For nearly half of all pregnant women worldwide, anemia is a daily reality. The condition, in which the body lacks enough healthy red blood cells to carry oxygen, is especially widespread in Indonesia, where nearly half of pregnant women and close to a third of teenage girls are affected, according to national health data cited in the research.
Severe anemia during pregnancy can nearly double a woman’s risk of dying during or after childbirth. An analysis of 17 studies now suggests that guava juice, used alongside standard iron therapy, could be a practical tool in addressing this persistent health problem.
Guava is a tropical fruit grown across Asia, Latin America, and other warm-weather regions. It is packed with vitamin C, which helps the body absorb iron more effectively by converting it into a form the gut can take in. The fruit also contains folic acid and other nutrients that support red blood cell production.
Researchers set out to determine whether drinking guava juice could measurably raise hemoglobin levels among Indonesian women, typically when taken alongside iron supplements. Published in BMJ Nutrition, Prevention & Health, the results suggest the answer is yes.
17 Studies, 726 Women, All From Indonesia
Researchers searched several medical databases for studies on guava juice and hemoglobin in Indonesian females and identified 17 that met their criteria, all conducted in Indonesia and published between 2019 and 2024. Altogether, those studies included 726 female participants, split between pregnant women and adolescent girls. Fifteen of the 17 used study designs that fell short of the gold standard, with only two qualifying as full randomized controlled trials. Twelve studies provided enough data to be combined into a formal statistical analysis.
Individual study sizes ranged from 15 to 230 participants, and most studies took place in urban settings. In the majority of cases, participants received guava juice in combination with iron supplements rather than guava juice on its own.
Guava Juice Plus Iron Outperformed Iron Supplements Alone
Pooling data from those 12 studies, representing 265 participants, researchers found that women who consumed guava juice showed an average hemoglobin increase of 1.71 grams per deciliter of blood. The team called this clinically meaningful, writing that an increase of this size “may shift individuals from mild or moderate anaemia to non-anaemic categories, improving fatigue, cognitive function and productivity outcomes.”
Breaking the data down by group, teenage girls saw an average hemoglobin increase of 1.52 g/dL, while pregnant women saw a larger average increase of 1.84 g/dL. That said, the size of the benefit varied widely from study to study, so the exact effect remains uncertain.
A separate look at five studies, involving 102 participants, compared guava juice plus iron supplements against iron supplements alone. Those receiving guava juice alongside iron came out ahead by an average of 1.29 g/dL, a difference the researchers described as statistically significant. Juice amounts across all studies ranged from 100 to 300 milliliters per day and intervention lengths varied, which partly explains why results were not uniform.
All Studies Came From Indonesia, and Most Lacked Rigorous Design
Every study included came from Indonesia, which means the findings may not automatically apply to women elsewhere with different diets, health conditions, or access to care. Heavy reliance on non-randomized study designs makes it harder to establish that guava juice itself caused the improvements. Several studies did not report how long the intervention lasted or exactly how much juice was consumed, making it difficult to pin down an ideal dose or duration. Larger, more rigorous research across multiple countries is needed before guava juice can be written into public health guidelines.
Still, the findings point toward something worth taking seriously. Anemia is deeply entrenched in many lower-income countries, and access to iron supplements is often limited by chronic supply problems and the reality that people do not always take the pills as directed. Guava juice is affordable across many tropical regions, widely familiar, and already woven into the food culture of many affected communities.
Scientists Destroyed a Few Dozen Neurons in a Fish and Watched Its Social Life Fall Apart
Researchers have captured the brain activity of a fish in the moments before it swims toward a companion, and the brain starts preparing that move several seconds before the fish does anything visible.
Published in Nature Communications, the study shows this is not a split-second reaction but a coordinated process playing out across multiple brain regions. Crucially, those patterns were specific to social situations. When researchers swapped the real companion for a moving dot, the predictive brain signature did not appear.
Scientists at the Hebrew University of Jerusalem pulled this off using zebrafish, tiny, nearly transparent fish whose brains can be imaged right through their skin. One fish was gently held in place with its tail free to move, while a companion swam freely nearby behind a clear barrier, close enough to see but unable to touch. A specialized microscope tracked more than 12,000 individual brain cells at once across 44 pairs of fish, with each session running 30 minutes. By reading those brain signals alone, researchers could tell whether a fish was about to approach its companion before any movement occurred, a predictive window rarely achieved in any animal.
What the Brain Does Before the Body Moves
Across those recordings, certain neurons in the midbrain and hindbrain became quieter several seconds before the fish moved toward its companion. At the same time, a small group of cells in a region called the pallium, part of the forebrain, became more active. When the fish was about to make a non-social movement instead, the pattern flipped.
A computer decoding those brain signals in any of the three regions could identify the upcoming social move with accuracy well above chance. Fish that moved in closer sync with their companions were also more likely to be heading toward them, and showed higher overall rates of social approach.
How early the brain signal appeared depended on what the companion was doing. When the companion had been swimming steadily in one direction for a while, the focal fish’s brain pattern shifted up to 10 seconds before any movement. When the companion had only just changed direction, the signal came much later. In other words, the fish’s brain wasn’t just tracking where its companion was. It was tracking how long it had been moving that way, and adjusting accordingly.
Variability between individual fish also showed up in their brain activity. Fish with more distinct neural patterns before approach movements had higher rates of actually approaching their companions, suggesting the clarity of the brain signal and the likelihood of social behavior are linked at the individual level. About 35 percent of fish in the study showed low approach rates, consistent with individual differences in social behavior observed in freely swimming zebrafish of the same age.
Removing Key Brain Cells Changes the Whole Network
To test whether the pallial cells were truly necessary for social behavior and not just correlated with it, the team used a laser to precisely destroy a small number of those cells, averaging around 46 neurons per fish, in nine fish. Movement ability and vision remained intact afterward, and neighboring cells were unaffected. Before the ablation, most fish preferred spending time near their companions. Afterward, social preference dropped significantly. A control group that underwent a sham procedure targeting a different, uninvolved brain region showed no change in social behavior whatsoever, ruling out the laser treatment itself as the cause.
After researchers re-imaged the brains of the treated fish during social interaction, the predictive brain signal had disappeared, not just in the pallium, but also in the midbrain and hindbrain. Removing a small cluster of cells in one region had dismantled the coordinated activity pattern across the entire network. Those pallial neurons weren’t just part of the system. They were necessary for it to work.
The rise of remote work since the pandemic has made businesses more reluctant to hire young, inexperienced workers and is the key driver of higher unemployment rates for recent college graduates, a study released Monday has found.
The study, by the Federal Reserve Bank of New York, compared occupations that can be done remotely — such as software development — with those that are done in person, such as nursing. The study finds that the unemployment rate among young college graduates in “remotable” jobs rose by about 1 percentage point from 2017-2019 to 2022-2024.
Yet for older workers in those fields — those aged 29 and over — the jobless rate declined slightly, leading to a notably higher unemployment rate for younger college graduates in remotable occupations compared with older workers.
Yet in non-remotable jobs, there has been little gap in the unemployment rates between older and younger college grads, the study finds. A similar pattern exists for those without college degrees, the New York Fed said.
The study, led by New York Fed research economist Natalia Emanuel, concludes that businesses are reluctant to hire new college grads into remote work because it is harder to train and mentor them if they work outside of the office. The authors of the study calculate that remote work is responsible for nearly two-thirds of the rise in the unemployment rate for young college graduates since the pandemic.
“Remote work has weakened incentives to hire young workers by impeding on-the-job training,” the study said. “Employers may not want to hire fresh graduates onto distributed teams because it is more difficult to teach them the requisite skills from afar.”
The study lands amid widespread concern over the employment prospects of college graduates as artificial intelligence makes inroads into a variety of white-collar jobs, including finance, law, entertainment, and media. This spring, college graduates have been booing references to AI during commencement speeches.
But the study notes that the worsening employment picture for young college grads pre-dates the development of artificial intelligence tools such as ChatGPT. And when the authors looked at the exposure different occupations had to AI, it found that AI had little impact on youth unemployment.
The unemployment rate for college grads under 29 rose 20% from before the pandemic to 3.7%, on average, in 2022-2025, the New York Fed said. For college grads aged 22 through 27, unemployment reached 5.8% last year, the highest outside the pandemic since 2012.
The study’s findings are consistent with the low-hire, low-fire state of the job market, where layoffs are low and the unemployment rate is mostly stable, but those out of work are struggling to find new jobs.
Women Over 50 With Low Protein Intake Face Dramatically Higher Odds of Losing Basic Physical Independence
Getting dressed, walking to the kitchen, or simply using the bathroom. These are everyday moments most people take for granted. But for millions of older adults across Europe, those tasks are becoming increasingly difficult. A large study tracking more than 38,000 adults across 27 countries has found that eating fewer protein-rich foods may be one warning sign linked to later physical difficulties, and the odds look different depending on age and gender.
Published in the journal Nutrients, the research drew on data from the Survey of Health, Ageing and Retirement in Europe and found that older adults who reported the lowest protein intake were more likely to develop muscle weakness and physical difficulties over time. Women between the ages of 50 and 65 in that lowest group had more than double the odds of difficulty using the toilet compared to women who ate more protein-rich foods.
Men with low protein intake were more likely to show weak grip strength, a well-established early warning sign of physical decline, while women were more likely to struggle with walking, bending, reaching overhead, and grocery shopping.
Low Protein Intake and Physical Decline: A 38,000-Person Dataset
Researchers analyzed data from 38,073 adults aged 50 and older across 27 European countries. Participants were first surveyed in 2019 and 2020, then followed up in 2021 and 2022, letting researchers track whether eating habits at baseline corresponded with physical difficulties that emerged over the following two years.
Rather than tracking exact grams of food, the study asked participants how often in a typical week they ate from three food groups: dairy products like milk, cheese, or yogurt; legumes and eggs; and meat, fish, or poultry. Researchers combined those answers into a single score, and those who fell in the bottom 10% were classified as having low protein intake.
Grip strength (how hard someone can squeeze with their hand) was tested using a handheld device, with scores below specific thresholds flagging potential muscle weakness. Participants were also asked whether they had lasting difficulty with activities from walking 100 meters and climbing stairs to bathing, using the toilet, and shopping for groceries.
Low protein intake was more common among people who were not physically active, those with higher depression levels, and those who had low grip strength at follow-up. People with higher education levels were somewhat more likely to eat protein-rich foods regularly, pointing to the role of nutritional knowledge and economic access.
Men and Women Face Different Odds With Low Protein Intake
Results broke down differently by age and gender, and in some cases, the gaps were wide.
For grip strength, men were most affected. Men aged 50 to 65 with low protein intake had about 39% higher odds of weak grip strength compared to men who ate more protein. Men 66 and older showed about 35% higher odds. For women 66 and older, the increased odds were about 21%. Younger women showed no clear connection to grip strength in the data.
Walking 100 meters showed higher odds of difficulty across all four groups. For tasks like bending, kneeling, and reaching overhead, women were more likely to show difficulty, while men were not. Tasks involving raw strength, like pushing or pulling heavy furniture, were more affected in men.
Among women aged 50 to 65, those in the lowest protein intake group had more than double the odds of reporting difficulty using the toilet, the standout finding of the study. Women in that same age group also had about 65% higher odds of difficulty shopping for groceries. Older women were more concentrated at the lower end of the protein scale, and the study authors note that older European women tend to eat smaller meals and fewer protein-rich foods than men.
Why Protein Matters More as Bodies Age
Protein is what the body uses to maintain and repair muscle. As people grow older, muscles become less efficient at using the protein they consume, meaning older adults generally need more protein, not less, to hold on to their strength and mobility. Many older people eat less than recommended due to reduced appetite, dental problems, lower income, or other health conditions.
Board-Certified Physicians Put Popular LLMs Through Their Paces, and Found Real Problems
When people feel a strange pain or notice a worrying symptom, more and more of them are skipping the doctor’s office and heading straight to an AI chatbot. It’s fast, free, and available at 3 a.m. But a study suggests that convenience might come with a serious catch: even the best-performing AI gets medical questions wrong roughly one out of every five times.
In a preprint study (not yet peer-reviewed) posted online by researchers from Penn State, four popular AI chatbots were put to the test using real and imagined health concerns submitted by university students, staff, and faculty. A panel of nine board-certified physicians then graded the AI responses. Overall results were mixed: impressive enough to turn heads, but flawed enough to raise real concerns about what happens when someone acts on bad medical advice.
Nearly one in four adults under 30 already use AI monthly for health-related guidance, according to data cited in the paper. Understanding what these tools get right (and wrong) is essential.
How Researchers Tested AI Chatbots on Health Questions
Researchers organized a university-wide competition in fall 2024. A total of 34 participants were invited to query one of four AI chatbots — ChatGPT-4o, ChatGPT-3.5, Gemini-1.5 Pro, and Llama3-8b — with health-related questions they might genuinely want answered. Participants could approach the task from one of three angles: as a patient describing personal symptoms, as a medical professional seeking diagnostic help, or through an out-of-the-box track that allowed for alternative medical query scenarios, such as analyzing images of handwritten prescriptions.
Competition entries generated 212 AI responses in total. Those responses were then divided among a panel of nine board-certified physicians, each of whom graded them on four measures: how valid the information was, the quality of the information, how well the AI reasoned through the problem, and whether the response could cause harm.
Gemini-1.5 Pro produced the largest share of responses, 140 out of 212, while Llama3-8b generated only 6. That imbalance matters when comparing models directly, and the researchers acknowledged it as a limitation.
What Doctors Found When They Graded the AI Responses
Across all four AI models, about 76% of responses were rated as valid by physicians. That sounds reasonable until the math flips: nearly one in four responses didn’t make the cut. For ChatGPT-4o, the highest-performing model, validity hit 84.6%, still leaving more than 15% of answers falling short. Llama3-8b landed at the bottom, with only half its responses rated as valid.
Which type of medical question was asked also mattered. Questions about obstetrics and gynecology scored the highest for accuracy, while neurology, internal medicine, and dermatology consistently ranked lower. Neurology cases in the study often involved rare conditions that are hard to diagnose under any circumstances, while dermatology relies heavily on visual examination — something a text-based chatbot simply cannot replicate.
Prompt length turned out to be a factor, too. Very short questions and very long, detailed ones both produced weaker results. Best performance came from medium-length queries, somewhere between 60 and 250 characters. Medical professionals said in follow-up interviews that the more specific and focused the question, the better the AI tended to perform.
Adding a Medical Encyclopedia Didn’t Always Help AI Chatbots
One of the study’s more surprising results involved a technique called Retrieval-Augmented Generation, or RAG, essentially giving the AI access to a curated library of medical textbooks, clinical guidelines, and research articles from a university medical school before it generates a response. Grounding the AI in vetted medical sources should, in theory, make its answers more reliable.
Seven medical professionals were recruited to compare standard AI responses against RAG-enhanced ones, side by side. For Gemini-1.5 Pro and Llama3-8b, the medical professionals actually preferred the standard, unenhanced versions by a wide and statistically significant margin. For the ChatGPT models, there was no significant difference either way.
Researchers stopped short of declaring RAG unhelpful overall, noting that the results varied by model and that future research should explore the approach further.
A new national survey found that nearly half of American adults (48%) feel their lives are seriously lacking in fun right now. Even more jarring, 12% say they can’t even remember the last time they had a full free day to enjoy themselves. It is not a trivial complaint. Researchers found that people who do manage to carve out regular fun report feeling less stressed, more motivated, and closer to the people they love. For the growing share of adults who can’t seem to get there, that gap has real costs.
On paper, fun sounds simple. In practice, it keeps losing to everything else on the calendar.
Why Americans Are Not Having Enough Fun
Talker Research surveyed 5,000 U.S. adults (100 per state) on behalf of Dave & Buster’s between April 21 and May 1, 2026. Participants were asked about how often they had fun, what they liked to do, what got in the way, and what might help them prioritize it more. All respondents were internet-accessible adults, surveyed online.
When asked what kinds of activities count as fun, the answers were decidedly low-key. Watching TV topped the list at 77%, followed by spending time with family or friends (69%), dining out (59%), outdoor activities (50%), personal hobbies (49%), and playing games (48%). A third of respondents (37%) said they regularly think of something fun to do, only to scale it back or cancel when something more pressing comes up. Another 33% said adult responsibilities frequently force them to scrap fun plans altogether.
The average American who says they are not getting enough fun estimates they would need about 17 extra hours per week to fix that.
The Biggest Obstacles to Having Fun as an Adult
Money and time are doing most of the damage. Among those who said it is harder to have fun than it was a decade ago (52% of respondents) the top explanations were straightforward: 51% said they can no longer afford the same activities, 45% said their social circle has shrunk, and 42% pointed to having more responsibilities than before.
Cost and budget pressures were the most commonly cited barrier to fun overall, flagged by 57% of respondents. After that came personal schedule conflicts (34%), work obligations (31%), friends and family not having time (29%), general burnout (22%), and not knowing what to do (16%).
When asked what would help them prioritize fun more, the answers pointed in a clear direction. More than half (55%) said low-cost options would make the biggest difference. Beyond price, respondents said more free time (41%), more exciting options to choose from (32%), better coordination with friends (29%), feeling like an activity was worth the investment (29%), and less stress at work (22%) would all help.
Fun Reduces Stress and Strengthens Relationships, Survey Finds
When fun does happen, people notice the difference. Nearly three-quarters of respondents (72%) said having fun helps them feel less stressed. More than half reported it made them feel more motivated (57%) and closer to the people in their lives (56%). And 89% said having fun with others helps them build and maintain stronger relationships.
“We’ve always believed that fun is one of the most powerful ways people connect,” said Melissa Powers, vice president of marketing at Dave & Buster’s. “Our State of Fun report makes it clear that people are craving more shared, in-person experiences & fun in their lives, but factors like cost, busy schedules and a lack of fresh entertainment options often get in the way.”
Powers also noted a broader pattern in how people are using their leisure time: “As life becomes increasingly busy and digitally driven, people are looking for places where they can connect in real life, share experiences and simply enjoy being together.”
Not everyone agreed that fun has gotten harder to come by. A smaller share (28%) said finding something fun to do is actually easier than it was 10 years ago. Among that group, the most common reasons were having fewer responsibilities (40%), having adult money (36%), being around people who enjoy having fun (34%), and having a better work-life balance (30%).
For most people, cheese is a guilty pleasure: something delicious but probably not great for you. That assumption may be worth revisiting. A recent study took a close look at three traditional British artisan cheeses and tracked how their bacterial communities and chemical profiles shifted from production to the moment they hit the dinner table. What researchers found raises real questions about what’s happening inside aging cheese and what that means for the trillions of microbes living in your gut.
Cheese has long been dismissed as a health-food nonstarter because of its fat and salt content. But scientists have been building a case for years that certain cheeses may actually reduce the risk of heart disease, strengthen bones, and even lower the odds of early death. No one has fully explained why. This new study, led by researchers at the University of Reading in the UK, takes a step toward answering that question by mapping exactly which bacteria are present in these cheeses and which chemical compounds they produce as the cheeses ripen.
Researchers studied three artisan cheeses made at Nettlebed Creamery in Henley, UK: a soft, white-rind cheese called Bix, a semisoft orange-rind cheese called Highmoor, and a firmer cheese called Witheridge that ages wrapped in hay. Each style represents a distinct cheesemaking tradition, and by the time the study was done, the differences between them were significant. The resultes are published in ACS Food Science & Technology.
How Researchers Tracked Bacterial Life Inside Artisan Cheese
To track changes in the cheeses, researchers collected samples at different stages of maturation and used two main tools. One was a DNA analysis technique that reads the genetic signatures of bacteria present in a sample, or essentially a census of microbial life inside each cheese. The other was a method that identifies and measures chemical compounds by exposing a sample to a powerful magnetic field. Together, these tools gave the team a detailed picture of both who was living in the cheese and what those microbes were producing.
Highmoor and Witheridge were sampled at a young stage, at a midpoint in maturation, and again when fully mature. Bix, which matures in just over a week, had only two sample points: young and mature. A fourth sample was also included: a version of Witheridge made with unpasteurized, or “raw,” milk, which allowed for a direct comparison with the standard pasteurized version.
What the Bacteria Revealed
Each cheese told a different story. Bix, the soft white-rind variety, had the shortest aging period — just nine days before packaging — and its bacterial population was dominated throughout by a species called Lactococcus lactis, recognized for its potential probiotic properties. Because Bix is also ripened using yeasts and molds that weren’t captured by the analysis method used in this study, the researchers noted that the cheese may actually have more microbial complexity than the data shows.
Highmoor, the orange-rind variety, showed a sharp jump in bacterial diversity between its young and midpoint samples, likely driven by the growth of rind bacteria during the washing process. In this technique, the cheese’s surface is repeatedly treated with a saltwater solution to encourage specific microbes responsible for its characteristic pinkish-orange color, pungent smell, and sticky texture. One bacterium found in Highmoor, Propionibacterium freudenreichii, is deliberately added to give the cheese its nutty flavor. It also produces a compound called propionate, which has been shown to have anti-inflammatory and antimicrobial properties and may play a role in regulating appetite and cholesterol production.
Witheridge, the hay-aged cheese, was the most dramatic case. Between its youngest and most mature samples, the number of observed bacterial species increased 3.8-fold. That’s the highest diversity seen across all three cheeses. Researchers believe the hay itself plays a role in this, stimulating the growth of bacterial species that wouldn’t normally thrive in a cheese environment, particularly during the months-long period when the cheese is vacuum-sealed with hay and left to ferment without oxygen. “As hay is a source of protein and fiber, we hypothesize that it stimulates the growth of bacteria that do not otherwise thrive in the cheese environment, particularly during the period where the hay was fermenting on the surface of the cheese anaerobically,” the authors write.
When the pasteurized version of Witheridge was compared to the raw milk version, the raw version showed a large number of bacterial species that couldn’t be accounted for. These were likely populations that survived because pasteurization, the heat treatment that kills many microbes, was never applied.
What the Chemistry Showed Inside Aging Cheese
On the chemical side, one of the most consistent findings across all three cheeses was the near-complete disappearance of lactose, the natural sugar in milk, as each cheese matured. In the youngest samples of Bix and Highmoor, lactose was clearly present. By the midpoint and mature stages, it was gone entirely. Bacteria convert lactose into other compounds, including lactic acid, as part of their normal metabolism. For people who are lactose intolerant, this could matter: mature cheeses appear to have their lactose almost fully consumed before they ever reach the shelf.
Amino acids, the building blocks of proteins, were barely detectable in young samples of all three cheeses but increased noticeably as each cheese aged. Witheridge had the highest concentrations of these amino acids among the mature cheeses, which the researchers suggest may be partly due to that cheese having the lowest moisture content, making everything more concentrated.
Small molecules produced by bacterial fermentation — increasingly linked to gut health — were also detected in the mature cheeses. Propionate was found in both mature Highmoor and mature Witheridge. Butyrate, a compound associated with maintaining the lining of the gut, was found in mature Bix and Witheridge; the paper notes it may originate from clostridia, a common contaminant in cheese whose spores can survive pasteurization, so its source in these cheeses is uncertain. These are the same compounds that gut bacteria produce when they ferment dietary fiber, and their presence raises the possibility that these cheeses could contribute similar compounds to the gut; though how they behave after consumption still needs testing in people.
One unexpected finding involved the white rind on Bix. A mold used to create that rind produces a type of dietary fiber that research suggests can influence the immune system and alter bacterial communities in the gut, potentially acting as a prebiotic, a substance that feeds and supports beneficial gut bacteria. That soft, bloomy rind, the part many people cut off and discard, may actually be one of the most nutritionally interesting components of the cheese.
Not everything in the data is good news. Witheridge contained relatively high levels of a compound called succinate. While succinate plays a role in energy metabolism and immune regulation, high concentrations of it in the gut have been linked to inflammation and the growth of harmful bacteria. The authors note, however, that this only becomes a concern in excessive amounts, and that in moderate quantities it can actually support immune defense. They also pointed out that the DNA-based method used to identify bacteria cannot distinguish between living and dead cells, which means some of the potentially beneficial bacteria found in the mature cheeses may no longer be alive by the time the cheese is eaten.
Ice Age Icebergs Left 3,000 Scratch Marks in the Great Lakes, and They Recorded Winds Blowing the Wrong Way
Thousands of grooves carved into the bottoms of ancient lakes, left behind by drifting icebergs thousands of years ago, have quietly preserved a record of how winds moved across North America during the last Ice Age. Researchers say these marks tell a story that scientists have struggled to piece together for decades.
Scientists from the University at Buffalo discovered more than 3,000 ancient scour marks, long shallow trenches carved by the undersides of drifting icebergs, preserved in the dry lake beds of the eastern Great Lakes region. The marks stretch across more than 1,000 kilometers and date back roughly 17,000 to 12,000 years ago, when a massive ice sheet still covered much of North America. Beyond its scale, the find reveals a powerful, persistent wind system that wrapped around the edge of the ice sheet like air flowing around a giant dome of high pressure, one that scientists had long suspected existed but had precious little evidence to prove.
That wind system sent easterly winds across the region for roughly 5,000 years, pushing icebergs generally westward to west-southwest. Those icebergs etched their paths into the lake floors below, acting like nature’s own wind vanes and leaving their record frozen in the earth.
Scratches in the Earth: How Scientists Found the Iceberg Marks
To find these marks, the research team combed through high-resolution digital terrain maps, detailed three-dimensional portraits of the land surface accurate down to half a meter. Using mapping software, they identified the scour marks as long, shallow trenches flanked by low ridges of pushed-up sediment on either side, the same way a plow kicks up soil on both sides as it cuts through a field.
Most marks were between about half a meter and five meters deep and ranged from a few hundred meters to several kilometers in length. Some of the icebergs responsible were enormous. Based on comparisons between the depth of the marks and ancient shoreline elevations, the tallest icebergs were estimated to have been more than 100 meters thick. By cross-referencing the scour marks with known ancient shoreline boundaries and ice margin positions, the team placed many marks into specific time windows spanning roughly 17,400 to 12,500 years ago.
Reading the Wind: What 3,377 Iceberg Tracks Reveal
When the team measured the direction of all 3,377 marks, the consistency across three separate regions was hard to ignore: the Lake Erie basin, the Lake Ontario basin, and the St. Lawrence Lowlands all told the same story. Marks pointed toward the west-southwest, with an overall average orientation of 258 degrees, give or take about 19 degrees, aligning almost perfectly with a wind blowing out of the east.
For additional confirmation, the team compared the scour marks against two other types of ancient landscape features shaped by wind: sand dunes and oval-shaped thermokarst lakes, formed when frozen ground thaws and collapses into depressions, which tend to align with their long axes perpendicular to prevailing winds. When the team translated those lake shapes into wind direction, the result lined up with the iceberg scours and dune fields, giving researchers three independent lines of evidence pointing to the same conclusion. Researchers also noted that the iceberg tracks did not aim toward ancient lake outlets or match the water-current patterns typical of modern Great Lakes, further supporting wind as the dominant steering force.
Why Ice Age Lake-Effect Storms Blew the Wrong Way
Easterly winds would have fundamentally changed the regional climate. Lake-effect snowstorms, the kind that batter cities like Buffalo, New York, during modern winters, are driven by cold winds blowing across open water from the west and northwest, dumping snow on the eastern and southern shores of the Great Lakes. During the Ice Age, the wind was running in reverse.
Easterly winds would have produced lake-effect precipitation on the western shores of the ancient lake basins instead. Since those Pleistocene lakes were also larger, broader, and deeper than today’s Great Lakes, lake-effect precipitation may have even been amplified. That reversed climate pattern may have left fingerprints in prehistoric plant and climate records that researchers have not yet fully explained.
Artist reconstruction of the Cretaceous Period sauropod dinosaur Nagatitan chaiyaphumensis, whose fossils were unearthed in Thailand, seen in this illustration on May 14, 2026. (Image: Reuters/Patchanop Boonsai)
Along a meandering river in a warm and arid region that is now Thailand roughly 113 million years ago, a plant-eating behemoth almost 27m long browsed on the treetops without much fear of predators due to its sheer size. This was Nagatitan chaiyaphumensis, the largest-known dinosaur from Southeast Asia.
Researchers have unearthed skeletal remains of Nagatitan, a member of the dinosaur lineage called sauropods known for having a long neck, long tail, small head and four columnar legs.
The fossils of this Cretaceous Period dinosaur were first spotted by a villager in Thailand’s northeastern province of Chaiyaphum. Scientists over a period of years then dug up spine, rib, pelvis and leg bones including a front leg bone – the humerus – measuring 1.78m long.
Based on the dimensions of its humerus and femur, the corresponding hind leg bone, the researchers estimated Nagatitan’s body mass at 25 to 28 tons. Its head and teeth were not among the fossils recovered, but the researchers have a good idea of its feeding preferences based on other sauropods.
“Nagatitan was probably a bulk browser that focused on consuming high volumes of vegetation that required little to no chewing such as conifers and possibly seed ferns,” said Thitiwoot Sethapanichsakul, a University College London doctoral student in palaeontology and lead author of the research published on Thursday in the journal Scientific Reports.
The climate was probably subtropical, with some forests, but also savanna-like and shrubland habitats. Nagatitan lived alongside various other dinosaurs as well as flying reptiles called pterosaurs. The rivers were teeming with crocodiles and fish including freshwater sharks.
The ecosystem’s largest predator was a relative of the giant African meat-eating dinosaur Carcharodontosaurus, probably about 8m long and around 3.5 tons.
“At that size, it was dwarfed by Nagatitan. At full size, Nagatitan likely had very little to fear in terms of predation,” Sethapanichsakul said.
Caring for a Loved One May Slow or Speed Mental Decline, Depending on the Burden
For millions of Americans, taking care of an aging parent, a sick spouse, or an ailing friend is simply part of life. But a new study finds that not all caregiving is created equal, and that how much care someone provides, and for whom, may be linked to how their memory and thinking skills change as they age.
Researchers tracking older adults in England over nearly two decades found that people who took on lighter caregiving duties, say a few hours a week helping an elderly parent, actually showed slower mental decline compared to people who weren’t caregivers at all. But those who provided very intensive care, cared for someone in their household, or cared for a spouse or partner showed the opposite: their cognitive test scores declined faster than non-caregivers.
Whether caregiving is good or bad for the caregiver’s own mind appears to depend entirely on the situation.
A Long Look at Caregivers Over Time
Published in the journal Age and Ageing, the study drew from a large, long-running survey called the English Longitudinal Study of Ageing, which tracks people aged 50 and older in private households across England. Researchers used data from nine rounds of interviews spanning 2004–2005 through 2021–2023.
To make a fair comparison, the team paired 2,765 caregivers with 2,765 non-caregivers who had similar backgrounds, matching them on factors like age, sex, health conditions, education, wealth, and relationship status. Caregivers in the study were, on average, 60 years old, and 56% were women.
Cognitive ability was tracked two ways. One test, naming as many animals as possible in one minute, served as a rough measure of executive function, the set of skills involved in organizing thoughts, switching between ideas, and solving problems. Researchers note the test captures only part of that broader skill set. A second test measured memory by having participants learn a list of ten words and recall them immediately and after a short delay. Both tests were repeated across multiple rounds, allowing the team to track how each person’s scores changed before and after they became a caregiver.
It’s Not Just Whether You Care, It’s How Much, and for Whom
When researchers looked at all caregivers as one group, they found no meaningful difference in cognitive decline compared to non-caregivers. Once they broke the data down by the type of caregiving, a far more revealing picture emerged.
People who provided between 5 and 9 hours of care per week showed a noticeably slower drop in executive function scores compared to non-caregivers. Those caring for a parent or parent-in-law also fared better cognitively, and caregivers helping someone who lived outside their own home showed slower decline than those providing care under their own roof.
On the other side, those caring inside the household or for a spouse or partner showed faster cognitive decline than non-caregivers, with statistically reliable results. Those providing 50 or more hours of care per week showed a similar pattern, though that result was somewhat weaker statistically. Caregivers in these situations tend to shoulder the heaviest burdens, often with little time off and limited ability to keep working. Memory followed a similar trajectory, though those effects were much weaker overall.
