 natural history museums to figure out how and why extinct sloths got so big.

Larger sloths weren’t restricted to pre-existing caves. Using claws that are among the largest of any known mammal, living or extinct, they could carve their own from bare earth and rock. Many of the caves they left behind are still around with claw-mark décor along the interior walls, evidence of their ancient nesting excavations.

This rare case of convergent evolution shows nature arriving at the same mind-altering molecule by two separate paths. The true reason fungi produce psilocybin remains unsolved, but theories range from predator defense to chemical communication. Beyond evolutionary intrigue, the discovery also offers new enzyme tools that could help produce psilocybin more efficiently for future medicines.

Ancient Molecule With a Modern Role
“This concerns the biosynthesis of a molecule that has a very long history with humans,” explains Prof. Dirk Hoffmeister, head of the research group Pharmaceutical Microbiology at Friedrich Schiller University Jena and the Leibniz Institute for Natural Product Research and Infection Biology (Leibniz-HKI).

“We are referring to psilocybin, a substance found in so-called ‘magic mushrooms’, which our body converts into psilocin – a compound that can profoundly alter consciousness. However, psilocybin not only triggers psychedelic experiences, but is also considered a promising active compound in the treatment of therapy-resistant depression,” says Hoffmeister.

Two Evolutionary Paths to Psilocybin
The study, carried out within the Cluster of Excellence ‘Balance of the Microverse’, reveals that fungi developed the ability to produce psilocybin on at least two separate occasions in evolutionary history. Psilocybe mushrooms rely on a familiar set of enzymes to make the molecule, while fiber cap mushrooms use an entirely different biochemical toolkit. Despite these very different methods, both groups arrive at the same compound. Scientists call this convergent evolution, when unrelated species independently evolve the same trait.