Too Much Caregiving Cancels Out the Mental Benefits
Researchers point to two competing theories. One, sometimes called the “use it or lose it” idea, holds that staying mentally and socially engaged helps keep the mind sharp. Light caregiving may provide exactly that stimulation: problem-solving, communicating, coordinating care, and staying attuned to another person’s needs.
That protective effect appears to have a breaking point. When caregiving becomes all-consuming, dominating a person’s days, disrupting sleep, and cutting them off from social connections and paid work, the toll may outweigh any cognitive benefits. Researchers tie this to the “stress process” framework, the idea that chronic, high-level stress wears down health over time. As the authors put it: “While caring may help preserve cognitive function, excessive caring demands appear to accelerate cognitive decline.”
Who Is Most at Risk, and What Families Should Know
The negative effects of intensive caregiving were not more pronounced for women or for people with less money. Women do disproportionately take on caregiving roles, the researchers noted, but the effect on cognitive test scores appeared similar regardless of gender or household wealth. People with lower wealth still started the study with lower cognitive scores overall, a gap present from the start, even if the caregiving effect itself didn’t differ by wealth.
People With Stronger Focus May Pay Less Attention to Social Media Posts, Study Finds
People who are better at managing their mental focus may pay less attention to social media content once they’re connected to the person or page sharing it. Researchers argue this may reflect strategy, not laziness.
Most people assume that those with stronger focus absorb more information. But a new study published in the Journal of Experimental Social Psychology turns that idea on its head. Researchers found that people with stronger mental focus actually engage less with posts and articles when they’re connected to the person sharing them, redirecting attention toward something else: mapping out who knows whom.
A team at the University of Bristol Business School and the University at Buffalo ran five separate studies on this. Forming an online connection with someone, becoming a friend, follower, or member of their group, didn’t make people more engaged with that person’s content. It made them less engaged with content and more focused on the social web surrounding it. The effect was strongest among people who scored higher on a working memory task.
Treating Social Networks Like a Hard Drive
Most people don’t memorize phone numbers because they trust the phone to hold onto them. Researchers argue that people do something similar with social media connections. Once connected to an information source, people may behave as if they don’t need to remember the content right away.
This concept is called cognitive offloading: memory work gets delegated to an external tool or system. Social networks function as one of those systems, and people who are best at managing their attention are also the best at recognizing when they can hand that job off.
How the Studies on Social Media and Working Memory Worked
Across the five studies, researchers used both real click behavior and memory recall tasks.
In the first study, 98 undergraduate marketing students were given the option to sign up for a fictitious student marketing group called Marketing Geniuses. About 43% chose to enroll. All participants then browsed a simulated Facebook page for the group, which included five posts and five member profiles. Every link was clickable, and researchers tracked what each student clicked.
Students who signed up clicked on fewer content links and more profile links, meaning they browsed posts less but explored who else was in the group more. This pattern was strongest among students who scored higher on a separate working memory test. Students who scored lower showed no meaningful difference in clicking behavior.
Working memory, as the researchers use the term, isn’t simply about memorization. It’s the ability to direct attention strategically, filter out distractions, and manage competing demands simultaneously. The test used to measure it asks participants to remember letter sequences while solving simple math problems, forcing the mind to juggle two tasks at once.
Friends Change Everything
In two follow-up studies, researchers recruited adults online and introduced them to a fictional professional named Mae O’Malley, an engineer who had developed a fitness app. Participants viewed her professional profile, which included her skills and a list of her connections.
One group was told they would be connected with Mae on a fictional networking platform. The other had no such connection. Both groups then completed a memory recall task covering what Mae knew and who she was connected to.
People connected to Mae recalled significantly less about her skills than those who weren’t connected, but recalled significantly more about her professional connections. This held even after accounting for how often participants used social media and how interested they were in Mae’s field.
In a follow-up version, researchers measured the same participants before and after forming a connection with Mae. Memory for her content dropped after the connection was formed while memory for her social connections went up, which rules out a simple practice effect.
The Real Trade-Off for High-Focus Users
A larger study with 400 participants added the working memory test to examine how individual differences shaped the effect.
Among participants with high working memory scores, being connected to Mae was associated with dramatically lower content recall. Among those with lower scores, connection status made essentially no difference.
For remembering who Mae knew, the pattern reversed. Higher working memory participants who were connected recalled more about Mae’s social web than their disconnected counterparts. Lower working memory participants showed no such shift.
A fifth study replicated the core findings using a university social media page. Participants who followed the page clicked fewer content links but paid more attention to follower links, with the effect again most pronounced among those with higher working memory scores.
Walking 8,500 Steps Daily May Help Prevent Weight Regain
Recent research has highlighted that walking approximately 8,500 steps each day might effectively prevent weight regain in individuals who have lost weight. Traditionally, the guideline for daily step count has been set at 10,000; however, this new finding indicates a lower threshold may suffice.
The study, conducted by specialists in the field of health and nutrition, found that maintaining this level of physical activity is crucial in solidifying weight loss achievements. The goal of 8,500 steps per day was determined based on observations of participants who had previously lost weight and aimed to sustain their new body weight.
Participants reported greater ease in adhering to this more attainable target compared to the higher 10,000 steps. The research implies that expectations around physical activity need to be re-evaluated to align better with individual capabilities without compromising health objectives.
Experts highlight that while walking is an effective and accessible form of exercise, the quantity should be tailored according to personal fitness levels. Consistency in this activity is deemed essential not only for physical health but also for mental well-being.
Dr. Emily Roberts, a prominent figure in weight management research, stated, “Walking is one of the simplest and most effective ways to maintain weight loss. Setting realistic targets can motivate individuals to stay active long-term.”
A large new analysis of randomized trials has found that regular exercise can meaningfully boost the odds of staying smoke-free, and that even a single short workout can blunt the urge to light up for up to 30 minutes afterward.
Quitting smoking has never been easy. Standard treatments like nicotine patches, prescription medications, and counseling can roughly double or triple quit rates, but in the real world, fewer than one in five people manages to stay smoke-free at the 12-month mark. Relapse is common, fueled by side effects, cost, limited access to specialists, and the persistent pull of cravings. For many people, medication isn’t an option at all, whether because of health conditions, cost, or simply a preference to avoid drugs. That gap has researchers looking hard at behavioral strategies, and exercise keeps rising to the top of the list.
A team of researchers conducted a systematic review and meta-analysis, a rigorous study that pools and analyzes findings from many individual trials, pulling together results from 59 randomized controlled trials involving more than 9,000 adults. Published in the Journal of Sport and Health Science, the analysis makes a compelling case that exercise deserves a serious role in how smoking cessation is approached, both by individuals trying to quit and by the healthcare providers helping them.
The Numbers Behind the Sweat
The analysis separated the 59 trials into two categories: studies that looked at what happens after a single workout session, and studies that tracked people who exercised regularly over a longer period.
On the long-term side, pooling data from 23 trials involving more than 5,500 participants, the researchers found that people in exercise programs were 15% more likely to stay smoke-free throughout a defined follow-up period compared to those in control groups. A separate measure, looking at whether people had avoided smoking in the seven days before a check-in point, showed an even stronger result: a 21% higher likelihood of remaining smoke-free among exercisers. Regular exercise was also linked to smoking fewer cigarettes per day, with an average reduction of about two cigarettes daily compared to non-exercising control groups.
Those numbers may not sound dramatic, but they matter. In the world of smoking cessation, modest improvements compound over time, and any strategy that chips away at tobacco use carries real health benefits.
When Just One Workout Makes a Difference
Perhaps the most immediately practical finding involves what happens right after a single exercise session. Across 10 trials, a single bout of exercise produced moderate-to-large reductions in cravings immediately after finishing, with effects still detectable at the 10-minute, 20-minute, and 30-minute marks post-exercise.
Intensity mattered. High-intensity exercise produced the largest drop in cravings, followed by moderate-intensity activity. Low-intensity exercise showed only a small effect that wasn’t statistically meaningful. Sessions as short as 5 to 30 minutes were found to be effective for managing acute cravings.
The proposed explanation involves brain chemistry. Exercise is thought to trigger temporary increases in the brain’s feel-good signaling systems, including pathways tied to dopamine and natural opioid-like compounds, while also reducing the stress hormone cortisol. These changes may dial down the reward-seeking pull that makes cravings so hard to resist.
Not All Exercise Is Created Equal
When it came to what type of exercise was most beneficial for long-term quitting, aerobic exercise, think brisk walking, cycling, or treadmill workouts, showed the clearest, most consistent benefits. Other forms like resistance training, yoga, and high-intensity interval training appeared in fewer studies and produced more mixed or limited results, though some suggested potential benefits for cravings. The researchers noted that the evidence base for these non-aerobic options is simply not yet large enough to draw firm conclusions.
Session frequency also appeared to play a role. Programs involving one to two sessions per week showed larger effects on staying smoke-free than those requiring more frequent sessions, though the researchers cautioned that this finding warrants careful interpretation given the variability across study designs.
A Tool Most Smokers Haven’t Tried
Unlike prescription medications, exercise is generally low-risk for most people and does not require a prescription, though people with heart, lung, mobility, or other health concerns should check with a clinician before starting vigorous activity. Unlike some digital programs or counseling services, exercise can often be done without internet access or a specialist, especially when it is as simple as a brisk walk.
The paper also notes that exercise may help with several problems that often make quitting harder, including mood, sleep, anxiety, depression, and post-cessation weight gain, all common forces that push people back toward cigarettes.
One notable gap: not a single trial in the entire body of evidence examined whether exercise helps people quit vaping or e-cigarettes. Given how rapidly e-cigarette use has grown and how common dual use, smoking traditional cigarettes while also vaping, has become, the researchers called this absence a critical oversight. Future research, the authors stressed, needs to address this directly.
Potato chips, frozen dinners, and diet soda don’t exactly have a reputation for being brain food. But a new study of more than 2,000 Australian adults suggests these foods may be chipping away at something far more concerning than a waistline: the brain’s ability to pay attention. And eating a salad on the side may not be enough to undo it.
For every 10% increase in the share of calories coming from ultra-processed sources, attention scores dropped by a small but measurable amount (about 0.05 points on the study’s scale), and a score used to estimate future dementia risk ticked upward. Both associations held up even after accounting for how closely participants followed a Mediterranean-style diet, widely considered the gold standard for brain-healthy eating. That detail matters because it suggests something about the processing itself may be driving the effect, not simply the absence of better food choices.
Published in Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring, the study doesn’t prove that ultra-processed foods directly cause cognitive problems. It captured a single snapshot in time rather than tracking people over years.
What Are Ultra-Processed Foods, and Why Do They Matter for Brain Health?
Scientists use a classification system called Nova, which sorts foods by how much industrial processing they’ve undergone rather than by nutritional content. At one end are whole or minimally processed foods like fresh fruits, vegetables, and plain meats. At the other end sit ultra-processed foods, industrial creations made largely from refined ingredients and chemical additives. Soft drinks, packaged salty snacks, processed meats, frozen ready meals, and flavored dairy desserts all fall into this category.
In Australia, these products make up roughly 42% of total calories consumed. In the United States and United Kingdom, that figure climbs above 50%. Participants in this study were right in line with the Australian national average, getting about 41% of their daily calories from ultra-processed sources.
How the Study Linked Ultra-Processed Foods to Attention
Led by Barbara R. Cardoso at Monash University, the research team analyzed data from 2,192 adults enrolled in the Healthy Brain Project, an online platform recruiting dementia-free people between the ages of 40 and 70. Most participants had a close family member with dementia, placing them at higher genetic risk for cognitive decline.
Participants filled out a detailed 130-item food questionnaire covering their eating habits over the previous 12 months, with every item classified using the Nova system. Cognitive function was measured using an established online test assessing processing speed, visual attention, visual recognition memory, and working memory, combined into two summary scores: one for attention, one for memory. Dementia risk was estimated using a tool called CAIDE, which weighs factors like age, cholesterol history, blood pressure, physical activity, and body mass index to predict 20-year dementia risk. The researchers also used a modified version of the CAIDE score that focuses only on changeable risk factors, though that version has not been independently validated as a dementia prediction tool.
Ultra-Processed Foods Linked to Worse Attention, Higher Dementia Risk Score
Higher consumption of ultra-processed foods was associated with worse attention scores, following a general trend where higher intake tracked with poorer performance. The effect remained across multiple rounds of analysis, even after accounting for Mediterranean diet adherence and body weight.
Ultra-processed food intake showed no connection to memory scores, a finding the authors noted aligns with previous research. Attention is foundational to learning and problem-solving, and disruptions there may surface before broader cognitive problems become apparent, a pattern documented in early stages of brain disease.
On the dementia risk front, each 10% increase in ultra-processed food consumption was linked to a 0.24-point rise on the modified CAIDE score, and that association held up after accounting for diet quality. The link with the original CAIDE score was weaker and lost statistical significance once Mediterranean diet adherence was factored in.
Salads Alone May Not Be Enough to Counter Ultra-Processed Food Risks
People who eat lots of ultra-processed food also tend to eat fewer fruits, vegetables, and other whole foods, so researchers have long struggled to separate the harm of junk food from the simple absence of better options. By adjusting for Mediterranean diet adherence, this team tried to isolate the processing question. The fact that the associations held up suggests something about the processing itself may matter.
The authors suggest several possible explanations, though none were directly tested in this study. Ultra-processing can strip away beneficial plant compounds, vitamins, and minerals while introducing potentially harmful substances from packaging materials, high-heat industrial cooking, and additives like emulsifiers and preservatives. Animal studies have shown some of these substances can disrupt gut microbes that communicate with the brain, potentially triggering inflammation and impairing nerve cell signaling. Ultra-processed foods are also strongly tied to obesity, diabetes, and high blood pressure, all of which damage blood vessels that feed the brain, and the researchers noted that attention is particularly sensitive to that kind of vascular damage.
A stick of chewing gum probably isn’t the first thing that comes to mind when thinking about cancer prevention. But a new study suggests it might be worth a second look. Researchers loaded a gum with proteins derived from an edible bean and tested it against the specific viruses and bacteria most strongly tied to head and neck cancer. In lab experiments using real patient samples, the results were notable enough to push this idea toward clinical trials.
All of this work was done in a laboratory, not in living patients. No one chewed the gum and was monitored for health outcomes. Human clinical trials will be needed before anyone can say whether it works in practice. Still, the early data offers an intriguing glimpse of what might be possible.
Head and neck cancer, the kind that strikes the mouth, throat, and tonsils, accounts for an estimated 890,000 new cases worldwide every year, with roughly half of patients dying after treatment. Radiation can disrupt the mouth’s bacterial balance, reducing helpful bacteria and allowing harmful microbes to increase. Scientists have known for years that three specific oral microbes, HPV and two types of bacteria called Porphyromonas gingivalis (Pg) and Fusobacterium nucleatum (Fn), show up at much higher levels in cancer patients and are tied to worse outcomes. The researchers behind this study argue that practical, affordable ways to lower these microbes in the mouth are still needed.
A team from the University of Pennsylvania, UCLA, the Veterans Administration Greater Los Angeles Healthcare System, and the University of Kansas Medical Center set out to address that. Their approach was simple in concept: load a chewing gum with plant-derived proteins that attack cancer-associated microbes right where they live. The results, published in Scientific Reports, suggest these gums could one day serve as a powerful add-on to existing cancer treatments or even as a preventive tool for people at high risk.
How the Bean-Based Chewing Gum Study Worked
This was a lab-based study, meaning the researchers collected real biological samples from cancer patients and healthy volunteers, then tested the gum ingredients on those samples rather than having patients chew the gum directly. Saliva samples came from patients treated at the VA hospital in Los Angeles, while mouth-rinse samples were collected at the University of Kansas Medical Center. In total, the study drew on samples from dozens of head and neck cancer patients and cancer-free participants.
The gum contains two active ingredients. The first is a protein called FRIL, found naturally in the lablab bean, a legume eaten around the world. FRIL works like a molecular trap: it latches onto sugar structures on the surface of viruses, clumping virus particles together into large clusters that can no longer infect cells. The second ingredient is protegrin-1, an antimicrobial peptide first identified in pigs that has already been tested in advanced human clinical trials for mouth sores caused by chemotherapy. Protegrin-1 is especially effective at killing certain types of bacteria thanks to its shape, which is locked in place by chemical bonds that make it unusually stable.
To test the antiviral gum, the team mixed bean gum extract with patient samples and measured how much HPV remained free in the liquid. For the antibacterial tests, they combined the bean gum extract with protegrin-1 and let the mixture sit with patient samples for one hour at body temperature. They then grew bacteria from the treated and untreated samples on specialized plates designed to detect specific microbes and counted the colonies that formed.
Bean Gum Cleared HPV and Killed 99% of Cancer-Linked Oral Bacteria
The HPV results were eye-opening. Researchers found the virus in every single saliva sample from cancer patients and in about 75% of mouth-rinse samples. When treated with the bean gum extract, about 93% of HPV in saliva was trapped and removed. In mouth-rinse samples, about 80% of HPV-positive cases showed the virus being clumped together, with 13 out of 22 positive samples showing complete virus removal. Spinning the samples at high speed without the bean extract did nothing to remove the virus. It was the FRIL protein doing the work.
Cancer patients harbored staggering amounts of the two dangerous bacteria compared to cancer-free participants. Saliva from cancer patients contained roughly 1,000 times more Pg and Fn than samples from healthy controls, and mouth-rinse samples showed about 100 times more. A single dose of the bean gum plus protegrin-1 combination wiped out more than 99% of both bacteria across all sample types, a reduction the researchers described as statistically highly significant.
Just as telling as what the treatment killed is what it spared. Streptococcus bacteria, which include many species that are normal, healthy residents of the mouth, survived the treatment largely intact. Many Streptococcus species produce protective sugar coatings that shield them from protegrin-1’s attack. The bacteria linked to cancer, Pg and Fn, lack this protection, making them vulnerable. That built-in selectivity is a real advantage over radiation therapy, which can disrupt the entire oral bacterial community without discrimination.
The study also screened for other microbes. A bacterium called Leptotrichia buccalis, tied to precancerous mouth conditions, turned up in 97% of cancer patients’ mouth-rinse samples at levels 100 times higher than in healthy participants, and the treatment killed more than 99% of it. A yeast sometimes linked to oral cancer, Candida albicans, appeared at low rates in cancer patients and was absent from all healthy participant samples.
Why a Chewing Gum Could Go Where HPV Vaccines Cannot
One-third of men globally are infected with HPV according to a major review of 65 studies spanning 45,000 males across 35 countries, and one-fifth carry the high-risk HPV-16 strain most commonly linked to cancer. Although HPV vaccines exist in more than 100 countries, the rate of throat cancer has actually increased since vaccination programs began. HPV vaccines are injected into muscle and trigger a body-wide immune response, but they do not produce the type of immune defense that protects the moist surfaces of the mouth and throat. Vaccinated individuals can still harbor and transmit the virus orally. A gum that traps and removes HPV directly in the mouth could, in theory, offer a layer of protection that vaccines currently cannot, though this potential has not yet been tested in real-world conditions.
Safety is also part of the picture. The bean powder carries an FDA designation as “Generally Regarded as Safe,” and the dose in a single gum tablet is more than 6,000 times less than the amount consumed safely in human toxicology testing. The chewing gum formula has already been submitted to the FDA and approved for evaluation in a clinical trial targeting coronavirus infection and transmission. The individual components have established safety profiles, but the effectiveness and safety of this specific formulation for targeting oral cancer microbes still need to be validated in human trials.
Beyond the surface of the mouth, the researchers point out that FRIL can enter human cells and block viruses at a deeper level, and that protegrin-1 has been shown to get inside head and neck cancer cells. Prolonged local delivery through chewing could, in theory, fight microbes both outside and inside cancer cells. Whether this plays out in a patient’s mouth remains to be demonstrated.
The top predator prowling the seas during the age of the dinosaurs 100 million years ago may have been the octopus.
New analyses of fossilized jaws reveal that massive, kraken-like octopuses once hunted alongside other marine predators. They boasted eight arms and long bodies that extended more than 60 feet (18 meters), rivaling other carnivorous marine reptiles.
“These krakens must have been a fearsome sight to behold,” University of Alabama paleontologist Adiel Klompmaker said in an email. He had no role in the new research.
Dinosaur fans know that late Cretaceous-era waters were ruled by sharp-toothed sharks and sea reptiles known as mosasaurs and plesiosaurs.
Why do octopuses get left out of the mix? Scientists have studied giant octopus relatives that roamed when dinosaurs were around, and researched some small octopuses that drilled into clams. But since their soft bodies don’t preserve well, it’s hard to figure out exactly how big the creatures got.
There’s also a perception that squishy invertebrates — creatures without backbones — weren’t formidable enough to join the ranks of top predators. But octopus’ beaks made of stiffened chitin are tough enough to crush shelled and bony critters.
In the new study, researchers studied the jaws of 15 ancient octopus fossils that were previously found in Japan and Canada’s Vancouver Island. They also identified 12 more jaws from Japan using a technique they created called digital fossil mining, which closely scans rocks in cross-sections to reveal fossils hiding inside.
They compared the jaws to that of modern-day octopuses to estimate how large the creatures may have been, and determined that the ancient octopuses ranged from 23 to 62 feet (7 to 19 meters) in length. The largest jaw was substantially bigger than that of any modern octopus, said co-author and paleontologist Yasuhiro Iba with Hokkaido University in an email.
They also found that the largest creatures’ jaws had significant wear and tear including scratches, chips and rounded edges, suggesting that “the animals repeatedly crushed hard prey such as shells and bones,” said Iba.
The findings were published Thursday in the journal Science.
Without access to the octopuses’ stomach contents, it’s hard to know for sure what they were eating or whether they truly competed with other top predators for their meals. They could have snacked on fish or snails, snatching prey with flexible arms and breaking it apart with their beaks.
Looking for octopus fossils in other places might help scientists get a clearer idea of how they factor into ancient food webs, said paleontologist Neil Landman with the American Museum of Natural History in New York.
“It’s a big old planet,” said Landman, who wasn’t involved with the new research. “So we have lots to look at to piece together the marine ecosystem through time.”
A stick of chewing gum probably isn’t the first thing that comes to mind when thinking about cancer prevention. But a new study suggests it might be worth a second look. Researchers loaded a gum with proteins derived from an edible bean and tested it against the specific viruses and bacteria most strongly tied to head and neck cancer. In lab experiments using real patient samples, the results were notable enough to push this idea toward clinical trials.
All of this work was done in a laboratory, not in living patients. No one chewed the gum and was monitored for health outcomes. Human clinical trials will be needed before anyone can say whether it works in practice. Still, the early data offers an intriguing glimpse of what might be possible.
Head and neck cancer, the kind that strikes the mouth, throat, and tonsils, accounts for an estimated 890,000 new cases worldwide every year, with roughly half of patients dying after treatment. Radiation can disrupt the mouth’s bacterial balance, reducing helpful bacteria and allowing harmful microbes to increase. Scientists have known for years that three specific oral microbes, HPV and two types of bacteria called Porphyromonas gingivalis (Pg) and Fusobacterium nucleatum (Fn), show up at much higher levels in cancer patients and are tied to worse outcomes. The researchers behind this study argue that practical, affordable ways to lower these microbes in the mouth are still needed.
A team from the University of Pennsylvania, UCLA, the Veterans Administration Greater Los Angeles Healthcare System, and the University of Kansas Medical Center set out to address that. Their approach was simple in concept: load a chewing gum with plant-derived proteins that attack cancer-associated microbes right where they live. The results, published in Scientific Reports, suggest these gums could one day serve as a powerful add-on to existing cancer treatments or even as a preventive tool for people at high risk.
How the Bean-Based Chewing Gum Study Worked
This was a lab-based study, meaning the researchers collected real biological samples from cancer patients and healthy volunteers, then tested the gum ingredients on those samples rather than having patients chew the gum directly. Saliva samples came from patients treated at the VA hospital in Los Angeles, while mouth-rinse samples were collected at the University of Kansas Medical Center. In total, the study drew on samples from dozens of head and neck cancer patients and cancer-free participants.
The gum contains two active ingredients. The first is a protein called FRIL, found naturally in the lablab bean, a legume eaten around the world. FRIL works like a molecular trap: it latches onto sugar structures on the surface of viruses, clumping virus particles together into large clusters that can no longer infect cells. The second ingredient is protegrin-1, an antimicrobial peptide first identified in pigs that has already been tested in advanced human clinical trials for mouth sores caused by chemotherapy. Protegrin-1 is especially effective at killing certain types of bacteria thanks to its shape, which is locked in place by chemical bonds that make it unusually stable.
To test the antiviral gum, the team mixed bean gum extract with patient samples and measured how much HPV remained free in the liquid. For the antibacterial tests, they combined the bean gum extract with protegrin-1 and let the mixture sit with patient samples for one hour at body temperature. They then grew bacteria from the treated and untreated samples on specialized plates designed to detect specific microbes and counted the colonies that formed.
Bean Gum Cleared HPV and Killed 99% of Cancer-Linked Oral Bacteria
The HPV results were eye-opening. Researchers found the virus in every single saliva sample from cancer patients and in about 75% of mouth-rinse samples. When treated with the bean gum extract, about 93% of HPV in saliva was trapped and removed. In mouth-rinse samples, about 80% of HPV-positive cases showed the virus being clumped together, with 13 out of 22 positive samples showing complete virus removal. Spinning the samples at high speed without the bean extract did nothing to remove the virus. It was the FRIL protein doing the work.
Cancer patients harbored staggering amounts of the two dangerous bacteria compared to cancer-free participants. Saliva from cancer patients contained roughly 1,000 times more Pg and Fn than samples from healthy controls, and mouth-rinse samples showed about 100 times more. A single dose of the bean gum plus protegrin-1 combination wiped out more than 99% of both bacteria across all sample types, a reduction the researchers described as statistically highly significant.
Just as telling as what the treatment killed is what it spared. Streptococcus bacteria, which include many species that are normal, healthy residents of the mouth, survived the treatment largely intact. Many Streptococcus species produce protective sugar coatings that shield them from protegrin-1’s attack. The bacteria linked to cancer, Pg and Fn, lack this protection, making them vulnerable. That built-in selectivity is a real advantage over radiation therapy, which can disrupt the entire oral bacterial community without discrimination.
The study also screened for other microbes. A bacterium called Leptotrichia buccalis, tied to precancerous mouth conditions, turned up in 97% of cancer patients’ mouth-rinse samples at levels 100 times higher than in healthy participants, and the treatment killed more than 99% of it. A yeast sometimes linked to oral cancer, Candida albicans, appeared at low rates in cancer patients and was absent from all healthy participant samples.
Why a Chewing Gum Could Go Where HPV Vaccines Cannot
One-third of men globally are infected with HPV according to a major review of 65 studies spanning 45,000 males across 35 countries, and one-fifth carry the high-risk HPV-16 strain most commonly linked to cancer. Although HPV vaccines exist in more than 100 countries, the rate of throat cancer has actually increased since vaccination programs began. HPV vaccines are injected into muscle and trigger a body-wide immune response, but they do not produce the type of immune defense that protects the moist surfaces of the mouth and throat. Vaccinated individuals can still harbor and transmit the virus orally. A gum that traps and removes HPV directly in the mouth could, in theory, offer a layer of protection that vaccines currently cannot, though this potential has not yet been tested in real-world conditions.
Safety is also part of the picture. The bean powder carries an FDA designation as “Generally Regarded as Safe,” and the dose in a single gum tablet is more than 6,000 times less than the amount consumed safely in human toxicology testing. The chewing gum formula has already been submitted to the FDA and approved for evaluation in a clinical trial targeting coronavirus infection and transmission. The individual components have established safety profiles, but the effectiveness and safety of this specific formulation for targeting oral cancer microbes still need to be validated in human trials.
Beyond the surface of the mouth, the researchers point out that FRIL can enter human cells and block viruses at a deeper level, and that protegrin-1 has been shown to get inside head and neck cancer cells. Prolonged local delivery through chewing could, in theory, fight microbes both outside and inside cancer cells. Whether this plays out in a patient’s mouth remains to be demonstrated.
It’s also worth noting the bean gum tablets used in these experiments had been stored at room temperature for up to 33 months and still worked. That kind of shelf stability could make the product practical and affordable at a global scale, particularly given that plant-based medicines approved by the FDA cost less than 3% of comparable drugs produced through other methods.
Some of the true crab species included in the study ‘Evolution of sideways locomotion in crabs’. Clockwise from top left: Two photographs of Tuerkayana hirtipes; Cardisoma carnifex (by Tsubasa Inoue); and Ocypode sinensis (by Junya Taniguchi) (CC BY 4.0) Credit: Tsubasa Inoue and Junya Taniguchi (CC BY 4.0)
A crab scuttling sideways across a beach is one of the most recognizable movements in the animal kingdom. The shuffle is so iconic that “crabwalk” has become part of everyday language. But scientists have long debated a deceptively simple question: Did crabs figure out this trick once, or did different groups independently arrive at it? A new study has an answer, and it turns out sideways walking appears to have evolved just once, a single behavioral shift that may have helped fuel the explosion of crab species across the planet.
Published in the journal eLife, the study filmed 50 living crab species and mapped their walking styles onto a family tree spanning hundreds of millions of years. Sideways movement appears to have originated in the ancestor of a massive group called true crabs. Based on previously published divergence estimates, that shift may have occurred around 200 million years ago near the start of the Jurassic period. According to the researchers, it may have helped crabs expand into a huge range of habitats, from deep-sea floors to tropical forests, and contributed to true crabs growing into roughly 7,900 species alive today.
Some lineages later reverted to walking forward again, multiple times independently. Those reversions tended to occur in species that had found other ways to avoid predators, like hiding inside clam shells or camouflaging themselves with seaweed. Once crabs no longer needed the escape advantage of darting sideways, some gave it up.
How Researchers Studied Crabs Walking Sideways
Scientists at Nagasaki University in Japan set up circular arenas, large plastic pools between roughly 2.5 and 4.5 feet across, filled with whatever environment each species naturally lives in. Each crab was given time to settle down, then released in the center and filmed for 10 minutes. Researchers tracked two landmarks on each crab’s shell frame by frame to determine which direction the animal moved relative to where its body was pointing.
Every movement was classified as forward, sideways, or backward, with backward movements rare enough to be excluded. A scoring system called the Forward-Sideways Index produced a value ranging from +1 for a purely forward-walking crab to -1 for a purely sideways-walking one. Of the 50 species studied, 35 were sideways movers and 15 were forward movers, with very little overlap between the two groups. Crabs, it seems, are fully committed to one direction or the other.
Crabs Walking Sideways Evolved Just Once on the Family Tree
Walking styles were then mapped onto an evolutionary tree of crabs built from genetic data covering 344 species. Statistical models pointed to a single origin of sideways walking at the base of a group that includes the vast majority of living true crabs. Earlier-branching lineages retained the forward-walking habit of their ancestors, and the probability that the common ancestor of all true crabs walked forward was estimated at 91 percent.
Model estimates put the number of independent reversions from sideways back to forward walking at around 10, while forward-to-sideways transitions happened roughly four times, mostly representing the original gain. One notable example: snow crabs likely underwent a secondary reversion back to sideways walking after their close relatives in the spider crab family had already switched to forward movement.
Why Crabs Walking Sideways Gave Them a Survival Edge
Sideways-walking crabs can bolt left or right with roughly equal swiftness, making their escape route unpredictable to a predator. Experiments with crab-like robots have backed this up: sideways movement turns out to be faster and more efficient than forward walking for a body built like a crab’s.
This escape advantage may help explain the species diversity gap between sideways-walking crabs and their closest relatives. Eubrachyura, the focal group where sideways movement dominates, contains about 7,468 described species, compared to just 110 in its nearest sister group and around 46 in the next closest relative.
If the external dating estimates hold, the origin of sideways walking lines up with the early Jurassic, right after the mass extinction that closed out the Triassic. That extinction would have opened ecological real estate: shallow marine habitats were expanding and competition was reduced. A crab that could escape predators by darting unpredictably in multiple directions would have had a serious edge. The researchers caution that separating the role of this behavioral shift from external factors like post-extinction opportunity will require further study.
The Crabs That Gave Up Sideways Walking
According to the authors, maintaining the sideways-walking body plan may come with tradeoffs, including changes to nerve wiring and joint flexibility that limit behaviors like burrowing and mating. When the pressure to escape predators was lifted by some other strategy, forward walking crept back in.
Many animals have converged on looking like a crab, a phenomenon called carcinization, but the study’s behavioral data show they don’t necessarily move like one. Porcelain crabs move mostly backward. King crabs and coconut crabs walk forward. Across the entire sweep of animal evolution, walking perpendicular to where your head points appears to be essentially a one-off invention, and only in true crabs has it stuck around long enough to reshape an entire group’s place in the natural world.
Interest in magic mushrooms has surged in recent years, and new federal data put a number on just how widespread use has become. A federal survey found that roughly 8 million Americans used psilocybin, the active compound in magic mushrooms, last year.
Buried inside that figure is a pattern researchers say doctors need to pay attention to: people who had recently experienced a major depressive episode were more likely to be among those using it.
As psilocybin inches closer to mainstream medicine, the question of who is using it outside of controlled settings, and why, is becoming harder to ignore.
A Federal Survey Tracks Magic Mushroom Use for the First Time
For the first time, the 2024 National Survey on Drug Use and Health included questions specifically about psilocybin. Run annually and designed to reflect the broader U.S. population, previous versions of the survey either grouped psilocybin with other hallucinogens or only asked whether someone had ever tried it in their lifetime. By asking instead about use within the past year, researchers got a much sharper picture of who is actually using it now.
Led by Kevin H. Yang of UC San Diego and Joseph J. Palamar of NYU Grossman School of Medicine, the study was published in The American Journal of Psychiatry and analyzed responses from 58,633 participants. An estimated 8 million people ages 12 and older, about 2.8% of the U.S. population, reported past-year use. Because the survey captures a single point in time and relies on self-reported data, the findings describe associations rather than cause-and-effect relationships.
Who is using it? Mostly younger, college-educated, higher-income men. Young adults ages 18 to 25 had higher odds of past-year use than the 35-to-49 age group, while people 50 and older had much lower odds. Black individuals had about 60% lower odds and Hispanic individuals about 31% lower odds compared to White individuals, and people with a college degree had more than two and a half times the odds of those without a high school diploma. Throughout the study, “odds” refers to how common something was in one group relative to another, not the likelihood that any one person would use psilocybin.
Cannabis Use Was Most Strongly Linked to Magic Mushroom Use
Other drug use showed the tightest connections. People who had used cannabis in the past year had more than 13 times the odds of also having used psilocybin, making it the most strongly associated factor by a wide margin. Past-year LSD use carried nearly eight times the odds, ketamine about six times, and MDMA roughly three and a half times. Cocaine was linked to about twice the odds, and misuse of prescription stimulants showed a similar association.
Researchers noted that psilocybin use “commonly co-occurs with other substance use within the same year, consistent with a shared experimentation pattern among individuals who use psychedelics.” For clinicians, that clustering is a practical signal: when a patient mentions using one psychedelic, a broader conversation about substance use is probably warranted, including a look at potential interactions with antidepressants.
People With Depression Were More Likely to Use Psilocybin
Among past-year psilocybin users, 23.1% had experienced a major depressive episode in the past year, compared to 8.4% of non-users. These figures reflect differences between groups, not a change in individual risk caused by psilocybin. After adjusting for demographics, income, education, and other substance use, people with a recent depressive episode still had 37% higher odds of having used psilocybin.
That association matters given the momentum behind psilocybin as a potential depression treatment. The FDA granted psilocybin its “breakthrough therapy” designation for treatment-resistant depression in 2018 and for major depressive disorder in 2019. Clinical trials have shown promise, but those trials involve careful screening, controlled dosing, and professional psychological support before, during, and after the experience. None of those safeguards exist when someone takes mushrooms on their own, and the authors pointed out that adverse effects from unsupervised use, including anxiety, paranoia, and prolonged psychological distress, have been documented, with poison center reports involving psilocybin on the rise.
Whether the link reflects self-medication, shared risk factors, or psychological distress from unsupervised use remains an open question. Earlier studies examining lifetime use found psilocybin was associated with lower odds of depression, a discrepancy researchers attributed to the difference in timeframe: past-year use captures people much closer in time to their current mental health status. Longitudinal research will be needed to sort out the direction.
What Comes Next as States Expand Legal Access to Psilocybin
Oregon launched a regulated psilocybin services program in 2023, and Colorado followed in 2025, with other states pursuing decriminalization. None of that changes psilocybin’s federal Schedule I status, but the legal landscape is shifting fast. Researchers argued that use is now common enough that psychiatrists are “likely to encounter patients who use it outside of clinical settings,” and that screening should become routine, especially for patients who use cannabis or other psychedelics and those dealing with depression.
Eight million Americans using a powerful psychedelic is not a fringe phenomenon. People struggling with depression appear to be showing up in that group at elevated rates, and that warrants serious, evidence-based attention from clinicians and policymakers alike.
Up to three in ten older adults die with significant amyloid plaques and Tau tangles in their brains yet never showed a single sign of mental decline while alive. Scientists have now identified a new mouse model that mimics this puzzling resilience, and the discovery was guided by artificial intelligence.
For decades, Alzheimer’s research has been shadowed by a strange paradox. Autopsies of elderly people who were mentally sharp until the day they died sometimes reveal brains loaded with the same protein damage found in patients with devastating dementia. An estimated 20 to 30 percent of cognitively intact older adults carry this level of brain pathology yet never lose their memory or thinking abilities, a condition researchers call “asymptomatic Alzheimer’s disease.” Nobody fully understands why some brains hold up while others collapse under the same burden.
A team at the University of California San Diego and Weill Cornell Medicine identified a living laboratory mouse that carries the molecular fingerprints of Alzheimer’s in its brain but learns and remembers just fine. The discovery came from an AI system trained to decode Alzheimer’s at the genetic level, sorting through large databases of human brain tissue data to identify a reliable genetic signature of the disease. Researchers then applied that signature to established mouse strains, revealing one that could serve as a stand-in for this silent form of Alzheimer’s. Having such a model opens the door to studying resilience directly and to developing treatments that could protect the brain before irreversible damage sets in.
AI Identified a New Alzheimer’s Mouse Model Using Gene Logic
The study, published in Acta Neuropathologica Communications, used a computational tool called the Boolean Network Explorer, or BoNE. Rather than looking for loose statistical correlations between genes, BoNE identifies strict, directional relationships between pairs of genes. These logical rules hold more stable across datasets than many traditional approaches, making them far less likely to shift depending on which group of patients is studied.
Researchers fed BoNE data from 70 cognitively normal individuals and 219 Alzheimer’s cases, and the tool produced a network of gene relationships capturing the core biology of the disease. From this, the team distilled a signature of 40 genes: 20 that ramp up in Alzheimer’s and 20 that dial down. When tested against 35 independent datasets spanning multiple brain regions, it outperformed 24 previously published Alzheimer’s gene signatures in its ability to tell diseased brains apart from healthy ones. It also picked up disease signals earliest in brain regions known to be affected first, confirming the AI had latched onto genuine disease biology rather than statistical noise.
From Human Data to a Living Mouse With Alzheimer’s Resilience
With a validated genetic signature in hand, researchers applied it to gene activity data from five widely used genetically engineered mouse strains. The goal was to find a mouse whose brain looked like Alzheimer’s at the molecular level but whose behavior told a different story.
A protein called Chromogranin A, or CgA, proved to be the key. CgA is found in nerve cells and support cells in the brain, its levels are elevated in the spinal fluid of Alzheimer’s patients, and it has been found tangled up with the toxic nerve fiber knots that characterize the disease. In earlier work, the researchers showed that deleting the CgA gene in mice engineered to develop a brain-tangling disease reduced damage and improved survival.
When the AI signature was applied to brain tissue from these CgA-deleted mice, the results split along sex lines. Male mice lacking CgA but carrying the disease genes showed Alzheimer’s-like molecular and pathological features, yet performed normally on tests of spatial learning and memory. Their brains had the disease markers; their minds did not. Female mice with the same genetic setup showed something more dramatic: their genetic scores clustered with healthy mice, and their brains showed additional layers of protection at every level examined.
Female Mice Showed Near-Complete Protection From Tau Damage
At the tiny junctions between nerve cells where memories are formed, healthy mice showed dense clusters of small bubble-like packages that ferry chemical signals across the gap. Diseased mice had lost most of them. Males lacking CgA recovered some of that density, but females lacking CgA came closest to matching healthy animals, retaining the kind of robust signaling machinery that memory depends on.
When researchers examined toxic Tau tangles, the sex divide was sharper still. Males lacking CgA still showed substantial tangles. Females lacking CgA were largely free of these tangles across multiple brain regions, with roughly a 23 percent reduction in one memory-center region and about a 33 percent reduction in another, compared to diseased mice.
These sex differences mirror a complicated reality in human Alzheimer’s research. Women face a higher lifetime risk of the disease and at symptomatic stages often carry a heavier Tau burden than men. But some studies suggest women may show greater early cognitive resilience, an advantage that appears to fade as disease advances. The mouse model captures this dynamic, pointing to female-specific protective mechanisms that may operate early but could eventually be overwhelmed.
Loneliness doesn’t just ache emotionally. For older adults across Europe, feeling persistently lonely is tied to measurably worse memory, though not because it speeds up decline over time. A large new study tracking more than 10,000 Europeans over six years found that adults reporting high loneliness had lower memory scores from the start, but loneliness was not associated with faster memory loss as people aged, suggesting the gap is present from the outset rather than opening up gradually.
Many researchers have long believed loneliness acts like a slow poison on the brain, gradually wearing down thinking skills and eventually increasing dementia risk. But this study, published in the journal Aging & Mental Health, adds an important wrinkle to that view. Prior evidence is genuinely mixed, with some studies finding loneliness accelerates cognitive decline and others finding no effect at all. What this research contributes is a closer look at memory specifically, across a large, geographically diverse sample, over a defined six-year window.
That scope matters. If loneliness is a marker of already-lower memory performance rather than a force that accelerates decline, it changes how doctors and policymakers should think about stepping in, and when.
How Loneliness and Memory Were Measured
Researchers drew on data from the Survey of Health, Ageing and Retirement in Europe, known as SHARE, one of the largest ongoing studies of aging across the continent. They analyzed information from three waves of data collection spanning 2012 to 2019, covering participants from 12 countries including Germany, France, Spain, Italy, Denmark, Sweden, the Czech Republic, Estonia, Slovenia, Switzerland, Belgium, and Austria.
Altogether, 10,217 adults aged 65 to 94 made up the final sample. All had completed a loneliness assessment at the study’s starting point and taken part in all three waves. People already diagnosed with Alzheimer’s or other forms of dementia, or who had trouble performing daily tasks, were excluded. Loneliness was measured using a three-question scale asking how often someone feels they lack companionship, feel left out, or feel isolated. Participants were sorted into low, average, and high loneliness groups; the low and average groups were combined and compared against the high loneliness group. About 7.7% fell into the high loneliness category.
Memory was tested at each wave using a word recall task. Participants heard a list of 10 words read aloud and tried to repeat back as many as possible within one minute for immediate recall, then did the same five minutes later for delayed recall.
Loneliness Linked to Lower Memory From the Start
At the study’s outset, the average immediate recall score was 5.4 out of 10 and delayed recall averaged 4.8. Adults with high loneliness started noticeably lower: immediate recall of 4.9 and delayed recall of 3.5, compared with 5.4 and 4.1 for everyone else. The differences were statistically significant.
When researchers tracked how memory changed over time, everyone’s scores declined slightly each year at roughly the same rate, regardless of loneliness level. High loneliness was associated with lower starting scores for both immediate and delayed recall, but had no measurable effect on how fast memory faded over six years.
Age was by far the strongest factor driving both lower baseline memory and faster decline. Adults aged 75 to 84 and those 85 and older showed significantly steeper drops compared to those aged 65 to 74. Diabetes also played a role in delayed recall, where it was linked to a faster rate of decline. Depression, high blood pressure, and poor self-rated health were all tied to lower memory scores at baseline but, like loneliness, didn’t change the speed of decline.
Being female, reporting good health, staying physically active, and participating in social activities such as volunteering, attending clubs, or taking classes were all linked to higher baseline memory scores.
Geographic patterns also emerged. Southern European countries reported the highest rates of high loneliness, while northern and central regions reported the lowest. Southern and eastern countries also showed weaker baseline memory scores, though researchers cautioned against reading those gaps as proof that geography causes memory problems. Historical factors, including nutritional hardship during and after World War II when many of these older adults were children, and socioeconomic stress could help explain the difference.
Good Friends, Less Pain, and a Sense of Purpose: What Helps Older Adults Flourish
(PeopleImages.com – Yuri A/Shutterstock)
Getting older doesn’t have to mean a decline in mental health. A sweeping new study of 2,024 older Canadians found that roughly 74% weren’t just free of mental illness but were genuinely flourishing, reporting frequent happiness, life satisfaction, and a sense of purpose. That’s a far more optimistic picture of aging than most people expect.
But what separates seniors who thrive from those who struggle? Researchers from the University of Toronto and the Public Health Agency of Canada analyzed a nationally representative survey to identify which factors are most strongly linked to what psychologists call “complete mental health.” Going well beyond the absence of a diagnosis, the concept requires no mental illness, suicidal thoughts, or substance use problems over the past year, plus a mix of frequent happiness, meaning, and strong social and psychological well-being.
Published in PLOS ONE, the study drew its data from the 2022 Mental Health and Access to Care Survey, conducted by Statistics Canada. Researchers restricted their analysis to respondents aged 65 and older living across the country’s ten provinces.
How Researchers Defined Complete Mental Health
Qualifying as having complete mental health required clearing three bars at once: no mental illness, substance use disorder, or suicidal thoughts in the previous 12 months; feeling happy or satisfied with life almost every day in the past month; and regularly experiencing a range of positive feelings, including things like feeling useful, having purpose, and generally liking who they are. About 95% of older adults in the sample met the first criterion, while roughly 74% cleared the full, higher bar.
That gap matters. Nearly one in five older adults wasn’t technically ill but also wasn’t flourishing, and the study set out to understand what made the difference.
Social Bonds, Spirituality, and Complete Mental Health in Later Life
Social support stood out as one of the most powerful factors. Older adults who said they could count on others to help manage major stress were about twice as likely to achieve complete mental health compared to those who couldn’t. Being married or in a long-term partnership also made a meaningful difference, with partnered individuals showing roughly 33% higher odds of flourishing even after accounting for other factors.
Religious or spiritual beliefs played a stronger role than many might expect. Older adults who rated religion or spirituality as “very important” in daily life had about twice the odds of complete mental health compared to those who said it held no importance. Researchers note that faith communities may offer both social connection and a framework for finding meaning during hard times, two things consistently tied to better well-being in later life.
Physical health mattered enormously. Older adults who rated their own health as excellent had more than three times the odds of complete mental health compared to those who rated theirs as poor. Freedom from chronic pain, the ability to handle household tasks independently, and getting adequate sleep were all independently linked to better outcomes. Moderate physical activity in the week before the survey was tied to 24% higher odds of flourishing.
Older adults without a history of childhood adversity, including abuse or exposure to domestic violence, also fared better, still linked to higher odds of flourishing even after accounting for many other factors.
When a Difficult Past Leaves a Mark
A person’s mental health history proved to be among the strongest predictors of flourishing. Older adults who had never been diagnosed with generalized anxiety disorder had three times the odds of complete mental health, while those without a lifetime history of major depression had about 1.8 times the odds. Never having had a substance use disorder also boosted the likelihood of flourishing.
Men were more likely than women to report both no recent mental disorders and overall flourishing, though the study did not examine reasons for that difference.
Geography produced one of the more counterintuitive findings. Living in a large urban center was associated with 38% lower odds of complete mental health compared to rural living, a pattern that aligns with other research, which has suggested that factors like social isolation, noise, and air pollution may play a role.
Income produced mixed and unclear results. Higher earnings weren’t tied to flourishing once other factors were accounted for. More puzzling, those in the lowest income bracket actually had the highest rates of being free from mental disorders, outpacing higher earners, an unexpected pattern that runs counter to most prior research. Researchers flagged the finding as inconclusive and said it needs further study.
For years, ‘Pohlsepia mazonensis’ was believed to be the earliest known octopus, with what appeared to be eight tentacles, eyes, and possibly an ink sas
The fossil had decayed so much before it was preserved that it created a case of mistaken identity lasting over a decade. (Image credits: University of Reading)
For over 20 years, a fossil named ‘Pohlsepia mazonensis’ was celebrated as the world’s oldest known octopus, dating back roughly 300 million years. It even made its way into the Guinness Book of World Records, shaping how scientists understood the evolution of these intelligent sea creatures. But new research now reveals that this ancient marine animal has been misidentified all along.
The fossil, was discovered at the Mazon Creek site in Illinois, USA. For years, it was believed to be the earliest known octopus, with what appeared to be eight tentacles, eyes, and possibly an ink sac, features that perfectly matched modern octopuses.
Using cutting-edge synchrotron imaging, scientists were able to peer deep inside the fossil like never before. What they found changed everything- rows of tiny teeth that simply do not match an octopus.
Lead researcher Thomas Clements from the University of Reading explained, “We basically used a wide selection of new analytical techniques to discover hidden anatomical characteristics within the rock. And we were able to determine that it is not an octopus, but is actually a very decomposed nautiloid.”
The fossil had decayed so much before it was preserved that it created a case of mistaken identity lasting over a decade.
Octopuses typically have fewer teeth per row, but this fossil had 11, a clear sign it belonged to a different group altogether. Instead, researchers now say the creature is more closely related to a nautilus, a shelled marine animal that still exists today.
So how did experts misread it for decades? The answer lies in decay.
Before fossilisation, the animal’s body had already started breaking down, masking key features like its shell. What remained looked soft and sack-like, eerily similar to an octopus.
Solid, liquid, gas. Most people learn about three states of matter in school and leave it at that. But deep inside planets far larger than Earth, where pressures millions of times greater than anything on our surface squeeze atoms into forms that defy easy description, matter can enter states that don’t fit neatly into any of those categories.
Now, a team of researchers has predicted a carbon-hydrogen compound that, under crushing pressure and extreme heat, enters a state where hydrogen atoms move in a tightly constrained way, mostly along a single direction while simultaneously spinning within a flat plane, like beads twisting on a wire as they slide along it.
Published in Nature Communications, the study used computer simulations to map how a simple carbon-hydrogen compound behaves under the kinds of pressures found deep inside massive planets. What emerged was a newly predicted state of matter, one in which carbon atoms lock into a rigid, corkscrew-shaped crystal framework while hydrogen atoms move in this constrained, partially rotational way. Researchers called this a “quasi-1D superionic” phase, distinct from solids, liquids, plastics, and even the three-dimensional superionic states scientists have studied for years.
To understand why any of this matters, it helps to know a bit about superionic materials. In a superionic state, one type of atom forms a solid crystal while another flows through it almost like a liquid. Superionic water ice, for instance, has been produced in laboratory experiments under extreme pressure, with oxygen atoms staying locked in place while hydrogen moves freely in all directions. Scientists believe such materials exist deep inside ice giant planets, helping to generate their famously lopsided magnetic fields. In the newly predicted quasi-1D state, hydrogen’s movement is tightly constrained to one dominant axis combined with rotation in a plane, and that directional bias shapes how the material conducts electricity and heat.
A New State of Matter Built from Carbon and Hydrogen
Researchers Cong Liu, R.E. Cohen, and Jian Sun relied on computational methods rather than attempting to recreate planetary interiors in a laboratory, combining first-principles physics simulations with machine-learning tools that allowed them to model atomic interactions over longer timescales and larger systems than traditional approaches alone would permit.
Starting from the question of which carbon-hydrogen structures could remain stable under enormous pressures, the team identified a compound with equal parts carbon and hydrogen (written as CH) that holds together above roughly 1,000 gigapascals. At those pressures, electrons rearrange themselves in a way that makes the material electrically conductive. But the really surprising behavior only emerged when the simulations turned up the heat.
As temperature rose, the carbon atoms locked into a rigid, spiraling lattice shaped like a corkscrew. Hydrogen atoms, meanwhile, began rotating within a flat plane while simultaneously drifting along a single perpendicular axis, the spinning-and-sliding motion described above. As temperatures climbed further, hydrogen eventually broke free of those constraints and began moving in all three directions, entering a more familiar 3D superionic state. At even higher temperatures, the whole compound melted into a fluid. Simulations produced a phase diagram charting all four states: solid, quasi-1D superionic, 3D superionic, and fluid, mapped across rising pressure and temperature.
What Makes This Phase Unusual
Because hydrogen moves mainly along one axis while also rotating within a plane, the material’s ability to conduct electricity and heat depends heavily on direction. Conductivity along the primary axis of hydrogen flow is notably higher than in perpendicular directions. Electronic transport dominates the overall conductivity; the contribution from the mobile hydrogen atoms themselves turns out to be negligible by comparison.
Carbon’s framework structure in this compound is also striking in its own right. It is “chiral,” meaning it cannot be overlapped with its own mirror image, much like a left hand cannot be placed directly over a right. That property emerges naturally from the extreme conditions, producing a twisting scaffold through which hydrogen threads its path.
What This Means for Giant Planet Science
Carbon-hydrogen chemistry in extreme environments has attracted scientific interest for years, partly because methane (the simplest hydrocarbon) is abundant in the atmospheres of ice giant planets. Under pressure, methane breaks apart, potentially producing materials including diamond. What happens to simpler carbon-hydrogen compounds under even more extreme conditions has been less understood.
Among the states predicted in this study, the 3D superionic phase falls within temperature and pressure ranges that, according to existing models of Neptune’s interior, may be relevant to that planet. The quasi-1D phase, however, requires pressures more extreme than what’s expected inside Uranus or Neptune specifically. The researchers themselves note that those pressures are unlikely to occur in those particular planets, and they make no direct claim of planetary or magnetic modeling relevance for the quasi-1D state. More massive worlds, sub-Neptune exoplanets in particular, could plausibly reach the conditions where this phase would stabilize.
Rather than a prediction about what’s happening inside Uranus or Neptune right now, this is better understood as a new piece in the larger puzzle of how carbon and hydrogen behave under compression, and what that might mean for the interior dynamics of a wider class of planets far beyond our solar system.
Why Directional Transport Changes the Picture
Many models of how giant planets generate magnetic fields assume that interior materials conduct electricity and heat equally in all directions. A material that conducts primarily along one axis would behave very differently, potentially channeling energy and electric charge in preferred directions through a planet’s deep layers.
Uranus and Neptune already have strikingly unusual magnetic fields compared to Earth’s. While Earth’s field is relatively symmetric and roughly aligned with its rotation axis, those of Uranus and Neptune are tilted, offset from the planetary centers, and far more irregular. Understanding why demands better models of what planetary interiors are made of and how those materials move heat and electricity, and results like this one help fill in that picture.
No probe has ever descended into the deep layers of Uranus or Neptune, and laboratory experiments capable of reaching the pressures involved are still in their early stages. Computational predictions like this one serve as a roadmap, giving experimentalists targets to pursue and giving planetary scientists new physical mechanisms to test against future data. NASA has identified a Uranus orbiter and probe as a high priority for the coming decades, and work like this will shape what scientists know to look for.
Every day, millions of people reach for hand soaps, cleaning sprays, and laundry products stamped with the word “antibacterial,” believing they’re getting extra protection. A growing body of evidence suggests those added germ-killing chemicals aren’t just unnecessary in most household situations. According to a new viewpoint paper published in Environmental Science & Technology, they may help create conditions that make dangerous infections harder to treat.
Drug-resistant bacteria, often called superbugs, already kill more than one million people a year worldwide. That toll is projected to reach two million annual deaths by 2050. Global health efforts have mostly zeroed in on antibiotic overuse in hospitals and on farms, but an international team of researchers argues there’s a critically overlooked front in that fight: the bathroom sink, the kitchen counter, and the washing machine.
Corresponding author Miriam L. Diamond, a professor at the University of Toronto, and her co-authors make the case that germ-killing chemicals in everyday consumer goods are seeping into waterways, soils, and even drinking water, creating conditions that breed resistant bacteria. Their paper calls for action at every level, from international health policy down to individual shopping choices.
The Chemical in Antibacterial Soap Turning Up Everywhere
At the heart of the paper’s concern is a chemical called benzalkonium chloride, sometimes listed on product labels as ADBAC. It belongs to a family of compounds called quaternary ammonium compounds, or QACs, and it shows up in hand soaps, cleaning sprays, clothing, plastics, and personal care products. Researchers have detected it in a wide range of places, including wastewater, rivers, soils, and even drinking water. Human studies have found it in blood and breastmilk.
When bacteria encounter low-level, repeated doses of benzalkonium chloride, concentrations too weak to kill them outright, something troubling happens. Resistant species thrive, and those bacteria develop resistance not only to the cleaning chemical itself but to clinically important antibiotics as well, including fluoroquinolones, beta-lactams, and tetracyclines, drug classes that doctors rely on to treat serious infections. Lab studies and real-world field research have documented this across gym surfaces, sewage sludge, soil, and drinking water sources.
Bacteria pull off this trick through several shared defense mechanisms: molecular pumps that flush out toxic chemicals, changes to their outer membranes, and the ability to swap resistance genes with entirely different species. Once those defenses develop, they stick around long after the chemical exposure ends.
Other germ-killing ingredients in consumer products raise similar concerns. Chlorhexidine, for example, has been shown in lab studies to encourage resistance in a dangerous bacterium called Klebsiella pneumoniae to colistin, described in the paper as a last-resort treatment used when nearly every other antibiotic option has failed.
From Household Drains to Drinking Water
One of the more alarming pathways described in the paper traces these chemicals from household drains to wastewater treatment plants and back into the broader environment. About a quarter of QACs used globally each year enter the environment through disposal, discharge, or runoff. Most of the rest flow to wastewater treatment plants, which also receive waste from hospitals carrying heavy loads of germ-killing chemicals and resistant organisms.
At those facilities, the chemicals mostly bind to solid waste byproducts, but liquid discharges can still carry concentrations high enough to favor resistant bacteria. Wastewater plants are themselves recognized hotspots for resistance: dense, diverse bacterial populations mingling under chemical stress create conditions that can help microbes trade resistance genes with one another. When contaminated solid waste is then spread on agricultural land, a common practice, the chemicals move into soils and surface waters, extending the problem further. Benzalkonium chloride is particularly persistent in waterway sediments because it binds tightly to particles, shielding it from breaking down.
Antibacterial Soap Offers No Clear Added Benefit Over Regular Soap
Perhaps the most uncomfortable conclusion in the paper is that many of these germ-killing products offer no clear added public health benefit in most everyday settings. Major health authorities, including the U.S. Food and Drug Administration, the U.S. Centers for Disease Control and Prevention, and the World Health Organization, already recommend plain soap and water over antibacterial soap for consumers, citing a lack of added benefit alongside concerns about ingredient toxicity and resistance.
Antibacterial laundry sanitizers land in the same category. According to the paper, disinfection is not necessary for routine household laundering, and ordinary detergent combined with hot water removes most microbes from fabrics just fine. Consumers are paying extra for products laced with chemicals that provide no safety advantage but quietly contribute to a worsening global health crisis.
A Four-Part Plan to Curb Antibacterial Overuse
Diamond and her co-authors lay out a four-part response. At the international level, they argue that global resistance frameworks should set explicit targets for reducing unnecessary germ-killing chemicals in consumer products and expand monitoring to track these compounds in wastewater and surface waters.
Nationally, governments should restrict germ-killing ingredients in household products where evidence of effectiveness is weak and resistance potential is clear. Worth noting, the United Kingdom has already introduced a private members’ bill to Parliament that would restrict antimicrobials in consumer goods. Public awareness campaigns should also correct widespread misconceptions about whether antibacterial products are actually necessary for daily hygiene.
On the industry side, the authors call for levies on environmentally persistent germ-killing chemicals as an economic push toward safer formulations. At the individual level, when genuine disinfection is needed at home, hydrogen peroxide and alcohol-based products can achieve similar or better germ-killing results in many situations, with shorter contact times and a lower demonstrated potential to drive resistance.
The true cost of middle-class living is doubling every eight years
In a darkened control room in Navi Mumbai, 100 operators oversee bots monitoring 30,000 ATMs across India.
Their cameras, sensors and bots do the work that 60,000 security guards once did.
That control room is a small window into something much larger.
Across India, the quiet machinery of automation has been reshaping – and in many cases, eliminating – the jobs that the middle class was built on. And the middle class is only now beginning to reckon with what that means.
As stable incomes come under pressure, many are turning to riskier ways of making money to bridge the gap.
Consider VS, a 27-year-old BTech graduate from a small town near Bhilwara city in western Rajasthan state. He earns 14,000 rupees ($151; £113) a month as a freelance salesperson.
Last year, he lost 1.3m rupees – nearly his entire family’s savings – trading Futures and Options (F&O) on the stock market. He is one of nine million Indians doing the same thing – and are collectively losing over $12bn a year. That figure is roughly equal to the federal government’s entire annual education budget.
These are not gamblers. They are educated, aspirational people with nowhere else to put their ambitions.
Or consider Rahul Singh, a delivery agent with a food delivery app. Singh explained that he borrowed money not just to finance his home renovation, which is a discretionary spend, but also for “covering essential expenses, such as rent, medical bills and any other unforeseen expenses, which were critical for survival”.
VS and Singh come from different layers of India’s vast middle class and they are socially and economically different. But their predicament is anything but different.
These are not cautionary tales about individual failure. They are portraits of a class under pressure – the 40 million income taxpayers who earn between 500,000 ($5,283; £3,969) and 10m rupees annually, and who form the productive core of the Indian economy.
Something is going wrong for them, as we discovered while researching our new book, and it is happening on multiple fronts at once.
White-collar job creation – the kind of employment that an engineering or commerce degree was supposed to guarantee – has fallen from 11% growth before 2020 to just 1% today, according to Naukri Jobspeak Index.
The decline didn’t begin with AI. Automation had been hollowing out middle-skill work since the early 2000s, quietly eliminating the clerical roles, bookkeeping jobs and sales positions that once absorbed India’s graduates.
But AI has dramatically accelerated the disruption. India’s IT services sector – the country’s largest graduate employer with eight million workers – is in active retrenchment.
The government’s own planning body, Niti Aayog, estimates that by 2031, AI could eliminate close to three million IT and customer service jobs. The CEOs of India’s most profitable companies speak openly to us about using AI to cut salary bills by a third.
At one large private bank, a single AI tool now handles 95% of customer queries that once required a 3,000-strong call centre team.
Into this contracting market, eight million new graduates arrive every year.
The results are becoming hard to ignore. At IIT Bombay – one of India’s top technology institutes that was once a near-guaranteed passport to prosperity – fresh graduates are leaving with lower salaries than their predecessors.
Across IITs nationally, 8,000 of 21,500 graduates remain unemployed. The IIT degree, long India’s most coveted credential, is beginning to look less like a golden ticket and more like a lottery.
Even for those who find work, something has quietly gone wrong with the economics of middle-class life.
Over the past decade, the average middle-class income taxpayer’s annual income has grown by around 50,000 rupees – roughly the price of a decent smartphone. In isolation, that sounds like progress. Against the actual cost of living, it is a slow erosion.
Recent research shows a vegetarian thali (an Indian meal comprising several small dishes) now costs 11% more each year, an entry-level car or motorcycle rises by 7 to 8% annually and medical costs climb at 14%.
Our estimate – based on spending patterns for typical middle-class households across rent (10-13%), food (7-9%), healthcare (around 14%) and education (8-10%) – suggests that the true cost of living is doubling roughly every eight years, implying an effective inflation rate of about 9% for this group.
A family that lived comfortably on 1m rupees in 2016 would now need close to 2m a year.
Their salary, in most cases, has barely moved. The middle class is on a treadmill, and every year the belt speeds up.
The debt is real, and it is growing.
The gap between what people earn and what life costs has to be filled somehow. Increasingly, it is being filled with borrowed money. India’s non-housing household debt as a share of income now exceeds that of the United States and China.
Nearly half of all Indian families have taken personal loans; 67% of borrowers had their first loan before the age of 30. For those carrying debt, nearly 40% of annual income goes to servicing it.
This borrowing isn’t building anything. It is financing holidays, smartphones, school fees and hospital bills – consumption and survival, not investment.
Between 5% to 10% of retail borrowers are caught in what lenders call a debt trap: taking new loans to pay old ones, with no clear exit.
In western Pune city’s Hinjewadi tech park, young engineers with degrees and debt queue up each morning for walk-in interviews at BPO firms, hoping to land data entry jobs paying 18,000 rupees a month. This is what the compression looks like at ground level.
The consequences are rippling outward.
FMCG volume growth has dropped from 11% some 14 years ago to 3% today. Car sales are stagnant. Consumer durables growth has collapsed from 11% to 1-2%.
When we speak with the leadership of India’s largest consumer companies, there is a particular expression – stunned, a little lost – that keeps appearing. The Indian consumer, they are slowly realising, has stopped spending. Not as a lifestyle choice but because they can’t – after a brief, post-Goods and Services Tax (GST)-cut burst of spending that now appears to be fading.
This matters beyond household balance sheets. Consumption accounts for 60% of India’s GDP. India’s post-1991 growth model was built on a specific and elegant logic: middle-class spending creates demand, demand creates jobs, jobs create more spending. A virtuous cycle, three decades in the making. That cycle has broken.
Nobody taught Ayumu to make a drum. Nobody taught him to keep a beat. Yet for more than two years, the 23-year-old chimpanzee living at a research center in Japan has been prying wooden floorboards off a walkway, repurposing them as percussion instruments, and staging structured, multi-part rhythmic performances. He is, as far as researchers know, part of a rare documented case of a chimpanzee repurposing objects as instruments and using them in extended, organized displays, and what he does with that instrument may offer clues about how human music evolved.
Where music came from is one of the more genuinely open questions in human evolutionary science. One leading theory holds that rhythmic sound-making grew out of older, emotion-driven vocal behaviors common across primates, a kind of ancient shared root between calling out and playing music. Ayumu’s behavior, spontaneous and untrained, offers a behavioral case that, for the first time, offers a behavioral case that brings together tool use, rhythm, and emotional expression in a way rarely documented in non-human animals.
Researchers at Kyoto University’s Center for the Evolutionary Origins of Human Behavior documented his performances over more than two years and published their findings in the Annals of the New York Academy of Sciences.
How Ayumu Invented His Own Chimpanzee Drumming Tool
Observations ran from February 2023 to March 2025. Whenever Ayumu’s displays could be heard, researchers filmed the sessions. Over the study period, they captured 89 distinct sequences across 37 observation days.
At least twice, Ayumu was filmed removing floorboards from the corridor walkway himself, meeting the scientific definition of tool-making. No other chimpanzee in the group consistently did the same. He had prior experience with electronic keyboards and touch panels at the center, but had never received any training in drumming or rhythm production. He arrived at this behavior entirely on his own.
Each recorded sequence was broken down into its parts: tool-assisted drumming, bodily drumming against a wire fence, object dragging, object rocking, walkway running, and object throwing. Two trained observers coded the footage independently and reached a strong reliability score. Statistical analyses then asked a simple question: was the order in which Ayumu moved through those behaviors random, or did it follow a pattern?
What Researchers Found in Ayumu’s Chimpanzee Drumming Displays
Ayumu’s sequences were not random. Two transitions occurred far more often than chance would predict: drumming consistently led to dragging, and dragging consistently led to throwing. That progression, from slow heavy percussion to rapid scraping to a climactic throw, resembles the introduction-development-climax structure of the pant-hoot, the chimpanzee’s signature long-distance call. In wild chimpanzees, object throwing is typically associated with the vocal peak of a pant-hoot, and the same pattern appeared here. Ayumu’s sequence closely resembled what pant-hoots do vocally.
His rhythm also held up under scrutiny. Analysis of the timing between drum hits showed that Ayumu favored a steady, even beat rather than random or erratic intervals. A regular beat is one of the most consistently documented features of human music across every culture ever studied. His sequences ran between two and fourteen distinct components each, with the whole performance sometimes lasting several minutes, far longer than the few seconds of drumming typically observed in wild chimpanzees.
When Ayumu drummed with the fabricated floorboard rather than his bare hands and feet, his rhythm was measurably more consistent. Studies of human drummers have found similar patterns. Tapping with sticks produces a more stable rhythm than tapping with fingers alone.
A Drummer Who Grins While He Plays
Perhaps the most unexpected detail was what was happening on Ayumu’s face. During many sessions, he displayed what primatologists call a play face, a relaxed open-mouthed expression associated with positive, non-aggressive arousal. On a handful of occasions, he also showed a silent bared teeth expression, typically linked to friendly, tension-reducing social signals. Neither expression had previously been documented during pant-hoot displays.
Researchers noted that “Ayumu’s drumming suggests not only a display, but also the experience of intrinsically positive emotions associated with the production of sounds, similar to human musical performance.” Research on human music across cultures has found that musical performance frequently expresses high-arousal, positive emotional states. Ayumu’s face during his performances fits that same profile.
Ayumu is the alpha male of his group of 11 adult chimpanzees, a social position researchers note may have contributed to his repeated use of loud, conspicuous drumming as a display. No other chimpanzee in the group adopted the same behavior consistently throughout the study.
That Fitness App May Not Be So Healthy After All, Especially For Teens
For most teenagers, a smartphone is as essential as a backpack. It’s how they talk to friends, follow trends, and increasingly, track what they eat and how much they exercise. But a sweeping new review of 35 studies covering more than 52,000 people, with an average age of just 17, finds that compulsive phone habits in young people may be closely tied to disordered eating, body dissatisfaction, and emotional overeating.
Published in JMIR Mental Health by researchers at King’s College London, the systematic review found a consistent association between problematic smartphone use and higher scores on eating disorder symptom tests across age groups and more than a dozen countries.
One longitudinal study within the review added a sharper edge to the findings: young people with higher problematic phone use at the outset developed more severe eating disorder symptoms a year later, but the reverse was not true. Eating disorder symptoms at baseline did not predict worsening phone dependency down the road.
Eating disorders affect roughly 8% of women and 2% of men over their lifetimes, with onset typically occurring in adolescence or young adulthood. Many more young people experience disordered eating without a formal diagnosis, with studies estimating that around 22% of adolescents show some form of problematic eating behavior.
Why Teens Are Especially Vulnerable to Smartphone-Linked Eating Disorders
Adolescence is a period when identity is still forming, and social comparison plays a major role in how young people see themselves. Smartphones provide a constant, frictionless channel for that comparison. As Dr. Johanna Keeler, the study’s first author and a Visiting Lecturer at King’s College London’s Institute of Psychiatry, Psychology and Neuroscience, explained: “Adolescence is a key stage of development as individuals evolve their sense of self by observing others. While smartphones might present an easy way for this to happen, being consistently exposed to idealised images can lead them to compare their own appearance with these ‘standards’, leading to poor self-esteem and appearance dissatisfaction, both risk factors for the development of an eating disorder.”
About one in four young people meet the criteria for what researchers call problematic smartphone use, or PSU, a pattern of phone dependency that resembles behavioral addiction. PSU involves an inability to cut back, constant preoccupation with the device, and withdrawal-like symptoms such as anxiety or restlessness when the phone is unavailable. It has already been tied to depression, anxiety, poor sleep, and reduced face-to-face social connection in young people. This review asked whether disordered eating belongs on that list. In the vast majority of included studies, the answer was yes.
It’s worth noting that most studies were observational snapshots rather than long-term trials, which means they can identify a relationship between phone habits and eating disorder symptoms but cannot prove one causes the other. The findings also apply mainly to young people without a formal eating disorder diagnosis.
The Seven-Hour Mark and What It May Mean for Young People
Screen time stood out across several studies. One study examining screen time categories found that young people using their phones for seven or more hours a day showed significantly higher odds of screening positive for disordered eating compared to those using them for around two hours. Users logging three to six hours daily did not show the same elevated risk, suggesting the relationship may become more pronounced at very high levels of use. Higher screen time was also tied to greater body dissatisfaction in multiple studies.
That said, screen time findings came from a relatively small number of studies within the review, and the overall quality of evidence was rated low by the research team due to study design limitations. The seven-hour figure is a signal worth watching, not a hard line.
Calorie Apps, Fitness Trackers, and the Hidden Risk for Teens
Social media’s connection to body image problems in young people is well established. Less examined is the role of calorie-tracking and fitness apps. Researchers note that behaviors central to eating disorders, including compulsive calorie counting, over-exercising, and obsessive body checking, are directly enabled by popular smartphone apps. Built around features designed to maximize engagement, daily streaks, push notifications, gamified progress bars, these tools could make it easier for vulnerable young users to monitor food and exercise in ways that tip from healthy habit into harmful obsession.
The study’s senior author, Professor Ben Carter of King’s College London, put the broader concern plainly: “Smartphones have become ubiquitous in our everyday lives. It is apparent from our study that, even for people without a diagnosis of an eating disorder, the overuse of a smartphone is associated with poor body satisfaction and altered eating behaviours, and is a potential source of distress.”
The authors also suggest that recommendation algorithms may amplify the problem. Platforms learn from user behavior and surface more of what keeps a person engaged. For a teenager already preoccupied with food or body image, that could quietly steer feeds toward thin-ideal imagery, extreme fitness content, and restrictive diet culture, without the user ever deliberately seeking it out. These are proposed mechanisms rather than findings measured directly in the studies, but they align with what broader research on social media and young people has shown.
That Fitness App May Not Be So Healthy After All, Especially For Teens
For most teenagers, a smartphone is as essential as a backpack. It’s how they talk to friends, follow trends, and increasingly, track what they eat and how much they exercise. But a sweeping new review of 35 studies covering more than 52,000 people, with an average age of just 17, finds that compulsive phone habits in young people may be closely tied to disordered eating, body dissatisfaction, and emotional overeating.
Published in JMIR Mental Health by researchers at King’s College London, the systematic review found a consistent association between problematic smartphone use and higher scores on eating disorder symptom tests across age groups and more than a dozen countries.
One longitudinal study within the review added a sharper edge to the findings: young people with higher problematic phone use at the outset developed more severe eating disorder symptoms a year later, but the reverse was not true. Eating disorder symptoms at baseline did not predict worsening phone dependency down the road.
Eating disorders affect roughly 8% of women and 2% of men over their lifetimes, with onset typically occurring in adolescence or young adulthood. Many more young people experience disordered eating without a formal diagnosis, with studies estimating that around 22% of adolescents show some form of problematic eating behavior.
Why Teens Are Especially Vulnerable to Smartphone-Linked Eating Disorders
Adolescence is a period when identity is still forming, and social comparison plays a major role in how young people see themselves. Smartphones provide a constant, frictionless channel for that comparison. As Dr. Johanna Keeler, the study’s first author and a Visiting Lecturer at King’s College London’s Institute of Psychiatry, Psychology and Neuroscience, explained: “Adolescence is a key stage of development as individuals evolve their sense of self by observing others. While smartphones might present an easy way for this to happen, being consistently exposed to idealised images can lead them to compare their own appearance with these ‘standards’, leading to poor self-esteem and appearance dissatisfaction, both risk factors for the development of an eating disorder.”
About one in four young people meet the criteria for what researchers call problematic smartphone use, or PSU, a pattern of phone dependency that resembles behavioral addiction. PSU involves an inability to cut back, constant preoccupation with the device, and withdrawal-like symptoms such as anxiety or restlessness when the phone is unavailable. It has already been tied to depression, anxiety, poor sleep, and reduced face-to-face social connection in young people. This review asked whether disordered eating belongs on that list. In the vast majority of included studies, the answer was yes.
It’s worth noting that most studies were observational snapshots rather than long-term trials, which means they can identify a relationship between phone habits and eating disorder symptoms but cannot prove one causes the other. The findings also apply mainly to young people without a formal eating disorder diagnosis.
The Seven-Hour Mark and What It May Mean for Young People
Screen time stood out across several studies. One study examining screen time categories found that young people using their phones for seven or more hours a day showed significantly higher odds of screening positive for disordered eating compared to those using them for around two hours. Users logging three to six hours daily did not show the same elevated risk, suggesting the relationship may become more pronounced at very high levels of use. Higher screen time was also tied to greater body dissatisfaction in multiple studies.
That said, screen time findings came from a relatively small number of studies within the review, and the overall quality of evidence was rated low by the research team due to study design limitations. The seven-hour figure is a signal worth watching, not a hard line.
Calorie Apps, Fitness Trackers, and the Hidden Risk for Teens
Social media’s connection to body image problems in young people is well established. Less examined is the role of calorie-tracking and fitness apps. Researchers note that behaviors central to eating disorders, including compulsive calorie counting, over-exercising, and obsessive body checking, are directly enabled by popular smartphone apps. Built around features designed to maximize engagement, daily streaks, push notifications, gamified progress bars, these tools could make it easier for vulnerable young users to monitor food and exercise in ways that tip from healthy habit into harmful obsession.
The study’s senior author, Professor Ben Carter of King’s College London, put the broader concern plainly: “Smartphones have become ubiquitous in our everyday lives. It is apparent from our study that, even for people without a diagnosis of an eating disorder, the overuse of a smartphone is associated with poor body satisfaction and altered eating behaviours, and is a potential source of distress.”
The authors also suggest that recommendation algorithms may amplify the problem. Platforms learn from user behavior and surface more of what keeps a person engaged. For a teenager already preoccupied with food or body image, that could quietly steer feeds toward thin-ideal imagery, extreme fitness content, and restrictive diet culture, without the user ever deliberately seeking it out. These are proposed mechanisms rather than findings measured directly in the studies, but they align with what broader research on social media and young people has shown.
Emotion Regulation: The Missing Piece
Several studies in the review pointed to difficulty managing emotions as a key connector. Young people who struggle to handle emotional distress are both more likely to reach for their phones compulsively and more vulnerable to disordered eating. PSU may function as a coping strategy that backfires: phones get used to soothe anxiety or sidestep negative feelings, but the habit may gradually erode emotional resilience and deepen exposure to triggering content.
In one study, disrupted sleep was linked to greater emotional distress and worse eating behavior, with heavy phone use acting as a connecting factor between them. For teenagers already navigating the pressures of adolescence, that chain reaction may be especially difficult to interrupt.
(Photo by Unsplash+ in collaboration with Getty Images)
6 in 10 Adults Don’t Lift Weights, but New Research Says Almost Any Routine Works
Six out of every ten American adults do zero strength training. A new analysis of more than 30,000 people suggests that overcomplicated advice may be one reason, and that the science of lifting weights may be far simpler than much of the fitness industry suggests.
Published in Medicine & Science in Sports & Exercise, the new position stand from the American College of Sports Medicine synthesizes 137 systematic reviews to produce the most evidence-based update to resistance training guidelines in nearly two decades. On a long list of training assumptions that have made strength work feel inaccessible to ordinary people, the analysis finds that many of them do not consistently hold up.
Regular strength work is tied to lower risks of cardiovascular disease, cancer, and diabetes, alongside measurable reductions in depression and better sleep quality. With only about 30 percent of American adults meeting minimum muscle-strengthening guidelines, those benefits are being left unclaimed on a massive scale.
Why Strength Training Advice Got So Complicated
Researchers at McMaster University led the analysis, pulling data from six major academic databases through October 2024. Studies ranged from first-time lifters to experienced athletes across all adult age groups, producing a dataset large enough to evaluate which training variables actually drive results and which ones have coasted on reputation.
Previous guidelines from 2009 leaned heavily on specific, detailed protocols, and some critics have argued that following them fully could require upwards of 20 hours of training per week. For most working adults, that is not an inconvenience. It is a dealbreaker. As the authors write, “we propose that individualizing programs to increase RT participation is, from our perspective, more important than conforming to specific RTx criteria outlined in previous Position Stands.” In other words, getting people lifting in whatever way fits their lives matters more than optimizing every detail of how they do it.
The evidence behind that shift is substantial. Training to complete muscular failure, the point at which another repetition is physically impossible, is not necessary for gains in strength, muscle size, or power. Stopping two to three reps short produces similar results in most cases, and potentially less strain. Free weights versus machines makes no meaningful difference in strength outcomes. Periodization, morning versus evening training, rest periods between sets, time under tension, and specialized techniques like drop sets did not consistently show clear advantages across studies. Coaching philosophies and bestselling fitness books have been built on these variables for decades. The evidence, drawn from more than 30,000 participants, does not consistently support them.
What Strength Training Research Actually Supports
Some variables do matter, and the analysis is specific. For maximum strength, heavier loads of at least 80 percent of a person’s one-rep max outperform lighter approaches. Two to three sets per exercise, at least two sessions per week, a full range of motion, and placing strength work at the start of a session rather than the end all produced consistent positive effects.
For muscle growth, at least ten sets per muscle group per week, with an emphasis on the lowering phase of each movement, produced the strongest results. For power, moderate loads between 30 and 70 percent of maximum, combined with intentionally fast lifting on the way up, were most effective.
Progressive overload, gradually increasing the challenge placed on a muscle over time, remains a foundational principle. Critically, this does not require constantly adding weight to the bar. More volume, adjusted frequency, or simply maintaining consistent effort as strength improves can all accomplish the same thing.
Why Almost Any Resistance Training Beats Doing Nothing
Elastic bands, home workouts, and circuit training all produced significant improvements in strength, muscle size, endurance, balance, and physical function compared with no exercise. Someone doing twice-weekly resistance band workouts in their living room is capturing most of what resistance training has to offer, and is well ahead of someone with a theoretically perfect program they never actually start.
Safety concerns, a well-documented reason many older adults avoid strength training altogether, are not strongly supported by current evidence. An analysis of more than 38,000 participants found that resistance training did not raise the risk of serious adverse events, and nonfatal cardiovascular complications occur substantially less often during weight training than during aerobic exercise. For healthy adults of any age, the risk profile is favorable.
Are multivitamins really good for longterm health? (Photo by Fida Olga on Shutterstock)
A pill that tens of millions of Americans already take every morning may do something scientists have long hoped to prove: slow the biological clock ticking inside their cells.
A large randomized clinical trial published in Nature Medicine found that adults who took a daily multivitamin-multimineral supplement for two years showed measurably slower biological aging compared to those who took a placebo. Researchers tracked the effect using epigenetic clocks, molecular tools that read chemical marks on DNA to estimate how fast a person’s body is aging, independent of how many birthdays they’ve had.
The effect was modest, not dramatic. But in a field where most anti-aging research involves extreme interventions like severe caloric restriction or experimental drugs, the idea that an over-the-counter multivitamin could register a detectable change in the biology of aging is worth taking seriously.
What Epigenetic Clocks Actually Measure
As people age, chemical tags accumulate on their DNA in predictable patterns. Scientists have learned to read those patterns as a kind of biological age, one that can differ meaningfully from a person’s actual age. Two 70-year-olds can look quite different at the cellular level. One’s cells may behave like those of a 65-year-old; the other’s may behave more like those of a 75-year-old. Those differences are linked to real health outcomes, including cognitive decline, cancer risk, and cardiovascular disease.
Researchers focused on two well-validated epigenetic clocks, PCGrimAge and PCPhenoAge, both trained to predict mortality and disease risk rather than simply estimate age. Adults taking a daily multivitamin-multimineral supplement, specifically Centrum Silver, showed a slower rate of increase on both measures over two years. Over that period, the difference translated to roughly two and a half to five months of reduced biological aging compared to placebo. That’s a small number, but it’s a number produced by a supplement most older Americans can walk into any pharmacy and buy for under $20.
Who Benefited Most From Daily Multivitamin Use
The data held a particularly interesting finding for people who were already aging faster than their chronological age at the start of the study. Among participants whose biological age was running ahead of their actual age, the multivitamin’s effect was considerably stronger than it was in the rest of the group. For those with the most accelerated biological aging at baseline, the slowing effect on PCGrimAge was considerably stronger than it was for participants whose biological age was tracking normally, while those in the normal or decelerated range saw little to no benefit at all.
A pattern in the nutritional data may help explain why. Participants with accelerated biological aging tended to have lower levels of key nutrients like folate and lutein at baseline, and multivitamin use appeared to raise those levels over time. One reasonable interpretation: when nutritional gaps are quietly driving faster cellular aging, filling them in may ease some of that biological strain. Since COSMOS participants were generally healthy older adults, the benefit could be even more pronounced in populations with poorer diets or greater nutritional deficiencies.
The trial also tested cocoa extract, rich in compounds called flavanols that have shown cardiovascular benefits in other research. Despite earlier lab-based signals that flavanols might influence DNA methylation, the cocoa extract had no meaningful effect on any of the five epigenetic clocks tested. The researchers suggested that its cardiovascular benefits, which have been documented in the broader COSMOS trial, may operate through biological pathways that these particular aging clocks don’t capture.
How The Multivitamin Study Was Run
The findings come from COSMOS, a large randomized, double-blind, placebo-controlled trial that enrolled more than 21,000 adults across the United States. For this specific analysis, 958 participants, women 65 and older and men 60 and older, were randomly selected for DNA methylation testing, with blood samples drawn at the start of the study and at one and two years of follow-up. Their average age was 70, and roughly half were women. Compliance was high throughout, with more than 91 percent of the multivitamin group still taking the supplement as directed at the two-year mark.
Five epigenetic clocks were evaluated in total. Statistically significant slowing appeared only in the two second-generation clocks, PCGrimAge and PCPhenoAge, though trends in the right direction were visible across most of the others. The third-generation clock, DunedinPACE, which measures the speed of biological decline across multiple organ systems, showed a nonsignificant trend toward slowing in the multivitamin group as well.
Low Testosterone May Worsen Fructose-Related Fatty Liver Risk
Most men past 40 have heard that testosterone drops with age. What far fewer know is that declining testosterone may increase vulnerability to fat buildup in t
he liver, especially in men who regularly drink sodas, fruit juices, or other high-fructose beverages.
New research in mice shows the combination of low testosterone and high fructose intake does something neither condition manages on its own: a rapid acceleration of fat buildup in the liver. That finding matters for a lot of men. Roughly 5.58 million Americans between the ages of 40 and 79 currently live with both low testosterone and excessive fructose consumption at the same time. Most likely don’t realize they fall into that overlap, and few conversations about low testosterone include any discussion of liver health.
Published in the American Journal of Physiology: Endocrinology and Metabolism, the study also uncovered a previously unrecognized piece of the puzzle. Changes in gut bacteria that cause a compound called pyruvate to accumulate and promote fat buildup in liver cells.
Low Testosterone and High Fructose Are Both More Common Than Men Realize
Testosterone begins declining gradually after a man’s 30s. About 17% of men between 40 and 79 meet the clinical definition of low testosterone, with symptoms often mistaken for normal aging: fatigue, abdominal weight gain, reduced muscle tone. What rarely enters that conversation is what low testosterone does to the liver, and how diet makes it worse.
At the same time, an estimated 43% of Americans consume more sugar than health guidelines recommend. Fructose, found in sodas, energy drinks, packaged snacks, and fruit-flavored beverages, is processed almost entirely by the liver. When it arrives in excess, the liver converts it into fat. Both low testosterone and high fructose intake are recognized risk factors for fatty liver disease, a condition estimated to affect about 30% of people worldwide. Their combined effect, however, had never been directly studied until now.
What Researchers Found When Both Risk Factors Were Combined
Researchers at Osaka Metropolitan University divided male mice into six groups. Some were surgically castrated to eliminate testosterone, while others underwent a sham procedure that left hormone levels intact. Within each group, mice received plain water, a 10% fructose solution comparable to many common soft drinks, or fructose water plus antibiotics to suppress gut bacteria. After eight weeks, the results were telling.
Castration alone did not significantly increase liver fat. Fructose alone produced only a modest, borderline rise. Combining both conditions drove liver fat and cholesterol levels well beyond what either factor caused independently, and histological analysis confirmed fatty changes in the liver that were absent in the other groups.
Liver enzymes that typically signal cell damage remained normal even in the worst-affected mice. That means the liver was accumulating fat silently, at an early stage before serious or irreversible damage sets in. Early fatty liver disease often produces no symptoms at all, which is precisely what makes it easy to miss.
How Gut Bacteria Drive the Damage
One of the more revealing results came from the antibiotic-treated mice. Animals that received both castration and fructose alongside antibiotics showed substantially less liver fat than those without the drugs. Since antibiotics suppress gut bacteria, that outcome pointed directly to the microbiome as a key driver.
Analysis of the bacteria living in the gut confirmed that the combination of castration and fructose shifted gut microbial composition in ways that neither condition produced alone. Measurements of chemical byproducts in the cecum, a pouch in the gut where many bacterial compounds collect, showed that levels of a molecule called pyruvate were significantly elevated only in the combined group. Antibiotic treatment brought those levels back down.
Pyruvate sits at a metabolic crossroads. Under normal conditions, gut bacteria convert it into other compounds and clear it efficiently. In the combined condition, certain bacterial species responsible for that conversion appeared less active, allowing pyruvate to accumulate and potentially influence liver metabolism. To confirm that pyruvate could directly drive fat accumulation, the team cultured isolated mouse liver cells with pyruvate, fructose, or both. Neither compound alone caused significant fat buildup. Together, they produced a sharp, statistically significant surge in fat inside the cells. As the researchers noted, this is “the first study to investigate the effects of pyruvate on the steatosis of primary hepatocytes.”
Pyruvate’s role here is worth pausing on. It has long been studied as an energy molecule, not a driver of liver disease. If further research confirms that gut-derived pyruvate contributes to fatty liver in humans, it could point toward a new and largely overlooked target for treatment, one tied directly to the bacterial landscape of the gut.
Separately, the researchers found that gene activity inside the liver itself also changed in the combined group, with genes governing fat production and fructose processing ramping up in ways that antibiotics did not reverse. That suggests the gut-pyruvate pathway is only part of the story, and that low testosterone and fructose together alter liver function through more than one route.
Severe COVID-19 raises lung cancer risk by 24%, study of 76 million Americans finds
Surviving a severe case of COVID-19 or influenza feels like crossing a finish line. Fever breaks, oxygen levels stabilize, and eventually life returns to normal. A major new study published in the journal Cell suggests that for people who were hospitalized with either virus, recovery may not be the clean ending it appears to be. Deep inside the lung tissue, the infection may leave behind a biological imprint that silently raises the risk of cancer later on.
Researchers at the University of Virginia, along with colleagues at the University of Pittsburgh, Mayo Clinic, and Cedars-Sinai Medical Center, analyzed de-identified health records from nearly 76 million American adults. People hospitalized with severe COVID-19 had roughly a 24 percent higher risk of subsequently developing lung cancer compared to people who had never been infected. That elevated risk held up after researchers accounted for smoking history, age, sex, and a range of pre-existing conditions. Severe COVID-19 was independently associated with higher lung cancer risk. People with mild or moderate COVID-19, by contrast, showed a modest decrease in lung cancer diagnoses, a contrast that makes the severity distinction difficult to dismiss.
The human data is correlational, meaning it cannot prove that infection directly causes cancer, and the observation window is still relatively short. But the association persisted after accounting for every major known risk factor the researchers could measure.
What the team set out to understand was not just whether the risk was real, but why. Their answer points to something the lungs carry long after the virus is gone.
How Severe COVID-19 and Flu Raise Lung Cancer Risk
To trace the mechanism, researchers infected mice with either SARS-CoV-2 or influenza A, allowed them to fully recover, and then introduced lung tumor cells. Previously infected animals consistently developed larger, faster-growing tumors and died sooner than mice that had never been infected. The pro-tumor effect from influenza was still detectable four months after the initial infection.
What the infection left behind was not the virus itself. Using a technique that maps which regions of DNA are switched on or off, the team found that severe respiratory infections produced durable changes in multiple types of lung cells, including immune cells, structural cells, and the cells lining the airways. Those changes caused the lungs to keep overproducing a protein called G-CSF long after recovery. G-CSF is a recruiting signal for neutrophils, white blood cells that normally arrive during infection, do their job, and leave.
In the post-viral lung, a specific subset of neutrophils accumulated in large numbers and stayed. Rather than protecting the host, they suppressed anti-tumor immune responses and made it easier for tumor cells to grow. At the same time, the immune system’s dedicated cancer killers, called CD8 T cells, were functionally weakened. Fewer were producing the proteins needed to destroy tumor cells.
The Biological Scar Behind the Lung Cancer Link
A central question was whether this altered immune state was a local lung phenomenon or a body-wide change. Researchers answered it by surgically joining the circulatory systems of two mice so they shared a bloodstream. When a previously infected mouse was paired with a healthy one, the abnormal neutrophil buildup in the infected animal’s lung tissue persisted. Healthy immune cells flowing in from the uninfected partner did not fix it. The lung had been changed on its own terms, independent of the rest of the body.
When researchers directly gave G-CSF to healthy, never-infected mice, those animals developed the same abnormal neutrophil buildup and showed faster tumor growth. Blocking the G-CSF signal in previously infected mice reduced the problematic neutrophils and slowed cancer progression. The protein driving all of this was not a remnant of the virus. It was being produced by a lung that the infection had durably rewired.
How COVID and Flu Vaccines May Reduce Lung Cancer Risk
Mice vaccinated against SARS-CoV-2 with an mRNA spike vaccine before virus exposure were fully protected from serious illness. When those vaccinated animals were later challenged with tumor cells, they showed substantially lower tumor burden than unvaccinated animals that had experienced full infection. A parallel experiment using an inactivated influenza vaccine produced the same result.
Severity mattered even in unvaccinated animals. Mice exposed to low doses of either virus, enough to cause only mild disease, did not show a meaningful increase in tumor burden. It was severe infection, the kind involving major lung inflammation, that drove the reprogramming. Vaccines, in these models, appeared to block not just the acute illness but the cancer-related consequences that followed it.
A Drug Combination That Reversed Post-Viral Tumor Growth
On the treatment side, researchers tested two drugs in post-COVID tumor-bearing mice. Reparixin, which blocks neutrophil recruitment, reduced the problematic neutrophils and partially decreased tumor burden. An antibody targeting PD-L1, a protein tumors use to hide from immune attack, produced modest improvement on its own. Together, the two drugs worked considerably better: tumor burden dropped, cancer-killing T cells increased inside tumor tissue, and more of those T cells were actively doing their job.
That combination, cutting off the neutrophil-driven immune suppression while restoring T cell function, suggests a treatment approach that could eventually be tested in people who survived severe COVID-19 or influenza.
For the tens of millions of Americans hospitalized with COVID-19 during the pandemic, and the millions more who have been seriously ill with influenza over the years, this study raises a question medicine has not yet fully confronted: whether severe respiratory viral infection should be considered a potential lung cancer risk factor alongside smoking history and occupational exposures.
The biological mechanism, demonstrated primarily in mice, still needs to be confirmed in humans, and prospective studies are needed before any formal recommendations can be made. But the depth of this work moves that conversation into considerably firmer scientific ground.
Somewhere between the ear and conscious awareness, something gets lost. A new study found that after just 12 minutes of passive exposure to labeled AI and human voices, the brain begins processing them as measurably distinct categories. Consciously, though, participants remained essentially unable to tell the difference. Their ability to correctly identify AI voices barely changed. Their brain activity, on the other hand, told a different story.
Published in eNeuro by researchers at Tianjin University and the Chinese University of Hong Kong, the study used brain recordings to track how the auditory system responds to AI-generated speech before and after a brief training session, then compared that neural data to what participants consciously reported. What emerged was a clear disconnect: the brain was quietly adapting to synthetic voices in ways that never surfaced as better detection ability. Researchers call it a neural-behavioral dissociation, and understanding it may hold the key to building training programs that can help people catch voice deepfakes before they cause harm.
“Our study shows that even when listeners cannot behaviorally distinguish AI-generated voices from real human voices, brief perceptual training enables their brains to detect subtle acoustic differences,” the authors wrote. Given how rapidly AI voice technology is advancing, and how easily it can be used for fraud and impersonation, closing that gap between brain and behavior is now a practical concern as much as a scientific one.
How Researchers Built and Tested the AI-Generated Voices
Three native Mandarin speakers, two women and one man, each recorded 67 short sentences. Those recordings were then fed into GPT-SoVITS, a widely available open-source voice-cloning tool, to produce two types of synthetic speech per speaker. One version was fine-tuned on each speaker’s own recordings, producing a close imitation of their voice. A second version was generated without additional fine-tuning, relying solely on short audio samples, which still sounded human but bore a weaker resemblance to the specific speaker.
Thirty adults between ages 20 and 32, all native Mandarin speakers with no neurological history, participated while wearing a 64-electrode EEG cap that records electrical brain activity in real time. In the first session, they listened to 297 randomly ordered sentences drawn from all three voice types and pressed a button after each one to label the speaker as human or AI. No feedback was given on their guesses.
Then came the training phase. Participants heard nine longer audio clips, one per speaker-voice combination, explicitly labeled as either human or AI. No instructions told them what to listen for. The whole thing lasted roughly 12 minutes. After that, a second test session began with a fresh set of sentences.
Why AI Voice Detection Fails at the Conscious Level
Behavioral results were discouraging but not surprising. Participants performed poorly at distinguishing human from AI speech in both sessions. Statistical analysis confirmed that training produced no significant improvement in conscious discrimination ability. What did shift was strategy: after training, participants became more likely to label voices as AI-generated overall, a sign of increased caution rather than sharpened skill.
Part of what makes conscious detection so difficult may come down to the acoustic properties of the voices themselves. Analysis of the speech recordings revealed that AI-generated voices differ from human ones in the fine, rapid fluctuations that characterize natural speech, the micro-level variations in how a voice moves through individual sounds. Modern AI synthesis does an impressive job mimicking the broad, overall character of a human voice, but it may fall short in precisely reproducing these moment-to-moment dynamics. These acoustic differences may contribute to why listeners struggle to identify synthetic voices, though the study did not establish this as a definitive cause.
Where the Brain and Behavior Split on Deepfake Voice Detection
EEG recordings told a story the behavioral data couldn’t. Using a method called temporal response function analysis, which tracks how closely the brain’s electrical activity follows the contours of incoming sound over time, researchers compared neural responses to human and AI voices before and after training. Before training, no meaningful neural distinctions emerged between voice types. After training, the brain showed clear, statistically significant differences in how it processed human versus AI speech at approximately 55 milliseconds, 210 milliseconds, and 455 milliseconds following each sound, spanning early acoustic processing all the way through to higher-level interpretation.
In plain terms, after just 12 minutes of labeled exposure, the brain had begun responding differently to AI and human voices, even as the individual kept pressing the wrong button.
Broader analyses of brain wave patterns and spatial electrical activity across the scalp found no significant differences between voice types, suggesting the training effect was specific to how the brain tracks fine acoustic detail in real time rather than reflecting widespread changes in neural activity.
What Short-Term Training Could Mean for Catching AI Voice Fakes
The neural data suggests the auditory system may already register subtle differences between human and AI speech, even when listeners cannot consciously act on them. Rather than building a detection skill from scratch, future training programs might help listeners learn to use acoustic cues the brain already registers.
Twelve minutes of passive, labeled exposure was enough to reshape brain responses but not enough to change behavior. Researchers suggest that longer training, or protocols designed to direct a listener’s attention toward the acoustic cues that distinguish human from synthetic speech, could eventually bridge that gap. Whether hearing a familiar person’s voice cloned by AI would make detection easier or harder is an open question the study’s design could not address, but it is one with obvious real-world stakes.
AI voice-cloning tools are already being used to impersonate relatives, employers, and public figures, and most people tested under controlled conditions cannot reliably identify them. The auditory system’s sensitivity to synthetic voices, quiet as it is, may offer a foundation for training programs that haven’t yet been built. Getting that sensitivity into conscious awareness is the next challenge.
Most men past 40 have heard that testosterone drops with age. What far fewer know is that declining testosterone may increase vulnerability to fat buildup in the liver, especially in men who regularly drink sodas, fruit juices, or other high-fructose beverages.
New research in mice shows the combination of low testosterone and high fructose intake does something neither condition manages on its own: a rapid acceleration of fat buildup in the liver. That finding matters for a lot of men. Roughly 5.58 million Americans between the ages of 40 and 79 currently live with both low testosterone and excessive fructose consumption at the same time. Most likely don’t realize they fall into that overlap, and few conversations about low testosterone include any discussion of liver health.
Published in the American Journal of Physiology: Endocrinology and Metabolism, the study also uncovered a previously unrecognized piece of the puzzle. Changes in gut bacteria that cause a compound called pyruvate to accumulate and promote fat buildup in liver cells.
Low Testosterone and High Fructose Are Both More Common Than Men Realize
Testosterone begins declining gradually after a man’s 30s. About 17% of men between 40 and 79 meet the clinical definition of low testosterone, with symptoms often mistaken for normal aging: fatigue, abdominal weight gain, reduced muscle tone. What rarely enters that conversation is what low testosterone does to the liver, and how diet makes it worse.
At the same time, an estimated 43% of Americans consume more sugar than health guidelines recommend. Fructose, found in sodas, energy drinks, packaged snacks, and fruit-flavored beverages, is processed almost entirely by the liver. When it arrives in excess, the liver converts it into fat. Both low testosterone and high fructose intake are recognized risk factors for fatty liver disease, a condition estimated to affect about 30% of people worldwide. Their combined effect, however, had never been directly studied until now.
What Researchers Found When Both Risk Factors Were Combined
Researchers at Osaka Metropolitan University divided male mice into six groups. Some were surgically castrated to eliminate testosterone, while others underwent a sham procedure that left hormone levels intact. Within each group, mice received plain water, a 10% fructose solution comparable to many common soft drinks, or fructose water plus antibiotics to suppress gut bacteria. After eight weeks, the results were telling.
Castration alone did not significantly increase liver fat. Fructose alone produced only a modest, borderline rise. Combining both conditions drove liver fat and cholesterol levels well beyond what either factor caused independently, and histological analysis confirmed fatty changes in the liver that were absent in the other groups.
Liver enzymes that typically signal cell damage remained normal even in the worst-affected mice. That means the liver was accumulating fat silently, at an early stage before serious or irreversible damage sets in. Early fatty liver disease often produces no symptoms at all, which is precisely what makes it easy to miss.
How Gut Bacteria Drive the Damage
One of the more revealing results came from the antibiotic-treated mice. Animals that received both castration and fructose alongside antibiotics showed substantially less liver fat than those without the drugs. Since antibiotics suppress gut bacteria, that outcome pointed directly to the microbiome as a key driver.
Analysis of the bacteria living in the gut confirmed that the combination of castration and fructose shifted gut microbial composition in ways that neither condition produced alone. Measurements of chemical byproducts in the cecum, a pouch in the gut where many bacterial compounds collect, showed that levels of a molecule called pyruvate were significantly elevated only in the combined group. Antibiotic treatment brought those levels back down.
Pyruvate sits at a metabolic crossroads. Under normal conditions, gut bacteria convert it into other compounds and clear it efficiently. In the combined condition, certain bacterial species responsible for that conversion appeared less active, allowing pyruvate to accumulate and potentially influence liver metabolism. To confirm that pyruvate could directly drive fat accumulation, the team cultured isolated mouse liver cells with pyruvate, fructose, or both. Neither compound alone caused significant fat buildup. Together, they produced a sharp, statistically significant surge in fat inside the cells. As the researchers noted, this is “the first study to investigate the effects of pyruvate on the steatosis of primary hepatocytes.”
Pyruvate’s role here is worth pausing on. It has long been studied as an energy molecule, not a driver of liver disease. If further research confirms that gut-derived pyruvate contributes to fatty liver in humans, it could point toward a new and largely overlooked target for treatment, one tied directly to the bacterial landscape of the gut.
Separately, the researchers found that gene activity inside the liver itself also changed in the combined group, with genes governing fat production and fructose processing ramping up in ways that antibiotics did not reverse. That suggests the gut-pyruvate pathway is only part of the story, and that low testosterone and fructose together alter liver function through more than one route.
For middle-aged men managing declining testosterone, this raises a question that almost never comes up in clinical settings: what role is diet playing alongside it? As the researchers put it, “risk factors for hepatic steatosis can exert a greater impact on disease development through complex mechanisms under certain conditions.” For millions of American men, that may describe their situation right now, without anyone having told them so.
These popular beverages often have many other ingredients, like vitamins and plant extracts. Here’s what you should know about them.
(Art: The New York Times/Javier Jaen)
A growing number of Americans, especially younger ones, are reaching for energy drinks in order to stay up late or level up their workout. About two-thirds of teens report drinking them at least occasionally, and most who drink one a day are under 35.
These beverages can have 100mg to 300mg of caffeine per serving, usually more than a cup of black coffee. There’s no question that high doses of caffeine can boost your energy. But energy drinks often include other healthy-sounding ingredients, such as B vitamins and plant extracts, which brands claim can boost focus and stamina or reduce fatigue.
“I generally greet that with a healthy dose of skepticism,” said Joe Zagorski, a toxicologist and assistant professor at Michigan State University. He added that there was very little scientific evidence showing any health benefit from the additives and vitamins in energy drinks.
Most likely, Dr Zagorski said, “the vast majority of the effects you’ll get from an energy drink are because of the caffeine.”
WHAT’S IN ENERGY DRINKS?
It can be difficult to know for sure. That’s because some products are marketed as beverages, while others are marketed as supplements, meaning they are regulated differently. Beverages are generally required to list ingredients, though not the exact amounts, Dr Zagorski said. But those marketed as supplements may not be required to list individual ingredients at all. Some use vague terms, like “focus blend” or “energy blend” to describe their ingredients.
Exactly what’s in an energy drink varies by brand, but here are a few common ingredients.
PLANT-DERIVED CHEMICALS
Energy drinks typically contain plant-based ingredients or extracts, including guarana, yerba mate and green tea, said Dr John Higgins, a cardiologist at the University of Texas Health Science Center at Houston who researches energy drinks. Some of these botanicals act like stimulants, but others simply contain additional caffeine, which isn’t always included in the amount listed on the label. This means regular drinkers may exceed 400mg of caffeine a day, the safe upper limit for most people, Dr Higgins said.
Energy drinks can also contain ginseng and ginkgo biloba, which are not technically stimulants but can increase blood flow. Combined with caffeine, some such ingredients can lead to adverse effects, like heart palpitations or increased blood pressure, said Dr Anna Svatikova, a cardiologist at the Mayo Clinic in Rochester, Minnesota, who’s done research on energy drinks and heart health.
B VITAMINS
B vitamins are essential for helping your body convert food into energy, and they’re commonly found in energy drinks, said Richard Bloomer, a professor and director of the Center for Nutraceutical and Dietary Supplement Research at the University of Memphis.
But some of the beverages contain amounts of Vitamin B2 (riboflavin), B3 (niacin), B6 (pyridoxine) and B12 (cobalamin) that exceed the recommended daily value, Dr Higgins said. Long-term, high doses of B vitamins could lead to low blood pressure, liver damage and neuropathy in some instances.
Most people get all the Vitamin B they need from a balanced diet, Dr Bloomer said, and they’ll excrete the excess in their urine. There’s a lack of clinical evidence that consuming more than you need will increase your energy or focus, Dr Svatikova added.
Vitamin B deficiency is more common in older adults, people with gastrointestinal issues and vegans or those on other restricted diets. A blood test is needed to determine if you’re Vitamin B deficient, but if you are, you’re better off taking a supplement than consuming an energy drink, Dr Bloomer said.
AMINO ACIDS
Energy drinks often include small amounts of amino acids like taurine, which is found in protein-rich foods, like meat and fish; and your body produces it naturally, Dr Svatikova said. There is some limited evidence that taurine combined with caffeine can enhance performance and exercise capacity, she said.
Taurine can have side effects, though. It may interact with antidepressants and other medications. Research in animals has shown a connection between caffeine, taurine and heart arrhythmias.
Some energy drinks also contain L-theanine, an amino acid found in tea leaves. Older, small studies have shown that when paired with caffeine, it may improve mood, cognition, focus and alertness. But larger, longer-term studies are needed to confirm this, Dr Svatikova said.
More research is also needed to better understand the long-term health impact of consuming taurine and L-theanine individually or together, Dr Svatikova said.
ADDED SUGAR
Energy drinks can contain significant amounts of added sugar, sometimes up to 60g per serving, said Dr Bloomer, who called the beverages “a can of sugar water with added caffeine.”
The US Department of Agriculture now recommends limiting added sugars to no more than 10g per meal and suggests avoiding “sugar-sweetened beverages,” including energy drinks.
Excess sugar is known to increase irritability and raise the risk of obesity, cardiovascular disease and diabetes, Dr Svatikova said.
SHOULD YOU AVOID ENERGY DRINKS?
The occasional energy drink is probably safe for most healthy people, Dr Zagorski said. But pay attention to the serving size: One bottle or can may contain multiple servings, which he said could dramatically increase your caffeine and sugar intake.
You should know your individual caffeine tolerance, Dr Svatikova added. For some, excess caffeine can cause jitters, irritability, sleeplessness, an upset stomach, anxiety, heart palpitations, irregular heartbeats, increased blood pressure and, potentially, cardiac arrest, she said.
It’s also not fully clear how additional ingredients in energy drinks, like plant extracts, could contribute to these effects, Dr Svatikova said.
Microwave ovens use non-ionising radiation to heat food. It is harmless in itself, but using plastic containers for the food can increase the risk.
Used with the right utensil, microwave ovens do not increase the risk of cancer, shares Dr Sharma. (Pexel)
Cancer is still considered to be a death sentence in many households, and because the disease is becoming increasingly common, it is understandable for people to be extra cautious about things of regular use that can increase their risk.
Radiations have long been considered carcinogenic. As a result, there has been a fear of microwave ovens, which, as the name suggests, use microwave radiation to heat or cook food, increasing the risk of cancer.
However, that is not exactly the case, noted Dr Jayesh Sharma, Raipur-based oncologist with over 25 years of experience. Taking to Instagram on February 23, he explained why microwaves are generally safe, and what is the one thing we should be cautious about while using the gadget.
Can microwave oven cause cancer?
According to Dr Sharma, the answer to the question is both yes and no, though in a majority scenario, it is the first option.
“Microwave is a type of electromagnetic radiation,” explained the senior cancer surgeon. “And from a biological perspective, they are of two types: ionising and non-ionising.”
Ionising radiations are those which have sufficient energy to hit an atom and split it into pieces. Thus, when an ionising radiation hits the DNA molecule, it can result in mutations at an atomic level of the DNA and therefore increase the risk of cancer.
Examples of such radiation are ultraviolet rays, X-rays, and radiation released during a nuclear explosion, shared Dr Sharma.
Non-ionising radiation does not have enough energy to break apart an atom. “The best example of non-ionising radiation is visible light,” shared Dr Sharma.
Microwave is also a non-ionising radiation that has even less energy than visible light rays, he noted. As such, there is no chance of microwave radiation breaking any atom. It can only be used to heat up food.
“If heating food leads to cancer, then it would apply to all cooking methods,” noted the oncologist. Since that is not the case, heating food in a microwave oven is safe.
Hidden danger of microwave oven use
Despite microwave ovens being generally safe and non-carcinogenic, there is one thing to keep in mind while using them to heat food. One often gets food delivered in plastic containers from restaurants and uses microwave ovens to heat food in the container itself.
A cancer diagnosis upends every aspect of an individual’s life, from sleep and appetite to work and relationships. All of it shifts the moment a doctor delivers that news. Now, a sweeping study finds how a patient reacts to such news may influence their risk of dying sooner.
Researchers found that cancer patients who developed anxiety, depression, or another mental health disorder within the first year of their diagnosis were 51% more likely to die from any cause during the roughly three years that followed, specifically months 12 through 35 after diagnosis, than patients who did not.
That figure comes from an analysis of nearly 372,000 cancer patients across the University of California health system, one of the largest studies of its kind ever conducted in the United States. The findings were published in Cancer, the peer-reviewed journal of the American Cancer Society. What sets this study apart from earlier work is its foundation.
Instead of relying on patient surveys or self-reported symptoms, researchers used clinically documented diagnoses pulled directly from a decade’s worth of hospital records. These were conditions a doctor confirmed, not just feelings a patient described on a questionnaire. It’s worth noting that the study is observational, meaning it identifies an association between mental health disorders and earlier death, but cannot prove that one directly causes the other.
When a Cancer Diagnosis Triggers a Mental Health Crisis
Researchers pulled records from all University of California-affiliated hospitals, tracking adult patients newly diagnosed with cancer between 2013 and 2023. To keep the analysis clean, only patients with no prior mental health history were included. The question was simple: how many would develop a new psychological condition, such as an anxiety disorder, depression, or a psychotic disorder, within 12 months of learning they had cancer?
About one in ten did. Of the nearly 372,000 patients studied, roughly 39,700 received a new mental health diagnosis within that first year. Generalized anxiety disorder was the most common, making up 43% of new cases. Major depressive disorder came next at 35.5%, followed by reactive and adjustment disorder at around 10.5%.
The timing of these diagnoses was itself revealing. Mental health conditions started ticking upward about three months before a cancer diagnosis was even officially recorded, likely because patients were already living with symptoms that sent them to a doctor in the first place. Then came a sharp spike in the six months right after the cancer diagnosis landed. That concentrated early window became the heart of what researchers wanted to study.
Mental Health and Cancer Survival: The Numbers Behind the Risk
In the first 12 to 35 months after diagnosis, patients who developed a mental health condition were 51% more likely to die from any cause than those who did not, even after researchers accounted for age, sex, race, and other existing health conditions. That’s a substantial gap.
It didn’t last forever. By years three through five, that elevated risk dropped to 17% above average. By years five through ten, the difference had essentially vanished. The association between mental health disorders and survival was strongest early on, hitting hardest in that vulnerable early stretch.
For patients who developed a mental health disorder and were also prescribed medication for it, antidepressants, anti-anxiety drugs, or antipsychotics, the early mortality risk was steeper still, more than double that of patients with no mental health diagnosis. Researchers suggest this may reflect how severe those cases were, since doctors typically prescribe psychotropic medications for moderate to severe symptoms. However, because the study did not include data on cancer stage or why specific medications were prescribed, it cannot determine whether the higher risk reflects symptom severity, more advanced cancer, or other factors entirely.
Not All Cancers Hit the Same Way
The type of cancer a patient had mattered too. Pancreatic cancer patients, who face a disease with roughly an 11% five-year survival rate, were more than three times as likely to develop a new mental health condition compared to prostate cancer patients, who served as the study’s comparison group. That gap makes sense intuitively. A diagnosis with a brutal prognosis generates a different kind of fear than one with high survival odds. But mapping that intuition across hundreds of thousands of patients gives it a weight that gut feeling alone cannot.
Among patients who did develop a mental health condition in that first year, breast cancer was the most commonly represented cancer type at 16.6% of that group, followed by blood cancers like leukemia and lymphoma at 13.3%.
A Prescribing Pattern Worth Examining
Of the patients who received a new mental health diagnosis, 35% were prescribed at least one psychotropic medication. Benzodiazepines, sedatives like Valium and Xanax, turned out to be the most commonly prescribed, with nearly a quarter of all cancer patients in the cohort receiving one at some point. That rate ran well ahead of SSRIs, the antidepressant class that clinical guidelines generally recommend first for anxiety and depression.
Researchers flagged that as worth paying attention to. The study did not test whether benzodiazepines directly increased mortality in this group, but the authors noted that prior research has linked these drugs to higher mortality risk and adverse interactions in patients with serious medical conditions, raising questions about whether cancer patients are consistently getting the most appropriate psychiatric care.
That still leaves roughly two-thirds of patients who received a mental health diagnosis but no medication at all. Access, personal preference, or clinical judgment could all explain that, and the data cannot say which. What the data can say is that mental health conditions after a cancer diagnosis are common, cluster in a specific and early window, and are associated with measurable consequences for survival.
Javier G. Fernández (left) and Akshayakumar Kompa (right) holding a sample of the material at the IBEC laboratories. (Credit: Institute for Bioengineering of Catalonia)
Most things fall apart in water. Paper, cardboard, and many eco-friendly alternatives to plastic turn soft and useless the moment they get soaked. Researchers have now created a biodegradable material that does the opposite: submerge it, and it grows nearly 50% stronger.
That single property could matter enormously. Every year, the world generates roughly 400 million tons of persistent plastic waste, much of it designed specifically to resist water. Bottles, cups, food containers, and packaging dominate because few biodegradable materials have matched conventional plastics in wet conditions. Research published in Nature Communications suggests that a molecule already being produced by nature in enormous quantities may help close that gap.
The material is made from chitosan, derived from shrimp shells, combined with trace amounts of nickel. Chitosan comes from chitin, a structural molecule found in crustacean shells and insect exoskeletons, with an estimated renewable biosynthesis rate of about 100 billion tons per year globally. Most of it currently goes to waste, discarded as a byproduct of shrimp and crab processing, or used in low-value applications like water filtration. Despite that abundance, chitosan-based materials have long been held back by one stubborn flaw: they weaken and dissolve in water. The team, based at the Singapore University of Technology and Design and the Institute for Bioengineering of Catalonia in Barcelona, appears to have solved that problem using an approach borrowed from nature itself.
How a Shrimp Shell Material Becomes Stronger Than Common Plastics
The inspiration came from a sandworm. Researchers knew that when zinc is removed from the fangs of a worm called Nereis virens, the fangs lose their structural strength when submerged. That observation led the team to ask whether trace metals might help chitosan actually use water, rather than be weakened by it.
To test the idea, they dissolved chitosan flakes, sourced from shrimp-processing factory byproducts in India, in a weak acetic acid solution, roughly one-fifth the concentration of regular table vinegar. Nickel chloride dissolved in water was then mixed in, poured into molds, and dried. The result was a series of thin, green-tinted films at varying nickel concentrations.
In dry conditions, the films matched the strength of common plastics like polypropylene or polystyrene. Once submerged, they reached the range of engineering plastics such as polycarbonate and PETG, the kind used in water bottles and structural components. The researchers described this behavior as “never achieved artificially.”
To understand why, picture the chitosan chains as a loosely woven net. When nickel and water move into the gaps between those chains, they act like cinches, pulling everything tighter rather than loosening it. Most materials work in reverse, their internal structure loosening when water gets in. This one locks down.
A Biodegradable Plastic Alternative Built to Survive Water
When a freshly made film is first submerged, about 87% of the nickel washes out. Only a small fraction of what was originally added actually drives the strengthening effect. That released nickel is not discarded. The researchers built a zero-waste production cycle in which the wash water from one batch feeds directly into the next. As the paper noted, “the nickel content of a discarded AAA battery (2.2 g) would be sufficient to manufacture more than a dozen typical drinking cups (4.7 g each) using nickel-doped chitosan.”
The team molded the material into cups and containers and confirmed it holds water without leaking for at least a week. A film more than three square meters in area was produced without processing problems, suggesting the approach is not confined to laboratory scales. In a standard soil burial test, the material reached its half-life in about four months. Most conventional plastics take centuries under the same conditions.
Both chitosan and nickel have existing FDA-approved medical uses individually, though the combined material would require further safety evaluation before any medical applications move forward.
No new synthetic polymer chemistry was required here. Shrimp shells and a trace of a common metal, combined with a process inspired by how crabs build their exoskeletons, produced something rare in synthetic materials: a substance that performs better in water than in dry air. The researchers believe medical applications and waterproof coatings for other biodegradable materials are realistic next steps, with more complex shaping and large-scale manufacturing still to be worked out. For now, what exists is a proof of concept built from seafood scraps and a battery’s worth of nickel, and the early results are hard to ignore.
The Findings Raise New Questions About Alzheimer’s Prevention
Doctors have long advised older adults to control their blood pressure, treat depression, and reduce stroke risk as key steps toward protecting their brains from Alzheimer’s disease. A new study suggests that advice, while sound, may be leaving out a major environmental risk factor.
Analyzing nearly 28 million Medicare patients over nearly two decades, researchers at Emory University found that long-term exposure to fine particle air pollution is linked to higher Alzheimer’s risk, largely independent of high blood pressure, depression, or stroke. In other words, those familiar conditions barely explain the connection. High blood pressure, depression, and stroke together accounted for less than 8% of the relationship between dirty air and Alzheimer’s. The findings suggest pollution may influence Alzheimer’s risk through pathways not explained by these common conditions.
If air pollution damages aging brains through pathways not fully explained by cardiovascular or mental health conditions, then managing those conditions alone won’t fully protect people. For the millions of older Americans already living with high blood pressure or a history of stroke, the air outside their windows may be posing a risk that no prescription can address. The study was published in PLOS Medicine.
How Researchers Measured Air Pollution and Alzheimer’s Disease Risk
Fine particulate matter, or PM2.5, refers to microscopic particles produced by car exhaust, power plants, wildfires, and industrial emissions. Small enough to travel deep into the lungs and, research suggests, small enough to eventually reach the brain, these particles may trigger inflammation and the buildup of toxic proteins linked to Alzheimer’s.
Researchers assigned pollution exposure estimates to each participant based on their ZIP code, drawing on a model that combined satellite imagery, EPA monitoring data, land-use records, and weather information. For each person, the team calculated a five-year rolling average of PM2.5 exposure and used statistical models to connect that exposure to Alzheimer’s diagnoses while controlling for age, sex, race, income, region, and other variables.
More than 57% of participants were women, over 89% were white, and the average age at entry was approximately 76. About 3 million of the nearly 28 million participants developed Alzheimer’s over the study period. Each meaningful increase in five-year average PM2.5 exposure (about 3.8 μg/m³) was associated with roughly an 8.5% higher risk of developing Alzheimer’s.
Stroke Survivors Face an Even Greater Air Pollution and Alzheimer’s Disease Risk
While high blood pressure and depression didn’t appear to change how strongly air pollution affected Alzheimer’s risk, stroke told a different story. People with a history of stroke showed a slightly larger effect: the same increase in PM2.5 was linked to about a 10.5% higher Alzheimer’s risk compared to 8.8% among those without stroke.
One possible explanation is that stroke weakens the blood-brain barrier, the protective boundary that normally keeps harmful particles from entering brain tissue. When that barrier is compromised, pollution-related inflammation may get through more readily, speeding up the neurodegeneration associated with Alzheimer’s. People with stroke may also have impaired glymphatic clearance, the brain’s natural waste-removal system, leaving it less equipped to flush out the toxic proteins that accumulate in Alzheimer’s.
Why This Reframes Conventional Thinking on Dementia Prevention
When the Emory team asked how much of the pollution-Alzheimer’s relationship could be explained by hypertension, stroke, and depression, the numbers were small. High blood pressure accounted for about 1.6% of the association, depression for 2.1%, and stroke for 4.2%. “Our findings suggest that PM2.5 exposure was associated with increased AD risk, primarily through direct rather than comorbidity-mediated pathways,” the authors wrote in PLOS Medicine. “Stroke may modestly increase susceptibility.”
Prior studies had produced conflicting results on this question, but most were limited by small sample sizes or methods that didn’t fully account for how exposure, chronic conditions, and disease outcomes interact over time. With nearly two decades of follow-up data, this analysis had both the scale and the statistical tools to get a cleaner answer.
Is the street you live on lined with leafy trees, or mostly grass and pavement? That simple difference might be affecting your heart in ways scientists are just beginning to understand.
A study tracking nearly 90,000 nurses across America for 18 years found neighborhoods with more visible trees showed about 4% lower rates of heart attack and stroke, while areas with more grass showed about 6% higher rates. These are relative differences comparing neighborhoods with varying amounts of visible vegetation, not guaranteed changes for any one person. After analyzing 350 million street-view photographs using artificial intelligence, researchers discovered that not all green space appears equal for cardiovascular health.
For decades, public health experts have urged people to get outside and enjoy nature. Parks, gardens, open spaces: it all seemed equally beneficial. But this research reveals something more complicated. From high above, a satellite can’t tell the difference between a tree-shaded avenue and a grass-covered suburb. Both look green. Yet for your cardiovascular system, the distinction matters.
How Scientists Measured Trees and Cardiovascular Disease Risk
Researchers used Google Street View images from across the country, training computers to identify exactly what appeared in each photo: trees, grass, shrubs, and other plants. They created detailed maps showing what someone would actually see walking through urban and suburban areas nationwide.
Then they matched those maps to health records from the Nurses’ Health Study, which has been following female nurses since 1976. The 88,788 women in this analysis lived everywhere from dense cities to rural towns. Every two years, they reported any heart attacks or strokes, which researchers verified through medical records. Over 18 years, doctors confirmed 6,065 cardiovascular events.
Even after accounting for smoking, diet, exercise, income, education, and air pollution levels, the pattern held. Trees seemed to protect hearts. Grass didn’t.
Why the Association Might Exist
Researchers suggest several reasons why trees and grass might show different associations with heart health, though the study didn’t directly prove these pathways.
Trees may offer protective mechanisms that grass cannot. Their leaves trap pollution particles that would otherwise enter lungs. A mature tree canopy cools a neighborhood far more effectively than a lawn. That’s critical during heat waves that stress the cardiovascular system. Thick branches muffle traffic noise, and prior research has linked chronic noise exposure to higher blood pressure and heart disease risk. Tree-lined streets also tend to encourage more walking and social interaction, and shaded sidewalks feel more inviting than exposed concrete.
Grass offers few of these potential benefits. Regular mowing creates noise and air pollution. Grass provides minimal cooling on hot days and does little to filter pollutants from the air. Open, sun-baked stretches of grass don’t exactly invite leisurely strolls.
Importantly, the study’s authors note that grass might also signal something else about a neighborhood rather than directly causing harm. Areas dominated by lawns but lacking trees often have sprawling, car-dependent layouts where people drive everywhere instead of walking. The analysis couldn’t fully separate grass itself from these neighborhood design patterns, meaning the observed associations could reflect these broader environmental differences.
The findings held across wildly different settings: crowded cities and quiet suburbs, polluted areas and clean ones, wealthy neighborhoods and modest ones, North and South, East and West. Whatever’s going on, it’s not limited to one type of community.
The Distance That Matters
The protective effect showed up most clearly within the 500-meter neighborhood buffer researchers used as their main measure, about one-third of a mile from someone’s home. Right outside your front door matters less than you might think. When researchers looked only at the immediate 100 meters, the associations mostly disappeared. But expand to the neighborhood level, and the pattern emerged strongly.
That’s actually good news for urban planning. You don’t need every single yard packed with trees. What matters is creating tree-covered neighborhoods where canopy extends over streets and sidewalks, cooling and cleaning the air across a wider area. One homeowner planting a tree helps a little. A community planting hundreds helps a lot.
What This Means for Your Neighborhood
Cities nationwide face tough choices about trees right now. Climate change brings more droughts, diseases, and storms that kill urban forests. New construction often means cutting down mature trees. Tight budgets force parks departments to choose between planting trees or maintaining grass.
This research offers clear guidance: prioritize trees. The findings suggest tree planting may deliver more cardiovascular benefit than investments focused mainly on turfgrass. Protecting existing mature trees during development could be as important as adding new parks.
Dr. Peter James, who led the study at the University of California, Davis, pointed out that scientists have been measuring green space wrong for years. “Aggregating green space into a single exposure category limits epidemiological research and potential interventions to increase health-promoting green space,” his team wrote.
Street-view imagery changes that. Computers can now analyze what people actually see at ground level, distinguishing between a tree canopy overhead and a stretch of grass beside the road. That specificity makes the research far more useful for anyone trying to improve public health through urban design.
What We Still Don’t Know
The study, published in Environmental Epidemiology, followed only female nurses, 93% of them white, which raises questions about whether the same patterns apply to men or more diverse populations. The researchers could track where participants lived but not where they spent their days or whether they actually went outside. Someone living on a tree-lined street who never walks there might not get the same benefits.
The harmful associations with grass might not be directly caused by the grass itself but rather by the kinds of neighborhoods that tend to have lots of grass and few trees. The analysis couldn’t fully separate those overlapping factors.
Interestingly, when researchers included traditional satellite-based greenness measures in their analysis, those showed no association with heart disease once street-level tree and grass measurements were accounted for. This reinforces that what matters isn’t just whether an area looks green from space, but what specific plants people actually see and experience at ground level.
Experts have acknowledged significant technical challenges, including the wall’s survival in extreme Antarctic conditions and long-term ocean exposure.
Scientists have raised concerns over the Thwaites Glacier, which is nicknamed the “Doomsday Glacier,” as it is melting at an unprecedented rate because of climate change fueled by human activities. The rapid melting rate would result in a rise of global sea levels by 65cm, putting millions at risk of coastal flooding.
Notably, Thwaites Glacier contributes 4% to global annual sea-level rise, and its collapse could destabilise the West Antarctic Ice Sheet, which would cause catastrophic sea-level rise. The glacier’s melting is a pressing concern, with researchers drilling into the ice to study the impact of warm ocean water.
In an effort to mitigate the impact, a team of scientists and engineers is proposing a radical solution: building a 150-meter-tall underwater wall to block warm ocean currents from melting the glacier, Euro News reported.
The proposed wall, which is a part of the Seabed Anchored Curtain Project, would stretch 80km across the seabed in front of the glacier, protecting it from warm ocean waters. The project involves a three-year research phase to design, test, and construct the curtain, with a budget of $10 million.
“We are proud to support the Seabed Curtain project, a groundbreaking initiative in climate research and ocean preservation in the Arctic,” Thomas Wilhelmsen, Chair of Tom Wilhelmsen’s Foundation, said as quoted on the official website.
“The project’s innovative approach to reducing ice melting in the Arctic Ocean through technology and collaboration across disciplines strongly aligns with the foundation’s values of sustainability, knowledge, and international cooperation.”
“We believe this project has the potential to make a meaningful contribution to the global climate effort and help protect vulnerable ecosystems in the northern regions.”
Americans trying to shed pounds are paying far more than they realize. In a survey of people actively working toward weight loss, participants spent an average of $12,308 in 2025 alone, exposing what researchers call a quiet but persistent “weight tax” that extends well beyond gym memberships and salad bars.
This financial burden touches nearly every corner of daily life, from the grocery store to the doctor’s office. For the 2,000 U.S. adults surveyed by Talker Research on behalf of Hims, Inc., the costs pile up through specialty clothing, repeated diet attempts, fast food purchases, and medical expenses tied to weight-related health conditions.
Survey participants estimate they could save roughly $197 each month if they finally reached their target weight. That adds up to more than $2,300 per year, money that could fund vacations, pay down debt, or boost retirement savings.
Where Americans Spend the Most on Weight Loss
More than half of respondents (56%) believe they’d save money by cutting back on fast-food meals once they reach their goal weight. Another 52% pointed to lower grocery bills as a major source of potential savings. Fast food might seem convenient when energy is low or motivation wanes, but those drive-through runs add up quickly. Specialty diet foods, meal replacement shakes, and organic produce marketed for weight loss often carry premium price tags compared to standard groceries.
Clothing costs represent another drain on wallets. Nearly one in three respondents (31%) said they’d spend less on new clothes once they reached their target size. For some, this means no longer replacing items that no longer fit after weight fluctuations. About 26% specifically mentioned savings from no longer purchasing “big and tall” specialty clothing, which typically costs more than standard sizes.
Healthcare expenses linked to weight management also take a toll. Roughly 22% of participants expect to save on medical costs once they reach their goals, including fewer doctor visits, lower insurance copays, and reduced spending on medications for conditions like high blood pressure or diabetes. Managing chronic conditions can easily run into thousands of dollars annually even with insurance coverage.
The Fad Diet Cycle Draining Bank Accounts
One of the more frustrating sources of spending comes from cycling through various diet and fitness programs that promise quick results but rarely deliver lasting change. About 19% of respondents expect to save money by no longer bouncing between fad diets, juice cleanses, and short-term weight loss programs.
Over the past decade, survey participants reported trying and failing to reach their target weight an average of six times. Each attempt brings its own costs: signing up for a new program, buying specialized foods or supplements, purchasing workout equipment or clothing, and sometimes paying for medical supervision or coaching.
Dr. Craig Primack, Head of Weight Loss at Hims & Hers, noted the pattern many patients face. “In my experience, most patients living with obesity aren’t just beginning a weight loss journey,” he said. “They’ve been navigating it for years, often a lifetime. Each failed attempt not only erodes hope, but comes with real financial consequences.”
He added: “For too many Americans, the pursuit of better health has become a cost they simply can’t afford. Evidence-based, personalized care that’s designed for continuity and priced for long-term use offers a more sustainable path forward.”
What Weight Loss Could Mean Beyond the Scale
Financial relief isn’t the only benefit respondents hope to gain. Having more energy during the day topped the list at 61%, followed by fitting into smaller clothing sizes (57%), sleeping better at night (56%), eating smaller portions (56%), and lowering their BMI (53%).
Better sleep alone could have widespread positive effects on health, mood, and productivity. More energy throughout the day might mean being more active with family, performing better at work, or simply feeling more engaged with life.
How Americans Are Changing Their Weight Loss Approach in 2026
Heading into 2026, many respondents plan to shift their strategies. Rather than chasing dramatic transformations or perfect adherence to rigid plans, people are emphasizing consistency, patience, and finding ways to move more throughout each day.
One survey participant captured this mindset: “I’m concentrating on consistency this year instead of perfection. I want to prioritize sleep and water, keep a mindful eating journal, and engage in enjoyable physical activities every day. I’m convinced that I can achieve my desired weight and BMI by acknowledging little accomplishments and using self-compassion.”
This approach moves away from all-or-nothing thinking that often leads to burnout. Small, sustainable changes may not generate dramatic “before and after” photos that flood social media, but they’re more likely to stick over time.
Motivation remains high among those surveyed. More than three-quarters (77%) said fitting back into their favorite clothes by year’s end serves as a key driver pushing them forward.
Would a $5,000 Reward Change Everything?
The survey revealed just how powerful financial incentives might be. More than eight in 10 respondents (86%) said they would pursue their weight loss goals with much greater intensity if a $5,000 reward awaited them at the finish line.
For many people, immediate financial incentives might provide stronger motivation than abstract health benefits years down the road. While most employers and insurance companies don’t offer five-figure weight loss bonuses, some are beginning to experiment with smaller financial incentives, reduced insurance premiums, or wellness program rewards for hitting health milestones.
Why Access and Affordability Keep Americans Stuck
Dr. Primack pointed to systemic issues that make sustained weight loss difficult for many Americans. “Affordability, access, and fragmented care remain some of the biggest obstacles standing between people and long-term success on their health and wellness journeys,” he said. “Many people cycle through disconnected diets, programs and appointments that add up quickly without providing consistent, sustained support.”
Coordinated care that brings together nutrition guidance, physical activity support, and medical oversight in one place could help reduce both costs and dropout rates. When people bounce between separate appointments with nutritionists, personal trainers, and doctors who may not communicate with each other, care becomes expensive, time-consuming, and often contradictory.
Around the world, Taylor Swift’s fan base skews female. (Credit: rblfmr on Shutterstock)
Taylor Swift’s latest album, “The Life of a Showgirl,” generated a cultural whirlwind: chart-topping success, social media saturation and frenzied debate over her artistic evolution.
Nonetheless, despite this warm reception, opinions on Swift are deeply polarized by party. Democrats are far more likely to view her positively; Republicans are more likely to hold negative views. This partisan divide remains in place even after accounting for age, gender and other demographic differences.
We are political scientists who conduct research on public opinion. In our just-published study, “Mirrorball Politics,” we draw on national survey data to examine how Americans feel about Swift and what those feelings reveal about our politics. What we find is striking: Swift has become a cultural mirror, reflecting our society’s deepest social and political fault lines.
In other words, liking or disliking Swift has become yet another way Americans signal who they are politically. Young women love her, but young men don’t – and that gap matters.
This is part of a broader trend in which cultural preferences and political identity have collapsed into each other. The type of beer you drink, the kind of car you drive, the stores you shop at and now the musical artists you admire have become markers of political belonging – and difference.
Popular entertainment used to be a common space where Americans, regardless of whether they were Republicans or Democrats, could come together and have some fun. Those shared spaces are shrinking – and with them the opportunity for connection across partisan divides.
The Swifties Gap
That’s why feelings toward Swift offer warning signs for the future of American politics.
One of the starkest divides we found is between young men and young women. Gen Z women – those born between 1997 and 2012 – admire Swift. Gen Z men, not so much. On a 100-point scale measuring attitudes toward Swift, young women averaged 55, while young men averaged 43 – a statistically significant difference that was not present among older Americans.
This gender gap mirrors the widening political divide among younger Americans that played a pivotal role in the 2024 presidential election. Although a modest gender gap has been a consistent, defining feature of American electoral politics since 1980, the gap among young Americans is huge.
Young women are markedly progressive in their politics. Young men, by contrast, are trending rightward.
Many young men express skepticism toward feminism, discomfort with shifts in gender norms and a growing attraction to more conservative cultural messaging.
Haters Gonna Hate
This yawning gender gap is also reflected in views regarding Swift.
The strongest predictor of negative views of the singer, aside from partisanship, is “hostile sexism.” This is defined as negative attitudes toward women and a sense that men should dominate.
Our study finds that individuals who believe that women’s achievements come at men’s expense, or that women have too much power, are far more likely to dislike Swift. This effect is especially strong among men and particularly among Republican men.
Swift’s enormous success, artistic autonomy and cultural influence appear to trigger anxieties about women’s power in public life. The backlash is not about her lyrics or her image. It’s about what she represents: a confident, self-directed woman at the center of American culture.
This dynamic reveals the broader challenges facing women in positions of authority, including in politics. Hostile sexism remains a force in American society and a formidable barrier for any woman aspiring to the presidency.
Swift As A Visible Symbol
Swift didn’t create these divisions – she is simply reflecting them back. But the intensity of the reaction to her success reveals how conflicted America remains about women’s power.
Our study also shows that people who scored high on hostile sexism were much more likely to hold negative views of Kamala Harris during the presidential election of 2024. This mirrors findings from earlier research showing that hostile sexism was one of the strongest reasons voters did not support Hillary Clinton in 2016.
Taking a moment to reflect before judging your own performance sounds like solid advice. But new research suggests that for people experiencing anxiety symptoms, pausing to second-guess themselves might deepen their self-doubt.
Scientists at University College London and the University of Copenhagen have discovered that anxiety-driven underconfidence grows stronger the longer someone takes to judge how they did on a decision they just made. The study, published in Psychological Medicine, analyzed confidence ratings from 1,447 people across multiple decision-making tasks. For anxious individuals, extra time for introspection actually makes their self-doubt worse.
The researchers found that people with higher anxiety symptoms accumulate negatively biased thoughts about their performance over time, deepening underconfidence as they spend more time reflecting.
How Scientists Measured Confidence in Real-Time
Researchers pooled data from four experiments where participants completed visual decision-making tasks, such as identifying which color appeared more frequently on screen or remembering objects from a brief display. After each decision, participants rated their confidence on a scale, and scientists measured how long they took to provide that rating.
The study collected information about participants’ anxiety levels using standardized questionnaires and tracked gender differences across the sample. Sample sizes for individual experiments ranged from 300 to 433 participants, all recruited online. The researchers excluded trials with unusually fast or slow response times to ensure data quality.
Anxiety and the Snowball Effect
The key finding emerged when researchers plotted confidence levels against the time participants took to report them. For people with higher anxiety symptoms, confidence dropped more steeply as they spent additional seconds contemplating their performance. The gap between low-anxiety and high-anxiety individuals widened with every passing moment of reflection.
This pattern held across multiple experiments and different types of tasks, showing the effect is robust and not limited to one specific scenario.
What makes this particularly notable is that the effect worked in the opposite direction for gender-related underconfidence. On average, women reported lower confidence than men immediately after making decisions, but that gap narrowed when they took more time to reflect. By the longest response times, the gender difference in confidence essentially disappeared.
Computational Models Reveal Why Time Helps Some but Hurts Others
To understand what drives these opposite patterns, researchers built a computational model based on drift-diffusion theory, which treats decision-making as an evidence accumulation process. Information builds up over time until it crosses a threshold that triggers a choice.
The team extended this framework to model different sources of distorted confidence: two kinds of confidence drag. One involves starting with a lower baseline of confidence. The other involves a downward pull that grows the longer someone thinks about their performance.
When they fit this model to individual participants’ data, anxiety stood out because confidence got worse with more reflection time, suggesting negative self-doubt built up during that extra time. People with anxiety symptoms showed both a lower starting point for confidence and this ongoing accumulation of negative thoughts about their performance.
Gender-related underconfidence, by contrast, stemmed only from that lower starting point, without the ongoing buildup of negative thoughts.
What the Patterns Might Mean
One possibility is that extra reflection gives anxious people more room to replay mistakes or imagine they got it wrong, even when their performance hasn’t changed. For the gender gap, extra time may let people double-check the decision in their mind and override a snap feeling of being probably wrong.
The study also offers a potential window into why anxiety might fuel rumination: the tendency to get stuck in negative thought loops. If people with anxiety symptoms are accumulating biased negative evidence about their abilities over time, extended reflection literally makes them feel worse about themselves, creating a feedback loop that reinforces self-doubt.
It’s worth noting that this study looked at split-second confidence ratings in simple online tasks, not treatment approaches or real-world performance reviews. The study focused on immediate post-decision reflection, typically lasting only a few seconds. Whether these patterns extend to longer-term rumination or self-evaluation remains an open question. The tasks used were also relatively simple perceptual and memory challenges, so whether the same dynamics would apply to evaluating performance in complex real-world situations like job interviews or creative projects is unclear.
When former athletes with severe brain damage experience cognitive issues, doctors have been quick to blame Alzheimer’s disease in recent years. Notably, however, autopsies later revealed many of those patients actually had no Alzheimer’s at all. They had chronic traumatic encephalopathy (CTE). Researchers estimate CTE was misdiagnosed as dementia in 40% of advanced cases.
The finding comes from a Boston University study of 614 brain donors, including 366 with CTE. Among the 99 donors with advanced CTE who had been diagnosed with dementia during life, only 17% of physicians correctly identified CTE as the cause. The misdiagnosis rate points to a troubling gap in how doctors recognize this disease.
The study, published in Alzheimer’s & Dementia, also revealed differences by disease stage. Among donors with the most severe CTE (stage IV), roughly 8 in 10 had dementia before death, compared to just 16% of those without CTE. Those with stage IV were more than four times as likely to have had dementia. But surprisingly, early-stage CTE showed no connection to memory problems at all. Moreover, despite common assumptions, CTE severity had no link to depression or behavioral issues.
How the Disease Progresses
CTE comes in four stages as abnormal proteins gradually spread through the brain. Early stages (I and II) involve small pockets of damage in the frontal regions. By stage III, the proteins reach deeper memory areas. Stage IV means widespread damage across much of the brain.
Family members of the deceased athletes filled out detailed surveys about memory problems, personality changes, and daily functioning before death. Researchers combined these accounts with medical records to determine who had dementia.
The connection became clear at advanced stages. Stage IV donors scored about twice as high on cognitive difficulty assessments as people without CTE. They struggled far more with basic tasks like managing finances or remembering appointments.
Early-Stage CTE Shows No Symptoms
Early-stage CTE showed no link to dementia or memory problems at all. Stages I and II looked essentially the same as having no CTE.
“It is uncertain if low-stage CTE clinically manifests,” the authors wrote. This suggests the brain can initially tolerate small amounts of damage before symptoms appear.
This finding challenges assumptions that any amount of CTE causes problems. The brain appears capable of withstanding limited damage without triggering memory loss or personality changes. It’s only when the disease reaches advanced stages that dementia becomes highly likely.
Why the Confusion Happens
Both CTE and Alzheimer’s attack memory first, and patients show similar symptoms in the doctor’s office. Former football players often struggle to recall recent events and conversations, just like Alzheimer’s patients do. Without a brain scan that can detect CTE, doctors often assume the more common diagnosis.
Vascular dementia accounted for another 10% of misdiagnoses, and 38% of doctors labeled the condition as “dementia unspecified or unknown.” Among all the physicians who diagnosed dementia in patients with advanced CTE, only 17% correctly identified CTE as the cause.
This raises a troubling possibility: some former athletes with dementia may be told they have Alzheimer’s when the real cause is CTE. The study can’t put a number on how often this happens among living people, but the mismatch researchers found in autopsy cases suggests it could be more common than anyone realizes.
Severe CTE Strongly Linked to Dementia
CTE severity had no connection to depression, anxiety, or impulsiveness in this study. That finding contradicts popular assumptions that CTE directly causes the mood and behavior problems many former athletes experience.
More likely, those symptoms come from multiple sources. Brain imaging often shows damage to white matter (the brain’s wiring) and blood vessels in former players. Chronic pain, sleep problems, and past substance use probably contribute too. CTE might be one factor among many, rather than the sole culprit for behavioral issues.
Some former athletes struggle with anger, depression, or impulsive behavior for years before memory problems appear. This study suggests those early struggles may not come from CTE itself, but from the accumulated toll of repeated hits, injuries, and the lifestyle that often accompanies professional sports.
Even after researchers accounted for blood vessel damage and other brain issues, the link between severe CTE and dementia held firm. Mood symptoms remained unconnected to disease stage.
What This Means for Athletes
The study focused almost entirely on male athletes, with 80% having played American football. Most with severe CTE had played at the college or professional level for many years. Those with the worst brain damage had typically started playing young and continued for decades.
The good news, if any exists here, is that mild CTE may not cause symptoms. The brain appears capable of withstanding limited damage without triggering memory loss or personality changes. The bad news is that once CTE reaches advanced stages, dementia becomes highly likely.
Researchers also found that age matters less than disease severity. Even when they looked specifically at donors 52 and older to control for natural aging, advanced CTE still carried the same elevated dementia risk. The disease itself, not just getting older, drives cognitive decline.
The Challenge of CTE Diagnosis
Right now, doctors cannot diagnose CTE in living people. Brain tissue must be examined under a microscope after death to spot the telltale protein deposits around blood vessels. This leaves athletes and their families in limbo, wondering whether symptoms stem from CTE or something else entirely.
Researchers are racing to develop imaging tests or blood markers that could spot the disease earlier. Such tools would help doctors distinguish CTE from Alzheimer’s and could potentially open the door to treatments if caught early enough.
Huge tornado near Omaha, Nebraska during a tornado outbreak on April 26th, 2024. (Photo by Jonah Lange on Shutterstock)
Tornado warnings sent to smartphones typically only give local residents around 15 minutes to take shelter. That’s barely enough time to gather family, grab essentials, and find somewhere safe to ride out the weather event. Now, scientists say they’ve identified atmospheric clues that appear up to an hour before a tornado touches down. These signals may someday help forecasters issue warnings earlier.
Researchers analyzing an experimental weather prediction system have pinpointed specific environmental patterns that helped separate storms that went on to produce tornadoes from similar storms that produced large hail instead. The work hints at a future where warnings could arrive with enough lead time for people to make better decisions about seeking shelter.
The key lies in what’s happening close to the ground. Tornado-producing storms showed dramatically stronger low-level wind patterns that favor rotation in the lowest 500 meters (roughly 1,600 feet) compared to storms that only hurled giant hailstones. These differences weren’t subtle. They persisted for the entire hour leading up to tornadoes and showed up consistently across storms from Texas to Nebraska.
Reading the Storm’s Environment
The Warn-on-Forecast System, developed by NOAA, updates every 15 minutes by ingesting the latest radar and satellite data. The weather model creates a constantly evolving picture of developing storms.
For this study, published in Weather and Forecasting, researchers examined 41 severe thunderstorms between 2017 and 2023. Fifteen produced tornadoes rated EF1 or stronger. That’s powerful enough to tear roofs off houses. The other 26 produced golf ball-sized hail or larger but no tornadoes.
The computer model revealed something forecasters couldn’t easily see before: small pockets of especially favorable low-level wind patterns in the storm’s inflow region. These conditions that favor tornado formation appeared much stronger and larger around tornado-producing storms.
Researchers also tracked how conditions changed as air flowed toward each storm during the hour before severe weather struck. Air feeding into tornadic storms encountered increasingly favorable conditions along the way, like a car accelerating downhill. Air approaching hail storms showed less dramatic changes.
The Cloud Base Connection
Another telling difference appeared overhead. Tornado-producing storms had cloud bases (the bottom of the clouds) that hung 1,600 to 3,300 feet closer to the ground than hail-only storms. Lower clouds mean the rotating column of air has less distance to stretch before reaching the surface.
This pattern held steady throughout the pre-tornado period, not just in the final minutes.
Interestingly, some atmospheric measurements that meteorologists typically examine showed little difference between the two storm types. The overall energy available to fuel storms and the rotation extending higher into the atmosphere were similar whether tornadoes formed or not. The crucial distinctions happened in that critical zone near the ground.
From Research to Reality
The study focused on storms in the Great Plains during May, when tornado season peaks. Whether these patterns hold true for winter tornadoes in the Southeast or storms in other regions remains an open question with the current sample size.
The Warn-on-Forecast System only runs on days when severe weather seems likely, and it covers specific geographic areas, meaning it misses plenty of tornadoes that occur on lower-risk days or outside its domain. The researchers examined a modest 41 storms, acknowledging that broader patterns might emerge with more data.
The model’s three-kilometer resolution means it can’t simulate actual tornadoes forming, but it captures the environmental conditions that make them possible. For forecasters watching storms develop in real time, knowing which supercells are moving into these tornado-favoring setups could eventually translate into earlier warnings.
Creatine supplements can be particularly beneficial for building strength. (Credit: Chay_Tee on Shutterstock)
Creatine is one of the most popular sports supplements out there. It’s shown to help build muscle and improve strength, boost speed and power in athletes and benefit sports performance all round.
Research also suggests this superstar nutrient may have other health benefits, including for brain function, memory, bone health and even mood.
While creatine has been a mainstay supplement for gym enthusiasts, most of the research on this supplement’s benefits has been conducted on men. With recent increased advertising specifically promoting creatine for women, there is growing interest in whether this nutrient can also be equally beneficial for them.
It’s already clear from the research that creatine could benefit women by reducing fatigue during exercise. It may also be particularly beneficial for maintaining muscle as women get older.
Creatine is a natural compound produced in the body from several amino acids (the building blocks from protein). We can also get it from protein-rich foods, such as meat and seafood.
Creatine plays a role in short-term energy, particularly during intense exercise, helping us to recover quicker between exercises. This makes it possible to do more work each time we train, leading to around 20% greater performance gains when regularly taking the supplement.
We naturally use around 2g-4g of creatine per day. But as our bodies don’t store much creatine, this is why we need to consume it in our diet or get it from supplements. Think of it like a short-term energy store that needs topping up.
Around 1kg of raw beef or seafood would supply around 3g-5g of creatine. However, cooking can reduce creatine content. This makes it challenging to consistently get enough from the diet alone, which is where supplements can be useful.
Research also shows that vegans, vegetarians and women tend to have diets lower in creatine – meaning lower overall body stores. However, women do appear to store a bit more creatine in their muscles than men, suggesting they may respond to it slower or differently than men.
The most studied form of creatine is creatine monohydrate. This can be taken as a powder, capsule or gummy. If women consume around 3g-5g of creatine a day as a supplement, it will help gradually increase muscle creatine stores over a period of two to four weeks.
But if you’re looking to boost muscle stores faster, research shows taking around 20g of creatine a day for seven days (before dropping down to 3g-5g daily) can safely boost stores.
Creatine Benefits For Women
There are many factors which influence a women’s health over their lifetime. This includes hormonal changes, the gradual loss of muscle that comes with aging, loss of bone density and slower metabolism post-menopause – as well as fluctuating energy levels and poor concentration or focus.
Resistance exercise may be beneficial in mitigating some of these changes, particularly in supporting muscle mass and function, bone health and energy levels.
This is where creatine comes in. Doing resistance training for several weeks while taking around 3g-5g of additional creatine per day can enable you to maintain the quality and consistency of your training. This combination can be particularly beneficial for strength in mid to later life.
Women who take creatine consistently are shown to have improved muscle function, which ultimately can impact quality of life. There’s also some evidence that taking it alongside resistance training may support bone health in postmenopausal women – although not all studies agree on this.
It’s worth noting as well that creatine does not appear to lead to weight gain or cause a bulky, muscular appearance, which are often concerns for women thinking about taking the supplement.
More recently, research has been exploring whether creatine can affect brain health, cognitive function and possibly even mood in older women. Evidence also shows that in younger women, it can improve mood and cognitive function after a bad nights’ sleep.
There’s emerging evidence as well that taking 5g of creatine daily can help younger women sleep longer (particularly on days they’ve done a workout). The same dose may also improve sleep quality in perimenopausal women – possibly by supporting the energy required by the brain.
Another study also reported greater reductions in depressive symptoms in women taking 5g of creatine daily alongside antidepressants, compared to those just taking antidepressants.
Given many women report experiencing symptoms such as “brain fog,” poor concentration, stress, low energy and poor sleep during their menstrual cycle and throughout the menopause, this could make creatine a low-cost solution for many of these symptoms. However, a higher dose of creatine may be needed daily (around 5g-10g) to increase the brain’s creatine stores.
A group of volunteers spent days locked in a small hotel room with people actively infected with flu. They played games, shared objects and exercised together in conditions designed to help the virus spread. Yet not a single person caught influenza.
The unexpected finding comes from a well-designed study that set out to answer a basic question: how does flu really spread?
Influenza, the virus responsible for flu, is known to spread through aerosols (microscopic droplets) released when an infected person coughs, sneezes or even breathes normally. It can also pass from person to person via contaminated surfaces such as door handles or phones, known as fomite transmission.
How efficiently the virus spreads depends on several factors, including how much virus an infected person sheds, the temperature and humidity of a room and how close people are to one another.
To tease apart which of these factors matter most, researchers at the University of Maryland in the US ran a real-world transmission experiment using people who had caught flu naturally.
They brought together groups of participants in a hotel room, mixing people with active influenza infections, referred to as donors, with uninfected volunteers, referred to as recipients. The aim was simple: see whether flu would spread under conditions designed to favor transmission.
Despite prolonged close contact over several days, no recipient became infected.
This approach differed from earlier studies in which healthy volunteers were deliberately infected with influenza for research. By using naturally infected “donors,” the researchers hoped to better reflect how flu spreads outside the laboratory.
Two versions of the experiment were carried out. In one, a single donor shared a room with eight recipients. In the other, four donors shared with three recipients. Donors were aged 20 to 22, while recipients were aged between 25 and 45.
The room was kept at temperatures and humidity levels thought to favor influenza transmission, at 22°C to 25°C, and 20% to 45% humidity. Before quarantining the participants, the researchers closed off major uncontrolled air pathways – such as windows, doors and a leak in the fan coil units – to deliberately create low ventilation and poor air quality.
Over three to seven days, participants spent hours together in the confined space. They played card games at close range, took part in dance or yoga classes and passed around shared objects such as markers, microphones or tablet computers.
The researchers monitored transmission by measuring virus levels in exhaled air, saliva and mouth swabs from donors. Shared objects and the room air were also tested for viral particles. Participants recorded symptoms including coughing, sneezing, headaches and other common signs of flu.
Why Transmission Failed
Several samples from donors confirmed active influenza infection. But none of the recipients tested positive. A few reported mild symptoms such as headaches, but there was no clear evidence of flu infection in any of them.
The researchers suggest three main reasons why transmission may not have occurred: low virus shedding from donors, partial immunity among recipients and the way air circulated in the room.
Children are widely thought to drive the spread of influenza, but this study involved only adults. Adult donors in the experiment released relatively small amounts of virus. This may reflect the strains they were infected with, their age or the fact that they showed few symptoms. Very little coughing or sneezing was observed, which would have limited the amount of virus entering the air.
Recipients may also have been less susceptible. They had all lived through many flu seasons and several had received flu vaccinations in previous years, with one vaccinated in the current season. This prior exposure may have given them some background immunity.
Although temperature and humidity were set to favor transmission, the high level of air recirculation caused by fans may have disrupted clouds of virus-laden air. Instead of lingering around donors, these plumes may have been broken up and diluted, reducing how much virus recipients inhaled.
Taken together, the findings point to coughing and sneezing as key drivers of influenza spread, particularly from people who shed large amounts of virus, sometimes described as super spreaders. Immunity in those exposed and air movement in indoor spaces also appear to be crucial.
The study does not suggest that influenza is harmless or difficult to catch. Each year, millions, and possibly billions, of cases occur worldwide, with strong evidence that aerosol transmission plays a central role. Instead, it shows that the circumstances that allow flu to spread are more nuanced than simply sharing a room with an infected person.
Around the world, Taylor Swift’s fan base skews female. (Credit: rblfmr on Shutterstock)
Taylor Swift’s latest album, “The Life of a Showgirl,” generated a cultural whirlwind: chart-topping success, social media saturation and frenzied debate over her artistic evolution.
Nonetheless, despite this warm reception, opinions on Swift are deeply polarized by party. Democrats are far more likely to view her positively; Republicans are more likely to hold negative views. This partisan divide remains in place even after accounting for age, gender and other demographic differences.
We are political scientists who conduct research on public opinion. In our just-published study, “Mirrorball Politics,” we draw on national survey data to examine how Americans feel about Swift and what those feelings reveal about our politics. What we find is striking: Swift has become a cultural mirror, reflecting our society’s deepest social and political fault lines.
In other words, liking or disliking Swift has become yet another way Americans signal who they are politically. Young women love her, but young men don’t – and that gap matters.
This is part of a broader trend in which cultural preferences and political identity have collapsed into each other. The type of beer you drink, the kind of car you drive, the stores you shop at and now the musical artists you admire have become markers of political belonging – and difference.
Popular entertainment used to be a common space where Americans, regardless of whether they were Republicans or Democrats, could come together and have some fun. Those shared spaces are shrinking – and with them the opportunity for connection across partisan divides.
The Swifties Gap
That’s why feelings toward Swift offer warning signs for the future of American politics.
One of the starkest divides we found is between young men and young women. Gen Z women – those born between 1997 and 2012 – admire Swift. Gen Z men, not so much. On a 100-point scale measuring attitudes toward Swift, young women averaged 55, while young men averaged 43 – a statistically significant difference that was not present among older Americans.
This gender gap mirrors the widening political divide among younger Americans that played a pivotal role in the 2024 presidential election. Although a modest gender gap has been a consistent, defining feature of American electoral politics since 1980, the gap among young Americans is huge.
Young women are markedly progressive in their politics. Young men, by contrast, are trending rightward.
Many young men express skepticism toward feminism, discomfort with shifts in gender norms and a growing attraction to more conservative cultural messaging.
Haters Gonna Hate
This yawning gender gap is also reflected in views regarding Swift.
The strongest predictor of negative views of the singer, aside from partisanship, is “hostile sexism.” This is defined as negative attitudes toward women and a sense that men should dominate.
Our study finds that individuals who believe that women’s achievements come at men’s expense, or that women have too much power, are far more likely to dislike Swift. This effect is especially strong among men and particularly among Republican men.
Swift’s enormous success, artistic autonomy and cultural influence appear to trigger anxieties about women’s power in public life. The backlash is not about her lyrics or her image. It’s about what she represents: a confident, self-directed woman at the center of American culture.
This dynamic reveals the broader challenges facing women in positions of authority, including in politics. Hostile sexism remains a force in American society and a formidable barrier for any woman aspiring to the presidency.
A group of volunteers spent days locked in a small hotel room with people actively infected with flu. They played games, shared objects and exercised together in conditions designed to help the virus spread. Yet not a single person caught influenza.
The unexpected finding comes from a well-designed study that set out to answer a basic question: how does flu really spread?
Influenza, the virus responsible for flu, is known to spread through aerosols (microscopic droplets) released when an infected person coughs, sneezes or even breathes normally. It can also pass from person to person via contaminated surfaces such as door handles or phones, known as fomite transmission.
How efficiently the virus spreads depends on several factors, including how much virus an infected person sheds, the temperature and humidity of a room and how close people are to one another.
To tease apart which of these factors matter most, researchers at the University of Maryland in the US ran a real-world transmission experiment using people who had caught flu naturally.
They brought together groups of participants in a hotel room, mixing people with active influenza infections, referred to as donors, with uninfected volunteers, referred to as recipients. The aim was simple: see whether flu would spread under conditions designed to favor transmission.
Despite prolonged close contact over several days, no recipient became infected.
This approach differed from earlier studies in which healthy volunteers were deliberately infected with influenza for research. By using naturally infected “donors,” the researchers hoped to better reflect how flu spreads outside the laboratory.
Two versions of the experiment were carried out. In one, a single donor shared a room with eight recipients. In the other, four donors shared with three recipients. Donors were aged 20 to 22, while recipients were aged between 25 and 45.
The room was kept at temperatures and humidity levels thought to favor influenza transmission, at 22°C to 25°C, and 20% to 45% humidity. Before quarantining the participants, the researchers closed off major uncontrolled air pathways – such as windows, doors and a leak in the fan coil units – to deliberately create low ventilation and poor air quality.
Over three to seven days, participants spent hours together in the confined space. They played card games at close range, took part in dance or yoga classes and passed around shared objects such as markers, microphones or tablet computers.
The researchers monitored transmission by measuring virus levels in exhaled air, saliva and mouth swabs from donors. Shared objects and the room air were also tested for viral particles. Participants recorded symptoms including coughing, sneezing, headaches and other common signs of flu.
Why Transmission Failed
Several samples from donors confirmed active influenza infection. But none of the recipients tested positive. A few reported mild symptoms such as headaches, but there was no clear evidence of flu infection in any of them.
The researchers suggest three main reasons why transmission may not have occurred: low virus shedding from donors, partial immunity among recipients and the way air circulated in the room.
Children are widely thought to drive the spread of influenza, but this study involved only adults. Adult donors in the experiment released relatively small amounts of virus. This may reflect the strains they were infected with, their age or the fact that they showed few symptoms. Very little coughing or sneezing was observed, which would have limited the amount of virus entering the air.
Recipients may also have been less susceptible. They had all lived through many flu seasons and several had received flu vaccinations in previous years, with one vaccinated in the current season. This prior exposure may have given them some background immunity.
Although temperature and humidity were set to favor transmission, the high level of air recirculation caused by fans may have disrupted clouds of virus-laden air. Instead of lingering around donors, these plumes may have been broken up and diluted, reducing how much virus recipients inhaled.
Taken together, the findings point to coughing and sneezing as key drivers of influenza spread, particularly from people who shed large amounts of virus, sometimes described as super spreaders. Immunity in those exposed and air movement in indoor spaces also appear to be crucial.
The study does not suggest that influenza is harmless or difficult to catch. Each year, millions, and possibly billions, of cases occur worldwide, with strong evidence that aerosol transmission plays a central role. Instead, it shows that the circumstances that allow flu to spread are more nuanced than simply sharing a room with an infected person.
Not everyone sheds virus at the same level and not everyone is equally vulnerable. Aerosol spread is most likely during coughing and sneezing, so people with these symptoms should isolate where possible and wear a well-fitted mask to reduce virus release into the air. Good ventilation and air circulation are especially important in small, poorly ventilated spaces.
Committing to an exercise regimen isn’t easy, but a younger brain is a strong motivator. When researchers asked middle-aged adults to practice aerobic exercise regularly for a year, their brains became significantly “younger,” so to speak.
After 12 months of regular workouts, participants’ brains appeared about seven months younger than when they started. MRI scans analyzed by machine learning algorithms showed measurable structural changes associated with younger brains.
Scientists checked several likely explanations for why this may have happened, and none of them panned out. Fitness improved. Blood pressure didn’t budge. Weight stayed the same. Brain growth factors didn’t show clear changes. None of those factors accounted for the brain age shift.
“The pathways by which these effects occur remain unknown,” researchers from the University of Pittsburgh and AdventHealth Research Institute wrote in the Journal of Sport and Health Science.
The study tracked 130 adults between ages 26 and 58, none of them particularly active to start. Half were assigned to an exercise program, half to a control group that just received general health information. The exercise group committed to 150 minutes of moderate aerobic activity per week, the same recommendation countless doctors give to their patients. Two sessions per week happened in a university lab with supervision, and the rest at home (walking, jogging, treadmills, bikes, ellipticals, etc.).
What Brain Age Actually Measures
To better understand “brain age,” researchers fed thousands of MRI scans into a computer, teaching it what a typical 30-year-old brain looks like versus a typical 50-year-old brain. The patterns involve brain volume, structure, and other subtle neurological features.
When someone gets a brain scan, the computer predicts their age based purely on what it sees. If you’re 45 but your brain looks more like that of a typical 48-year-old, you’re aging faster than average. If your brain looks 42, you’re aging slower.
In other studies, each extra year on this brain-aging measure has been linked to about a 3% higher risk of developing dementia down the road. People whose brains look older than their age tend to die earlier and show cognitive decline sooner. Your brain age in midlife may be forecasting your mental sharpness in your 70s and 80s.
The Fitness Connection Nobody Can Explain
Before the study started, researchers found something in the baseline measurements. People who were more fit had younger-looking brains. For every meaningful bump in measured cardio fitness, brain age looked nearly two years younger on average.
So when the exercise group got fitter over the year (and they did, measurably) researchers expected that would explain everything. It didn’t. Yes, fitness improved. Yes, brain age dropped. However, the statistical analysis showed fitness improvements didn’t account for the brain changes.
Body composition? No change in either group. Blood pressure? Same story. BDNF, a protein often linked to brain health, didn’t show a clear, meaningful increase in exercisers, and it didn’t explain the brain age changes anyway.
The researchers ticked through the usual suspects they’d measured. Nothing added up.
“That was a surprise,” said lead author Dr. Lu Wan, a data scientist at the AdventHealth Research Institute, in a statement. “We expected improvements in fitness or blood pressure to account for the effect, but they didn’t. Exercise may be acting through additional mechanisms we haven’t captured yet, such as subtle changes in brain structure, inflammation, vascular health or other molecular factors.”
What Might Be Happening (Besides What They Measured)
Of course, the brain doesn’t exist in isolation. Exercise triggers a cascade of changes throughout the body, and researchers only measured a handful of possibilities.
Maybe exercise altered inflammatory signals in ways the study didn’t capture. Perhaps it improved blood flow to the brain through mechanisms that wouldn’t show up in simple blood pressure readings. Mitochondria, the tiny power plants in cells, might have gotten more efficient. Metabolic changes could have occurred that weren’t tracked.
Alternatively, brains may have responded to exercise through pathways science hasn’t fully mapped yet. The study wasn’t designed to measure every possible mechanism, just the most obvious candidates.
What researchers do know is that 150 minutes of weekly aerobic exercise (two and a half hours, broken up however one wants) was enough to produce measurable changes in brain structure within a year.
Why Your 30s, 40s, and 50s Matter
Most brain aging studies focus on people in their 70s and 80s, after cognitive decline has already started. This study deliberately targeted younger adults because midlife appears to be a pivot point.
Risk factors that show up in your 40s (high blood pressure, obesity, inactivity) predict dementia risk 20 or 30 years later. But midlife is also when intervention might matter most. Your brain is still resilient enough to respond, but aging processes have begun.
The participants in this study weren’t elderly, weren’t sick, and weren’t already showing cognitive problems. They were regular people, two-thirds of them women, averaging 41 years old. Most were sedentary, reporting less than 100 minutes of exercise per week before the study started. In other words, they looked like a lot of American adults.
Their brains at the study’s start were aging normally on average, though individual participants varied quite a bit. Twelve months of exercise changed that trajectory.
The Exercise Program That Worked
Nothing about the workout regimen required a gym membership or special equipment. Participants walked, jogged, or used whatever cardio equipment they had access to. Heart rate monitors ensured they worked hard enough, breathing heavily but still able to talk, working at about 60-75% of their maximum heart rate.
The group stuck with it remarkably well. They completed 93% of their prescribed exercise minutes. Lab attendance hit 73%, and people made up the difference at home.
Meanwhile, the control group’s fitness declined slightly over the year, as tends to happen when sedentary people stay sedentary. Their brain age drifted slightly upward on average.
The pandemic also complicated things. Some participants couldn’t complete final assessments, and for several months in 2020, lab sessions shut down entirely. Still, 89% of the exercise group returned once facilities reopened, and the results held.
Why did this community burn one woman’s remains in such a visible, spectacular way? (Credit: T.Photo on Shutterstock)
Near the equator, the Sun hurries below the horizon in a matter of minutes. Darkness seeps from the surrounding forest. Nearly 10,000 years ago, at the base of a mountain in Africa, people’s shadows stretch up the wall of a natural overhang of stone.
They’re lit by a ferocious fire that’s been burning for hours, visible even to people miles away. The wind carries the smell of burning. This fire will linger in community memory for generations − and in the archaeological record for far longer.
We are a team of bioarchaeologists, archaeologists and forensic anthropologists who, with our colleagues, recently discovered the earliest evidence of cremation – the transformation of a body from flesh to burned bone fragments and ashes – in Africa and the earliest example of an adult pyre cremation in the world.
It’s no easy task to produce, create and maintain an open fire strong enough to completely burn a human body. While the earliest cremation in the world dates to about 40,000 years ago in Australia, that body was not fully burned.
It is far more effective to use a pyre: an intentionally built structure of combustible fuel. Pyres appear in the archaeological record only about 11,500 years ago, with the earliest known example containing a cremated child under a house floor in Alaska.
Many cultures have practiced cremation, and the bones, ash and other residues from these events help archaeologists piece together past funeral rituals. Our scientific paper, published in the journal Science Advances, describes a spectacular event that happened about 9,500 years ago in Malawi in south-central Africa, challenging long-held notions about how hunter-gatherers treat their dead.
The Discovery
At first it was just a hint of ash, then more. It expanded downward and outward, becoming thicker and harder. Pockets of dark earth briefly appeared and disappeared under trowels and brushes until one of the excavators stopped. They pointed to a small bone at the base of a 1½-foot (0.5-meter) wall of archaeological ash revealed under a natural stone overhang at the Hora 1 archaeological site in northern Malawi.
The bone was the broken end of a humerus, from the upper arm of a person. And clinging to the very end of it was the matching end of the lower arm, the radius. Here was a human elbow joint, burned and fractured, preserved in sediments full of debris from the daily lives of Stone Age hunter-gatherers.
We wondered whether this could be a funeral pyre, but such structures are extremely rare in the archaeological record.
Finding a cremated person from the Stone Age also seemed impossible because cremation is not generally practiced by African foragers, either living or ancient. The earliest evidence of burned human remains from Africa date to around 7,500 years ago, but that body was incompletely burned, and there was no evidence of a pyre.
The first clear cases of cremation date to around 3,300 years ago, carried out by early pastoralists in eastern Africa. But overall the practice remained rare and is associated with food-producing societies and not hunter-gatherers.
We found more charred human remains in a small cluster, while the ash layer itself was as large as a queen bed. The blaze must have been enormous.
When we returned from fieldwork and received our first radiocarbon dates, we were shocked again: The event had happened about 9,500 years ago.
Piecing Together The Events
We built a team of specialists to piece together what had happened. By applying forensic and bioarchaeological techniques, we confirmed that all the bones belonged to a single person who was cremated shortly after her death.
This was a small adult, probably a woman, just under 5 feet (1.5 meters) in height. In life, she was physically active, with a strong upper body, but had evidence of a partially healed bone infection on her arm. Bone development and the beginnings of arthritis suggested she was probably middle-aged when she died.
Patterns of warping, cracks and discoloration caused by fire damage showed her body was burned with some flesh still on it, in a fire reaching at least 1,000 degrees Fahrenheit (540 degrees Celsius). Under the microscope we could see tiny incisions along her arms and at muscle connections on her legs, revealing that people tending the pyre used stone tools to help the process along by removing flesh.
Within the pyre ash, we found many small pointed chips of stone that suggested people had added tools to the fire as it burned.
And the way the bones were clustered inside such a large fire showed that this was not a case of cannibalism: It was some other kind of ritual.
Perhaps most surprisingly, we found no evidence of her head. Skull bones and teeth usually preserve well in cremations because they are very dense. While we can’t know for sure, the absence of these body parts suggest her head may have been removed before or during the cremation as part of the funeral ritual.
A Communal Spectacle
We determined that the pyre must have been built and maintained by multiple people who were actively engaged in the event. During new excavations the following year, we found even more bone fragments from the same ancient woman, displaced and colored differently from in the main pyre. These additional remains suggest that the body was manipulated, attended and moved during the cremation.
Microscopic analysis of ash samples from across the pyre included blackened fungus, reddened soil from termite structures, and microscopic plant remains. These helped us estimate that people collected at least 70 pounds (30 kg) of deadwood to do the task and stoked the fire for hours to days.
We also learned that this was not the first fire at the Hora 1 site – nor its last. To our astonishment, what had seemed during fieldwork to be a single massive pile of ash was in fact a layered series of burning events. Radiocarbon dating of the ash samples showed that people began lighting fires on that spot by about 10,240 years ago. The same location was used to construct the cremation pyre several hundred years later. As the pyre smoldered, new fires were kindled on top of it, resulting in fused ashes in microscopic layers.
Within a few hundred years of the main event, another large fire was built again at the exact same place. While there is no evidence that anyone else was cremated in the subsequent fires, the fact that people repeatedly returned to the spot for this purpose suggests its significance lived on in community memory.
A New View Of Ancient Cremation
What does all of this tell us about ancient hunter-gatherers in the region?
For one, it shows that entire communities were engaged in a mortuary spectacle of extraordinary scale. An open pyre can take more than a day of constant tending and an enormous amount of fuel to fully reduce a body, and during this time the sights and smells of burning wood and other remains are impossible to hide.
This scale of mortuary effort is unexpected for this time and place. In the African record, complex multigenerational mortuary rituals tied to specific places are generally not associated with a hunting-and-gathering way of life.
Both age and menopause appear to influence attraction – but in different ways.
(Photo by oneinchpunch on Shutterstock)
Women’s preferences for masculine features in men shift as they age and transition through menopause, according to research exploring how attraction evolves throughout the female lifespan.
The small study of 122 Polish women aged 19 to 70 found distinct patterns across age groups and menopausal stages. Older women preferred men with fuller beards and lighter builds, while postmenopausal women rated feminized faces as less attractive compared to younger women.
Published in Adaptive Human Behavior and Physiology, the study examined how women at three different life stages evaluated photographs of men that had been digitally altered to show varying degrees of facial masculinity, beardedness, body shape, and muscle mass.
Age Shapes Preferences for Facial Hair and Build
Women’s age emerged as a significant factor in their assessments. Older women rated men with medium and full facial hair as more attractive than younger women did. This preference may reflect associations between beards and maturity, status, and resource acquisition rather than purely reproductive signals.
Light muscularity also became more attractive to older women. Well-built physiques signal genetic fitness and physical strength, traits that younger women in their reproductive years may prioritize. As women age and reproductive concerns diminish, lighter musculature suggesting health and approachability becomes more appealing than intimidating displays of strength.
Menopausal Status Shows Distinct Effects
Beyond age, menopausal status itself influenced some preferences. The research team included 45 premenopausal women, 30 perimenopausal women, and 47 postmenopausal women. Each viewed digitally modified photographs of a 22-year-old male model altered to show different facial structures, amounts of facial hair, body types, and muscle development.
Postmenopausal women rated feminized male faces as less attractive than women in other life stages. This finding is complicated, however, because age alone seemed to push preferences slightly in the opposite direction—older women across the board rated feminized faces as somewhat more attractive, but this effect was small.
Postmenopausal women also showed a trend toward rating V-shaped body silhouettes as less attractive, though this result was weaker and reached only borderline statistical significance. They perceived men with medium muscularity as more aggressive than other groups did. Age and menopausal status had no effect on how women judged social dominance.
What Might Explain These Changes
Hormonal changes during menopause may help explain these shifting preferences. Declining estrogen levels affect not just physical symptoms but potentially also how women perceive and evaluate potential partners. The study didn’t measure hormone levels directly, but the pattern fits with what researchers know about reproductive biology.
During reproductive years, women tend to prefer traits signaling genetic fitness and reproductive success, such as masculinized features, muscular bodies, and aggressive dominance. As women transition through menopause, their priorities may shift toward characteristics supporting long-term relationships and social cooperation rather than reproductive potential.
This aligns with the “grandmother hypothesis,” which explains the extended post-reproductive period in human females. After ovarian function ceases, women may redirect attention from mate selection toward caring for grandchildren and supporting family networks. A postmenopausal woman focuses on helping her daughters raise children rather than seeking partners with the best reproductive genetics.
Understanding Attraction Across the Lifespan
The findings suggest that attraction isn’t static across a woman’s life. What women find appealing in men appears to shift with different life stages in ways that may reflect changing biological priorities.
Researchers carefully modified the photographs to ensure consistent changes across all images. Women evaluated each variation on a 10-point scale for physical attractiveness, perceived aggression, and social dominance. The controlled methodology allowed the team to isolate which specific features drove different reactions across age groups.
The study focused specifically on secondary sexual characteristics—traits like facial structure, body shape, and hair distribution that distinguish males from females beyond reproductive organs. These features serve as biological signals that women may interpret differently depending on their life stage.
Whether a woman is in her reproductive years or post-menopause appears to influence what she notices and values in male appearance, though the mechanisms behind these changes require further research to fully understand.
Mice given processed fats struggled to adapt to winter.
Struggling to understand why your metabolism seems out of sync with the seasons? Your body might be stuck thinking it’s still summer, thanks to the types of fats lurking in processed foods. A study from the University of California, San Francisco, suggests it’s not just how much fat you eat, but rather the ratio of different fat types that may tell your internal clock what season it is.
Scientists discovered that mice fed diets low in certain types of fats showed a summer-like pattern, taking longer to sync with winter light cycles. These animals kept warmer body temperatures, a sign their metabolism stayed in summer mode. Diets with the same calories but different fat types produced completely different effects on how bodies tracked seasons.
Published in Science, the study shows that mouse brains have a built-in seasonal timer that reads the fats they eat. This discovery suggests modern diets rich in hydrogenated oils and processed fats might create similar confusion in humans, though scientists haven’t tested that yet.
Why Fat Type Acts Like a Seasonal Signal
In nature, many plants and animals pack more polyunsaturated fats (PUFAs) into their tissues during winter. It helps them stay flexible in cold temperatures. So a diet high in PUFAs signals winter, while a diet low in PUFAs signals summer—the season when animals naturally store energy for leaner times ahead.
Lead researcher Daniel Levine and colleagues zeroed in on a molecular switch that controls the body’s internal clock. Earlier work from the same lab had connected this switch to how mice and humans sense nutrients and regulate sleep timing.
When researchers fed mice high-fat diets that differed only in their fat composition, the differences were clear. Animals eating fewer polyunsaturated fats adjusted their daily patterns more slowly to winter lighting, taking about 40% longer than mice eating more of these fats. During summer lighting, these same mice adjusted faster, as if their bodies expected abundant food.
Looking at brain tissue, the team found that diets lower in polyunsaturated fats flipped this molecular switch in the hypothalamus, the brain’s control center for daily rhythms and metabolism. The change affected how cells produced signaling molecules and raised body temperature.
Genes Prove Fat Types Actually Control the Clock
To make sure this switch actually caused the effects rather than just happening alongside them, the team studied genetically modified mice. These animals were engineered so the switch couldn’t flip.
The results were clear: These mice adjusted to seasonal lighting at steady rates no matter what they ate. Regular mice? Their adjustment speed changed dramatically based on fat type.
The genetic evidence proved dietary fat composition actively controls how bodies track seasons, not just correlates with it. Mice unable to flip this switch became immune to the seasonal signals hiding in their food.
Fasting experiments revealed another layer. When mice went without food, the switch flipped to winter mode, and animals shifted their daily schedules earlier. Analyzing which genes turned on and off showed this change affected hundreds of genes involved in processing polyunsaturated fats into signaling molecules.
How Food Processing Erases Winter
To isolate what fat saturation does, researchers made two high-fat diets with identical calories. One used regular corn oil, naturally high in polyunsaturated fats. The other used partially hydrogenated corn oil, where industrial processing converts polyunsaturated fats into more saturated types.
Mice fed the hydrogenated oil showed the flipped switch, warmer bodies, fewer signaling molecules, and slower adjustment to winter lighting. The genetically modified mice? No diet-related changes at all.
Partial hydrogenation, the same process that creates trans fats, strips away the seasonal signal that would normally say “winter is here.” What’s left is a metabolism displaying summer patterns: warmer body temperature and delayed clock adjustment.
The experiments tracked male mice for weeks as they adapted to new lighting schedules mimicking seasonal changes. Researchers even used computer-controlled feeding devices to test calorie restriction, which had opposite effects, helping mice adjust faster to winter. This suggests total calories and fat type send separate seasonal messages to the body.
What This Might Mean for Humans
Processed foods are available year-round with altered fat compositions. Combined with artificial lighting, this could create “seasonal confusion” between internal clocks and the actual environment. Many processed foods go through hydrogenation or contain different fat ratios than seasonal whole foods. Even products without trans fats might have fat profiles that signal the wrong season.
The research team points out that humans with a genetic mutation affecting the same molecular switch develop a sleep disorder where they crash early and wake at dawn. This proves the pathway exists in humans—but whether dietary fats affect human daily rhythms the same way needs direct testing.
Deep beneath the surface of our planet lies the Earth’s core, a solid ball of iron under crushing pressure. Now, however, scientists conducting laboratory experiments have found evidence suggesting it may not be a uniform sphere after all.
Instead, lab tests on iron mixed with silicon and carbon show properties consistent with a layered structure, with different chemical compositions at different depths. If correct, this hidden structure would have formed as the core crystallized from the center outward, naturally sorting lightweight elements toward the outer layers while leaving the center more iron-rich.
The work addresses a puzzle that has bothered geophysicists for decades. When earthquake waves travel through the inner core, they move at different speeds depending on which direction they’re headed, a property called anisotropy. Stranger still, this effect isn’t uniform. The outer portions of the inner core show weak anisotropy while the central region shows much stronger anisotropy. A compelling explanation has been difficult to pin down – until now.
A research team at the University of Münster in Germany may have found an answer by recreating inner core conditions in their lab. They squeezed iron mixed with small amounts of silicon and carbon (proportions scientists think may match the actual core) to crushing pressures in a diamond vise while heating it to extreme temperatures. When they measured how this material would affect seismic waves, something clicked: the silicon-carbon mixture showed low anisotropy, roughly consistent with what seismologists infer for the outer portion of the inner core. Pure iron, by contrast, showed high anisotropy matching observations from the center.
The results, published in Nature Communications, suggest Earth’s core could be chemically stratified rather than uniform.
How Freezing Iron Could Have Created Layers
The core didn’t start out solid. As Earth cooled over geological time, conditions at the center eventually allowed iron to begin crystallizing despite the crushing pressure. That process continues today, with the boundary between solid inner core and liquid outer core slowly advancing outward.
Crucially, as molten iron freezes onto the growing inner core, silicon and carbon get incorporated at levels that depend on temperature and pressure. Studies of iron alloys show that cooler temperatures and lower pressures both favor more silicon and carbon dissolving into solid iron. Since pressure drops as you move from center to edge, each successive layer that crystallized could have incorporated progressively more of these lightweight elements.
Think of it like making rock candy. As sugar solution slowly crystallizes, different conditions at different times can create layers with slightly different properties. Except this is 800 miles across, made of iron instead of sugar, and formed over vast stretches of geological time. If the model is correct, the oldest, most iron-rich material sits at the center while younger, more silicon-and-carbon-rich material forms the outer layers.
Squeezing Samples to Extreme Pressures
The team couldn’t drill to the core, obviously. Instead, they brought approximations of core conditions to a lab in Germany using diamond anvil cells, which are devices that squeeze microscopic samples between two diamonds to create enormous pressures. They also heated the samples with electrical resistance.
The experiments hit pressures up to 128 gigapascals and temperatures up to 1,100 Kelvin. That’s not quite as extreme as the actual inner core, which experiences roughly three times more pressure and much higher temperatures; but close enough to help constrain models that project the behavior to true core conditions.
Powerful X-rays from a synchrotron facility revealed how the samples’ crystal structure deformed under stress. When iron is squeezed in one direction, the atomic layers can shift and align. This alignment controls how seismic waves travel through the material. By measuring the alignment in their tiny samples, the researchers could predict what earthquake waves might experience passing through a planetary volume of the same material.
Silicon and Carbon Change the Picture
The key finding: pure iron and the silicon-carbon alloy behave quite differently. Pure iron squeezed and heated to conditions approaching the core’s develops strong alignment that can make seismic waves travel several percent faster in one direction than another, often on the order of 6-7% in models. The iron-silicon-carbon mixture? Closer to 2%.
That’s consistent with what seismologists observe. The outer portion of the inner core shows roughly 2% anisotropy. The central region shows higher values, around 4-6%. If silicon and carbon concentrations increase toward the edge, as the crystallization process would predict, the seismic observations align with the laboratory findings.
The research also revealed that adding carbon strengthens the iron alloy significantly, making it more resistant to deformation. This affects how the material could develop its aligned structure over geological time as the core continues to evolve.
Why This Matters Beyond Cool Science
More broadly, because the core helps power Earth’s magnetic field through churning motions in the liquid outer core, understanding the solid inner core’s structure matters for modeling how this magnetic shield works. The field protects Earth’s surface from harmful solar radiation and has helped maintain habitable conditions over geological history.
Chemical layers in the solid inner core could influence heat flow and interactions at the boundary with the liquid outer core, potentially affecting the magnetic field’s pattern and stability. Knowing the inner core may have stratified structure helps scientists build better models of these deep Earth processes.
Mold lurking behind walls and under floors can sicken families for months before anyone realizes what’s wrong. Traditional mold testing requires swabbing surfaces, sending samples to labs, and waiting three to seven days for results, all while potentially harmful spores continue circulating through living spaces. Researchers at Germany’s Karlsruhe Institute of Technology have created an electronic “nose” that measures air samples in about 30 minutes and identifies toxic mold species with performance levels approaching laboratory-grade testing in controlled conditions.
AI-generated illustration of electronic nose for mold detection. (Image created by StudyFinds using Google Gemini)
The device works similarly to mold-detection dogs but eliminates the need for expensive animal training and provides something dogs cannot: precise identification of mold species. Published in Advanced Sensor Research, the study shows that sensor technology can distinguish between Stachybotrys chartarum and Chaetomium globosum, two of the most common and concerning molds found in water-damaged buildings. Both species thrive on moisture-compromised materials like drywall and wallpaper, producing metabolites linked to irritant and inflammatory responses in humans.
Indoor mold creates health and financial problems in many damp buildings. Current detection methods rely on visual inspection, air sampling, or surface swabs followed by laboratory culturing, a process that delays remediation efforts. While mold-detection dogs offer faster screening, their training is costly and time-intensive, and the animals can only signal mold presence without differentiating between species, a critical limitation when determining health risks and remediation strategies.
Electronic Nose Mold Detection Using Chemical Signatures
The innovative e-nose uses tin oxide nanowires as its sensing material. These microscopic wires change their electrical resistance when exposed to different volatile organic compounds, the chemical signatures that molds emit as metabolic byproducts. Each mold species gives off its own characteristic mix of gases that the sensor can recognize.
The device contains 16 individual sub-sensors, each coated with the same tin oxide nanowires but positioned to detect slight variations in the chemical signals. When ultraviolet light activates the nanowires, they become sensitive to gas molecules in the air. Mold compounds either directly oxidize or reduce the sensor surface, or they alter how oxygen interacts with it, changing the electrical resistance in measurable ways.
Researchers grew both mold species on two different substrates to simulate real-world variability: one substrate mixed agar with shredded gypsum board (mimicking drywall), while the other combined agar with wheat flour (representing paper and cellulose materials). Samples were incubated at 25 degrees Celsius with 60% humidity for at least 10 days until mold fully colonized the growth surface. The team conducted eight measurements for each mold species over two weeks. In their lab setup, each air sample was measured for about 30 minutes, and the system used that signal pattern to classify what it detected. The measurements generated about 324,000 data points through resampling.
Machine Learning Boosts Mold Detection Performance to 98.4%
The research team tested several approaches to classify the sensor data. Their initial method used conventional linear discriminant analysis, a statistical technique that finds patterns distinguishing different groups. This approach included seven categories: clean air, gypsum substrate alone, wheat substrate alone, and each mold species on each substrate type. Conventional analysis produced an F1-score of only 83.74%, with many samples overlapping. (Think of F1-score as a single report-card number that rewards both catching true mold signals and avoiding false alarms.)
The team then simplified the model by removing substrate dependency, merging samples into broader categories of Stachybotrys, Chaetomium, and “no mold.” When researchers created separate analysis systems for gypsum-based samples and wheat-based samples, the F1-score jumped to 92.64% for gypsum and 98.09% for wheat substrates.
The strongest results came from an ensemble approach combining multiple analysis models with a subsequent classification algorithm. This system creates numerous individual models, each trained on different subsets of the data, then synthesizes their predictions. The best-performing approach reached an average F1-score of 98.37% across all seven original categories, performance approaching laboratory-grade testing. To prevent false positives, the team implemented a majority voting system where the final prediction is only accepted if more than half of the individual models agree.
Translating Laboratory Success to Real Buildings
The study was conducted under controlled laboratory conditions, which differ substantially from occupied buildings. Real indoor environments contain numerous volatile compounds from building materials, cleaning products, cooking, and human activities that could interfere with mold detection. The researchers suggest that baseline measurements in mold-free areas of a building could allow mold detection using outlier analysis, flagging areas where chemical signatures deviate from the clean baseline.
The study focused on two mold species, but buildings commonly harbor others like Aspergillus and Penicillium. These also produce characteristic chemical signatures, suggesting the e-nose technology could expand to detect them. Additional research is needed to determine which species can be reliably identified individually versus which might be grouped into broader categories, and how well the sensors perform in actual buildings with naturally occurring mold contamination.
Star Trek pins with “Highly Illogical” and “Where No Man Has Gone Before” mottos on them. (Photo by KatarinaJenko on Shutterstock)
It might seem worlds away from the Earth we know. But can Star Trek teach us anything about the economics of our own society?
Set in the mid-23rd century, the original Star Trek series told the story of the starship Enterprise. Its crew were led by the human Captain James Kirk and the half-Vulcan Mr Spock.
From post-scarcity societies to hyper-capitalist alien cultures, the now legendary sci-fi franchise the show spawned offers surprisingly rich material for economists and curious minds alike.
As we wind down for the holiday season, let’s take a light-hearted journey into one of pop culture’s most enduring sci-fi universes.
A Society Without Money?
There is macroeconomics in Star Trek, but not as we know it. Scarcity seems much less of an issue in the Star Trek world.
That’s because, within the interstellar government known as The Federation, machines called replicators generate food and other objects. Money is claimed to be no longer used.
Some scholars interpret Star Trek’s relative absence of money in Marxian terms as a step towards a classless society. There are, however, passing references to “credits”. In one episode, a villain is accused of having used counterfeit currency to purchase a ship.
In another, Kirk describes a pile of diamonds as an “incredible fortune in stones.” It seems even in the 23rd century, money still has some uses.
Logic And Emotions
In one early episode, the engineer Montgomery “Scotty” Scott famously tells Captain Kirk he “can’t change the laws of physics.” But the laws of economics also still operate. Despite material wealth, everyone still only has 24 hours in their day and has to make choices.
There are still what economists call “opportunity costs”: doing one thing means having less time for another. So, we can learn about economics from Star Trek, just as we can from Star Wars.
Underpinning many classical economic theories was the concept of “homo economicus” or the “economic man”. This is the idea that humans are rational and self-interested and will always make decisions that maximise their personal benefit.
Spock seems to fit this description. He is unemotional, or at least suppresses his emotions. He prides himself on always making logical decisions.
More recently, however, the field of behavioral economics has challenged this view of human beings as perfectly rational.
It argues human beings are more like Kirk – we try to make good decisions but are sometimes swayed by impatience or influenced by a wide range of emotions. Behavioral economists are trying to predict what Kirk would do, rather than Spock.
Hyper-Capitalist Aliens
Across the entire franchise, viewers are introduced to a variety of alien races. They are at different levels of technological progress – but not that different.
One of the most vivid illustrations of economic behaviour comes from the Ferengi, who feature prominently in Star Trek: Deep Space Nine series. The Ferengi are a mercantile alien race whose culture revolves around the accumulation of wealth and profit. They aren’t members of the “post-money” Federation.
They live by a codified set of business maxims, the “Rules of Acquisition”. These rules reflect their deeply ingrained profit-seeking ethos. Some of the more memorable include:
These rules encapsulate the Ferengi’s relentless pursuit of profit, and their efforts to increase economic rent through various means including manipulation of market and institutional structures.
An Unscrupulous Boss
A prime example is Quark, the archetypal Ferengi who owns a popular bar and restaurant. Quark exploits his monopsony power – being the sole employer in a niche market – to underpay staff and impose harsh working conditions.
This is a practical demonstration of Rule 211: “Employees are the rungs on the ladder of success. Don’t hesitate to step on them.”
But in one episode, Quark’s employees go on strike, prompting him to use underhanded tactics to suppress collective bargaining and maintain control.
This storyline mirrors real-world labour market dynamics and the tension between capital and labour.
Monopoly Power
In the series Star Trek: Voyager, we see how access to key technology and asymmetric information can lead to monopoly power and exploitation.
In the episode “False Profits”, two Ferengi stranded on a primitive planet use replicator technology to produce goods, presenting themselves as divine sages.
Their technological advantage allows them to extract maximum rent from the unsuspecting locals.
Microplastics are linked to a number of health problems. (Photo by SIVStockStudio on Shutterstock)
Fathers exposed to microplastics before conception may be setting their daughters up for metabolic problems later in life. A new mouse study shows when male mice consumed plastic particles before breeding, their female offspring developed insulin resistance on a high-fat diet while male offspring remained largely unaffected.
Research from the University of California, Riverside found an unusual pattern. Female descendants of microplastic-exposed fathers showed significantly impaired insulin tolerance despite maintaining normal body weight and fat mass. Their brothers had reduced fat deposits but normal insulin function.
Male mice received microplastics daily for four weeks before mating with unexposed females. The dose matched amounts humans might encounter through everyday exposure to contaminated food and water. The fathers themselves showed no health changes from the exposure.
Daughters Develop Insulin Resistance
When fed a Western-style high-fat diet after weaning, female offspring from exposed fathers failed insulin tolerance tests. Blood glucose levels dropped more slowly after insulin injection compared to controls, showing their bodies struggled to respond properly to the hormone. This condition, called insulin resistance, increases risk for Type 2 diabetes and cardiovascular disease.
Examining liver tissue revealed why. Female offspring from microplastic-exposed fathers had elevated levels of inflammatory proteins. One protein called IKKβ acts as a central coordinator of inflammatory responses and has been directly linked to obesity-related insulin resistance in previous research. None of these changes appeared in male offspring.
Sperm RNA Carries Environmental Signals
The study, published in the Journal of the Endocrine Society, identifies a potential mechanism behind these sex-specific effects. Microplastic exposure substantially changed small RNA molecules in sperm. These molecular fragments act like instructions that can influence which genes turn on or off in developing embryos.
Scientists used an advanced sequencing technique that overcomes limitations of traditional methods by detecting chemically modified RNA molecules. The analysis uncovered more than 4,000 changes in small RNAs from sperm of microplastic-exposed mice.
To test whether these altered RNAs could affect development, researchers introduced three candidates into mouse embryonic stem cells. All three changed expression of genes important for metabolism and development. One RNA fragment increased expression of an inflammatory gene while decreasing a gene that helps cells respond to insulin. Two other RNA fragments decreased expression of genes involved in muscle development, gut formation, and glucose transport.
These experimental results in stem cells match some problems observed in female offspring: elevated inflammation and impaired insulin signaling.
Why Female Offspring Are More Vulnerable
The sex-specific pattern observed in this study fits with findings from other research on paternal environmental exposures. Studies have found that fathers fed high-fat diets or exposed to arsenic produced female offspring with glucose intolerance, while male offspring remained unaffected.
Scientists don’t fully understand why female offspring appear more vulnerable. Possibilities include differences in sex chromosomes, sex hormone effects, and distinct patterns in how male versus female embryos reset their gene activity patterns during early development.
Male offspring weren’t completely unaffected by paternal microplastic exposure, but their changes differed from their sisters. Males from exposed fathers had significantly reduced belly fat despite similar overall body weight. Female offspring showed the opposite pattern—reduced muscle mass with normal fat mass.
Human Microplastic Exposure
Humans face widespread exposure to microplastics through contaminated food, water, and air. Recent studies have detected plastic particles in human blood, placentas, liver, kidneys, and brain tissue. Researchers have also found them in testicular tissue, semen, and placentas.
The health consequences need more investigation, though emerging evidence links microplastics to increased cardiovascular disease risk, metabolic dysfunction, and premature aging. Most research has focused on direct exposure effects rather than potential impacts on future generations.
For decades, dietary guidelines have warned against high-fat cheese because of concerns about saturated fat and heart health. Now, a Swedish study that followed 27,670 people for nearly 30 years has uncovered a surprising benefit associated with fatty cheeses. Those who ate more high-fat cheese showed lower rates of dementia.
The research found that participants consuming at least 50 grams daily of cheese with more than 20% fat content had a 13% lower risk of developing dementia compared to those eating less than 15 grams daily. Compared with non-consumers, those eating 20 grams or more per day of high-fat cream showed a 16% lower dementia risk.
Not all dairy products showed these associations. Milk, fermented milk products (like yogurt), low-fat cheese, and low-fat cream showed no clear links to dementia risk overall. Butter was more complicated. In one analysis, higher butter intake was linked to higher Alzheimer’s risk. When it comes to brain health, the type and fat content of dairy products may matter more than simply eating “more dairy” or “less dairy.”
30-Year Study Tracked Nearly 28,000 People
Researchers used data from the Malmö Diet and Cancer cohort, where participants underwent detailed dietary assessments between 1991 and 1996. The evaluation combined three methods: a seven-day food diary, a 168-item food frequency questionnaire, and a 45-60 minute dietary interview conducted by trained personnel.
The study, published in Neurology, identified 3,208 dementia cases through Swedish health registries by December 2020. Cases diagnosed through 2014 underwent additional validation by trained physicians who reviewed symptoms, cognitive test results, brain imaging, and biomarkers when available. The validated cases included 1,126 with Alzheimer’s disease and 451 with vascular dementia.
Participants were followed from their baseline examination until dementia diagnosis, death, emigration, or December 2020 (whichever came first). The median follow-up period was about 25 years.
Genetics May Influence Cheese’s Brain Benefits
Among people without the APOE e4 gene variant, a major genetic risk factor for Alzheimer’s disease, eating more high-fat cheese was associated with a 13% lower risk of Alzheimer’s specifically. The gene variant had no effect on the cheese-dementia association overall, but it modified the relationship with Alzheimer’s disease itself.
About 30% of study participants carried at least one copy of the APOE e4 variant.
People who consumed the most high-fat cheese tended to be younger, have lower body mass indexes, and have higher education levels. They also had lower rates of diabetes, high blood pressure, cardiovascular disease, and stroke. They were less likely to use cholesterol-lowering medications. However, they were more likely to be current or past smokers and had higher alcohol consumption.
The researchers adjusted their analyses for age, sex, education level, physical activity, smoking status, alcohol consumption, family history of cardiovascular disease, marital status, living alone, diet quality, body mass index, and hypertension. Even after accounting for all these factors, the protective associations with high-fat cheese and cream remained.
Strongest Protection Against Vascular Dementia
High-fat cheese consumption showed particularly strong protective effects against vascular dementia, the second most common form of dementia caused by reduced blood flow to the brain. People eating 50 grams or more daily had a 29% lower risk of vascular dementia compared to those consuming less than 15 grams daily.
High-fat cream consumption also showed inverse associations with both Alzheimer’s disease and vascular dementia when researchers analyzed intake as a continuous variable rather than categories.
The researchers used specific thresholds to categorize dairy products. High-fat cheese meant more than 20% fat, high-fat cream meant more than 30% fat, and high-fat milk and fermented milk meant more than 2.5% fat.
How Researchers Tried to Reduce ‘Reverse Causation’
A major concern in dementia research is reverse causation (the possibility that early cognitive decline changes eating habits years before diagnosis occurs). Dementia can have a long preclinical phase during which subtle brain changes begin but symptoms haven’t appeared yet.
The researchers addressed this by excluding dementia cases that occurred within the first 10 years of follow-up. Surprisingly, this strengthened the protective associations with high-fat cheese, suggesting the findings aren’t simply due to sick people changing their diets before diagnosis.
The study also examined people who reported no substantial diet changes during a five-year follow-up examination. Among this subset, the associations weakened and no longer reached statistical significance, though they remained in the protective direction.
Why High-Fat Cheese May Benefit Brain Health
Cheese is a whole food with protein, calcium, and other compounds packaged together in a way that may affect how the body responds to it. Previous randomized controlled trials have shown that regular-fat cheese doesn’t cause the adverse changes in blood cholesterol that researchers once feared when they issued blanket warnings about saturated fat.
Some animal studies suggest that regular-fat cheese may provide metabolic benefits by altering gut bacteria and altering fat absorption. Regular-fat cheese has been linked to increased fecal fat excretion, meaning the body may absorb less of the fat consumed. The cheese-making process and fermentation may also create beneficial compounds not found in milk.
Mendelian randomization studies, which use genetic variants to infer causal relationships, have linked cheese consumption to lower risks of diabetes and high blood pressure (both risk factors for dementia).
An unmeasured factor would need to substantially increase dementia risk to completely explain away the observed protective association with high-fat cheese. That threshold exceeds the effect sizes of several established dementia risk factors like smoking, high blood pressure, and diabetes.
Butter consumption showed a different pattern. Among people consuming 40 grams or more daily, there was a 27% higher risk of Alzheimer’s disease compared to non-consumers. However, among participants with higher overall diet quality, butter consumption was inversely associated with dementia risk. The authors stress this finding is speculative and might relate to overall dietary fat intake (butter might be protective in an otherwise low-fat diet, but increases risk when added to a diet already high in fat).
Low-fat milk consumption showed an unexpected finding. People consuming 500 grams or more daily (about two cups) had a 24% higher risk of dementia when follow-up ended in 2014. However, this association wasn’t significant when the follow-up was extended to 2020, despite increased statistical power from more cases.
Neither high-fat nor low-fat fermented milk products showed associations with dementia risk in the overall analysis. Regular milk, regardless of fat content, showed no significant associations with dementia, Alzheimer’s disease, or vascular dementia.
The researchers conducted substitution analyses to estimate what might happen if people replaced 20 grams of high-fat cheese with equivalent amounts of other foods. Replacing high-fat cheese with milk, fermented milk, high-fat red meat, or processed meat was associated with increased dementia risk.
Stuck in front of our screens all day, we often ignore our senses beyond sound and vision. And yet they are always at work. When we’re more alert we feel the rough and smooth surfaces of objects, the stiffness in our shoulders, the softness of bread.
In the morning, we may feel the tingle of toothpaste, hear and feel the running water in the shower, smell the shampoo, and later the aroma of freshly brewed coffee.
Aristotle told us there were five senses. But he also told us the world was made up of five elements and we no longer believe that. And modern research is showing we may actually have dozens of senses.
Almost all of our experience is multisensory. We don’t see, and hear, smell and touch in separate parcels. They occur simultaneously in a unified experience of the world around us and of ourselves.
What we feel affects what we see and what we see affects what we hear. Different odors in shampoo can affect how you perceive the texture of hair. The fragrance of rose makes hair seem silkier, for instance.
Odors in low-fat yogurts can make them feel richer and thicker on the palate without adding more emulsifiers. Perception of odors in the mouth, rising to the nasal passage, are modified by the viscosity of the liquids we consume.
My long-term collaborator, professor Charles Spence from the Crossmodal Laboratory in Oxford, told me his neuroscience colleagues believe there are anywhere between 22 and 33 senses.
These include proprioception, which enables us to know where our limbs are without looking at them. Our sense of balance draws on the vestibular system of ear canals as well as sight and proprioception.
Another example is interoception, by which we sense changes in our own bodies such as a slight increase in our heart rate and hunger. We also have a sense of agency when moving our limbs: a feeling that can go missing in stroke patients who sometimes even believe someone else is moving their arm.
There is the sense of ownership. Stroke patients sometimes feel their, for instance, arm is not their own even though they may still feel sensations in it.
Some of the traditional senses are combinations of several senses. Touch, for instance involves pain, temperature, itch and tactile sensations. When we taste something we are actually experiencing a combination of three senses: touch, smell and taste – or gustation – which combine to produce the flavors we perceive in food and drinks.
Gustation, covers sensations produced by receptors on the tongue that enable us to detect salt, sweet, sour, bitter and umami (savory). What about mint, mango, melon, strawberry, raspberry?
We don’t have raspberry receptors on the tongue, nor is raspberry flavor some combination of sweet, sour and bitter. There is no taste arithmetic for fruit flavors.
We perceive them through the combined workings of the tongue and the nose. It is smell that contributes the lion’s share to what we call tasting.
This is not inhaling odors from the environment, though. Odor compounds are released as we chew or sip, traveling from the mouth to the nose though the nasal pharynx at the back of throat.
Touch plays its part too, binding tastes and smells together and fixing our preferences for runny or firm eggs, and the velvety, luxuriousness gooeyness of chocolate.
Sight is influenced by our vestibular system. When you are on board an aircraft on the ground, look down the cabin. Look again when you are in the climb.
It will “look” to you as though the front of the cabin is higher than you are, although optically, everything is in the same relation to you as it was on the ground. What you “see” is the combined effect of sight and your ear canals telling you that you are titling backwards.
The senses offer a rich seam of research and philosophers, neuroscientists and psychologists work together at the Centre for the Study of the Senses at the University of London’s School of Advanced Study.
In 2013, the centre launched its Rethinking the Senses project, directed by my colleague, the late Professor Sir Colin Blakemore. We discovered how modifying the sound of your own footsteps can make your body feel lighter or heavier.
We learned how audioguides in Tate Britain art museum that address the listener as if the model in a portrait was speaking enable visitors to remember more visual details of the painting. We discovered how aircraft noise interferes with our perception of taste and why you should always drink tomato juice on a plane.
While our perception of salt, sweet and sour is reduced in the presence of white noise, umami is not, and tomatoes, and tomato juice is rich in umami. This means the aircraft’s noise will taste enhance the savory flavor.
At our latest interactive exhibition, Senses Unwrapped at Coal Drops Yard in London’s King’s Cross, people can discover for themselves how their senses work and why they don’t work as we think they do.
For example, the size-weight illusion is illustrated by a set of small, medium and large curling stones. People can lift each one and decide which is heaviest. The smallest one feels heaviest, but people can them place them on balancing scales and discover that they are all the same weight.
Most people in relationships would never admit it out loud, but a surprising number are keeping their options open. One in six Americans currently in a relationship confesses there’s someone else in their life they’d actually leave their partner for if that person showed romantic interest.
That revelation comes from a new survey of 1,279 people in relationships, which uncovered some uncomfortable truths about modern commitment. While having a wandering eye is one thing, having a specific person in mind as a potential exit strategy takes it further.
The Gender Gap in Relationship Commitment
Research conducted by Talker Research as part of a lifestyle omnibus found that 16% of coupled Americans have identified someone who could pull them away from their current relationship. Men are far more likely to have this backup plan, with 19% admitting there’s someone they’d leave their partner for, compared to just 12% of women.
Perhaps even more telling: one in five Americans (20%) in relationships don’t actually consider their current partner to be their soulmate. Women are slightly more likely than men to feel this way, with 14% of women expressing doubt compared to 11% of men. The survey doesn’t prove these are the same people with backup plans, but the combination raises an obvious question. Why stay if the conviction isn’t there?
Millennials emerge as the generation most likely to believe in the soulmate concept and feel their current partner is “the one.” Maybe growing up immersed in romantic comedies set their expectations sky-high, or perhaps they’re just more willing to walk away from relationships that feel like compromises.
When Attraction Becomes Something More
Clinical psychologist Adam Horvath explained why these feelings might be more universal than people admit. “It is not uncommon to think we could leave our partner for the new, exciting, mysterious other one, but it matters how we respond to these feelings,” Horvath said. “If you often find yourself emotionally invested outside your relationship, that’s a signal to look at why your boundaries are dropping.”
Horvath emphasized that attraction to others doesn’t automatically make someone a bad partner. “We’re human. Attraction does not turn off when we say ‘I choose you.’ What matters is what we do with our feelings, and whether we’re honest with ourselves about why they’re there,” he explained. “Having a daydream about someone else isn’t rare or pathological, and it doesn’t automatically mean you are a bad partner, let alone that your relationship is doomed.”
The psychologist pointed out that noticing romantic interest in others is hardwired biology. “Developing feelings for someone is quite normal, as our brains are wired to notice a romantic interest. It’s biology, not betrayal,” he said.
The Fantasy Partner Problem
The trouble starts when people begin comparing their actual partner to a fantasy version of someone else. “Where it gets tricky is when we think these feelings are meaningful, and in fact, they are our way out. When we compare our real partner to a fantasy of someone else, and check out because ‘there’s something better,’” Horvath explained. “That’s less about the crush and more about something missing that the backup person represents: Playfulness, romance, excitement. Or sometimes simply just something new.”
For many Americans, monogamy might be more about choosing to stay than about not wanting to stray. Whether having a “what if” person in the back of your mind is normal human psychology or a red flag about your relationship depends on how each person handles it.
But the survey data tells a clear story. If these percentages hold nationally, they would translate to millions of Americans in relationships while simultaneously identifying someone they’d rather be with. That person at work who makes them laugh, the ex who got away, the friend who “gets them” in ways their partner doesn’t. These backup options aren’t just passing crushes but specific people who could theoretically change everything if they made a move.
Anyone who has beheld Luke “The Nuke” Littler’s stellar abilities on the darts circuit will have seen the exceptional talent he displays. In January, he became the youngest World Champion in history at just 17 years old. In October, he captured his first World Grand Prix title. But what does it actually take to become a professional darts player?
Many may be wondering whether darts skills are simply innate in some people, or if Littler is just an exceptionally quick learner.
Elite technique requires a combination of both physical and mental athleticism. You need to have the skills to hit very small targets when stepping up to the oche, all while maintaining the mental strength needed to stay composed under pressure – knowing that even the smallest miss can have big consequences.
1. Coordination
There are lots of different ways in which coordination – one of the critical functions of our nervous system – lends itself to success in darts. Every single throw requires a smooth and accurate trajectory.
Coordination is controlled by the cerebellum, which is located at the back of the brain. This complex region, sometimes referred to as “the little brain,” helps regulate both fine muscle control and posture. It’s a key region when it comes to darts skills.
For instance, the cerebellum helps with hand-eye coordination. To hit a perfect 180, you’re aiming for that tiny treble 20 on the inner ring, three times over. It requires the player to set that target, judge the distance from the board and calculate an appropriate angle at which to throw. It’s also critical in the learning process of how to improve your aim over time.
Stance, posture and balance are paramount too, and also coordinated by the cerebellum. Even the slightest wobble can affect the trajectory of the dart on release.
2. Arm Mechanics
A recipe for success also involves a honed and accurate throw.
The mechanics of a good throw include the transition between taking aim, the pullback move to gather energy, through to a smooth release and eliminating any jerks which might send the dart off course.
The chief muscle groups that allow for this are found in the hand, wrist and forearm. They contain multiple smaller muscles which flex and extend the wrist and fingers. These are capable of working together to enable a wide variety of precise movements in gripping, aiming and releasing the dart.
It’s generally quite difficult to target these small muscles by working out in the gym, so this is where training through repetition is key to nailing the right throw.
The throw is also governed by rhythm: the target setting, the speed of the pullback stroke and the timing of the release.
Every professional dart player has their own throw technique. For instance, Phil Taylor demonstrated a fast, yet measured throw, while Luke Littler favors a relaxed, instinctive rhythm. But the individual rhythm all goes back to those intricate nerve pathways and the small muscles which coordinate it.
3. A ‘Quiet Eye’
Obviously vision is also fundamental to darts – but it’s not as simple as just regarding the board.
This is where the concept of a “quiet eye” comes in – where the eyes lock in upon the target just before a throw is made. A quiet eye ensures the gaze remains fixed upon the target, ensuring the throw is accurate.
A quiet eye is a technique important in many sports other than darts – including clay shooting, snooker and archery. A quiet eye lends important visual information to the motor system, which allows for maximum synchronization between the brain and body.
Several studies have explored the effect the quiet eye phenomenon has on target sports and what underpins it. First, there’s evidence that shows expert players typically have a longer quiet eye phase than amateurs. Although this usually only amounts to half a second longer or so, this is still significant in coordinating between the brain and body, allowing the player to execute that perfect shot.
Second, the measured gaze of professional players appear to be more stable and unwavering – with no eye flicking or deviation from the target.
Through target fixation, critically timing their movements and repeating their shots, players can train their quiet eye.
4. The Brain And Body Connection
The connection between brain and body appears to be key – and is exemplified by players who lost their ability in darts.
There’s actually a condition referred to as “dartitis,” which is defined by an inability to throw. Dartitis is often associated with stress, fatigue or burnout.
It can even affect top players – most notably multiple World Champion Eric Bristow, who had to retrain in order to play normally again after developing dartitis. This can involve going back to basics and rebuilding the throw – sometimes even switching to the other hand.
Since researchers first established the link between diet, cholesterol and heart disease in the 1950s, risk for heart disease has been partly assessed based on a patient’s cholesterol levels, which can be routinely measured via blood work at the doctor’s office.
However, accumulating evidence over the past two decades demonstrates that a biomarker called C-reactive protein – which signals the presence of low-grade inflammation – is a better predictor of risk for heart disease than cholesterol.
As a result, in September 2025, the American College of Cardiology published new recommendations for universal screening of C-reactive protein levels in all patients, alongside measuring cholesterol levels.
What Is C-Reactive Protein?
C-reactive protein is created by the liver in response to infections, tissue damage, chronic inflammatory states from conditions like autoimmune diseases, and metabolic disturbances like obesity and diabetes. Essentially, it is a marker of inflammation – meaning immune system activation – in the body.
C-reactive protein can be easily measured with blood work at the doctor’s office. A low C-reactive protein level – under 1 milligram per deciliter – signifies minimal inflammation in the body, which is protective against heart disease. An elevated C-reactive protein level of greater than 3 milligrams per deciliter, signifies increased levels of inflammation and thus increased risk for heart disease. About 52% of Americans have an elevated level of C-reactive protein in their blood.
Research shows that C-reactive protein is a better predictive marker for heart attacks and strokes than “bad,” or LDL cholesterol, short for low-density lipoprotein, as well as another commonly measured genetically inherited biomarker called lipoprotein(a). One study found that C-reactive protein can predict heart disease just as well as blood pressure can.
Why Does Inflammation Matter in Heart Disease?
Inflammation plays a crucial role at every stage in the development and buildup of fatty plaque in the arteries, which causes a condition called atherosclerosis that can lead to heart attacks and strokes.
From the moment a blood vessel is damaged, be it from high blood sugar or cigarette smoke, immune cells immediately infiltrate the area. Those immune cells subsequently engulf cholesterol particles that are typically floating around in the blood stream to form a fatty plaque that resides in the wall of the vessel.
This process continues for decades until eventually, one day, immune mediators rupture the cap that encloses the plaque. This triggers the formation of a blood clot that obstructs blood flow, starves the surrounding tissues of oxygen and ultimately causes a heart attack or stroke.
Hence, cholesterol is only part of the story; it is, in fact, the immune system that facilitates each step in the processes that drive heart disease.
Can Diet Influence C-Reactive Protein Levels?
Lifestyle can significantly influence the amount of C-reactive protein produced by the liver.
Numerous foods and nutrients have been shown to lower C-reactive protein levels, including dietary fiber from foods like beans, vegetables, nuts and seeds, as well as berries, olive oil, green tea, chia seeds and flaxseeds.
Weight loss and exercise can also reduce C-reactive protein levels.
Does Cholesterol Still Matter for Heart Disease Risk?
Though cholesterol may not be the most important predictor of risk for heart disease, it does remain highly relevant.
However, it’s not just the amount of cholesterol – or more specifically the amount of bad, or LDL, cholesterol – that matters. Two people with the same cholesterol level don’t necessarily have the same risk for heart disease. This is because risk is determined more so by the number of particles that the bad cholesterol is packaged into, as opposed to the total mass of bad cholesterol that’s floating around. More particles means higher risk.
That is why a blood test known as apolipoprotein B, which measures the number of cholesterol particles, is a better predictor of risk for heart disease than measurements of total amounts of bad cholesterol.
Like cholesterol and C-reactive protein, apolipoprotein B is also influenced by lifestyle factors like exercise, weight loss and diet. Nutrients like fiber, nuts and omega-3 fatty acids are associated with a decreased number of cholesterol particles, while increased sugar intake is associated with a larger number of cholesterol particles.
Furthermore, lipoprotein(a), a protein that lives in the wall surrounding cholesterol particles, is another marker that can predict heart disease more accurately than cholesterol levels. This is because the presence of lipoprotein(a) makes cholesterol particles sticky, so to speak, and thus more likely to get trapped in an atherosclerotic plaque.
However, unlike other risk factors, lipoprotein(a) levels are purely genetic, thus not influenced by lifestyle, and need only be measured once in a lifetime.
Fossil fragments of a face as well as teeth were reassembled to produce the most complete cranium of a human ancestor from this time in the Horn of Africa. (Credit: Karen L. Baab. Scans provided by National Museum of Ethiopia. Photographs courtesy of M. Rogers and G. Suwa.)
The skull had the brow of a descendant but the face of an ancestor. When researchers finished reconstructing the DAN5/P1 cranium from Ethiopia’s Afar region, dated to between 1.6 and 1.5 million years ago, they found themselves staring at an evolutionary contradiction: a single individual who appeared to belong to two different chapters of human history at once.
Homo erectus, the species that first looked recognizably like us with its large brain, prominent brow ridge, and smaller teeth, has long been considered a turning point in human evolution. The species is often described as a package of changes arriving together, but this newly reconstructed skull from the Gona research area indicates the pieces did not always move in lockstep.
The brain inside DAN5/P1 was small, just 598 cubic centimeters, closer to the earlier Homo habilis than to the larger-brained Homo erectus fossils found in Kenya from the same time period. Yet its jutting brow ridge and certain features of the braincase matched Homo erectus. Its face, meanwhile, retained the flat cheekbones and narrow nasal opening of species that should have been fading from the scene.
An international team led by Karen L. Baab of Midwestern University published their findings in Nature Communications. After years of digital reconstruction using micro-CT scans, they pieced together a mostly complete Early Pleistocene Homo cranium from the Horn of Africa, only the sixth such specimen recovered from the continent. What emerged was a fossil that defies easy classification and complicates our understanding of how Homo erectus came to be.
“The presence of such a morphological mosaic contemporaneous with or postdating the emergence of the indisputable H. erectus craniodental complex around 1.6 Ma implies an intricate evolutionary transition from early Homo to H. erectus,” the researchers wrote.
How Researchers Reconstructed the Homo Erectus Skull
The DAN5/P1 fossil was discovered at the Dana Aoule North site in Gona, part of Ethiopia’s Afar region. Initially, only the braincase had been fully studied. The face remained a puzzle, broken into fragments during fossilization and cemented together by sediment over millennia.
To reconstruct it, the team took micro-CT scans of five facial bone fragments: portions of both sides of the upper jaw, a piece of the region below the eye sockets, part of the cheekbone, and several teeth including premolars and molars. From these scans, they generated 3D surface models that could be digitally manipulated and fitted together.
Reassembly required matching each piece according to anatomical landmarks. Sutures had to align. Break lines had to correspond. The frontal process of the upper jaw, for instance, had to be angled so it would properly meet the frontal bone while simultaneously matching curvatures implied by surrounding structures. After the face was assembled, the team attached it to the previously reconstructed braincase.
To account for uncertainty in how the face connected to the braincase, the researchers also created an alternative reconstruction with slightly different positioning. Both versions produced similar results in subsequent statistical analyses, lending confidence that the findings were not artifacts of reconstruction choices.
A Face from the Past on a Skull from the Future
Comparing DAN5/P1 to other early human fossils revealed its split identity. The braincase aligned with Homo erectus in several respects: a thick, projecting brow ridge with a continuous groove behind it, circular eye sockets, and the long, low profile characteristic of the species.
But the face pointed backward in time. The area below the eye sockets was flat from side to side rather than curving outward as in typical African Homo erectus. The nasal opening lacked the pronounced widening seen in roughly contemporaneous Kenyan fossils like KNM-ER 3733 and the adolescent KNM-WT 15000. The cheekbone’s attachment point sat more toward the front of the face than expected, a trait linked to earlier Homo species.
The roof of the mouth was large relative to brain size, placing DAN5/P1 closer to early Homo and to Homo erectus fossils from Dmanisi, Georgia, than to East African Homo erectus. The teeth were also substantial. The first and third molars fell within the size range of Homo habilis and at the upper end of variation for African Homo erectus.
Statistical analyses of skull shape placed DAN5/P1 within the Homo erectus range but nearest to two specific fossils: the adolescent KNM-WT 15000 from Kenya and the subadult D2700 from Georgia. When the researchers analyzed midface shape alone, DAN5/P1 clustered with Homo habilis specimens instead. Its single closest match in overall shape was KNM-ER 1813, a classic Homo habilis skull from Kenya.
“DAN5/P1 is, to our knowledge, the first African fossil to exhibit a mixture of H. erectus and early Homo features,” the team reported.
Two Populations, Two Evolutionary Speeds
The combination of ancestral and more advanced features in a single skull from this time period complicates the conventional timeline. By 1.6 million years ago, Homo erectus was supposed to have already arrived as a coherent package. Famous Kenyan fossils from roughly the same period, including KNM-ER 3733 and KNM-WT 15000, display the full suite of Homo erectus traits: larger brains, smaller teeth, wider nasal openings, and curved architecture below the eyes.
Yet DAN5/P1 lived at essentially the same time with a brain barely larger than Homo habilis, teeth to match, and a face that looked like it belonged to an earlier era. The brow ridge announced membership in Homo erectus. Almost everything else pointed to something more primitive.
The researchers interpret this as evidence that different populations of early humans were evolving at different rates across East Africa. The rift basin landscape, combined with low population densities, may have allowed groups in the Horn of Africa and the Lake Turkana region of Kenya to diverge over time. The Horn of Africa population, represented by DAN5/P1, retained more ancestral features. The Kenyan population developed more derived characteristics.
“The evolutionary contrasts in brain size and face morphology embodied by the broadly contemporaneous DAN5/P1 and Kenyan fossils, KNM-ER 3733 and KNM-WT 15000, imply complex population structure rather than simple coexistence of two different lineages,” the researchers wrote.
This interpretation casts Homo erectus as a species showing substantial regional variation rather than uniform characteristics everywhere it lived.
Advanced Tools Found at the Same Site as Small-Brained Fossil
Both simple and advanced stone tools turned up at the DAN5 site. Mode 1 tools, basic cores and flakes, appeared alongside Mode 2 Acheulean tools, the more sophisticated hand axes associated with Homo erectus.
Acheulean technology is typically linked to larger-brained populations. The longstanding assumption has been that expanding brains drove technological innovation. But at Gona, these advanced tools appear in the same context as a fossil with a brain volume comparable to Homo habilis, the earlier species credited only with simpler tools.
Evidence from the site also points to a broadened diet and access to animal resources. A similar pattern appears at Dmanisi in the Republic of Georgia, where small-brained fossils occur alongside evidence of meat consumption and varied tool use.
“The Gona evidence, along with that from Dmanisi, hints that key behavioral/technological innovations may precede major morphological transformations,” the team noted.
If accurate, the assumed connection between brain size and cognitive ability in early human evolution may have been less direct than researchers believed.
Surprising Similarities to a Much Younger Species
DAN5/P1 also shares certain features with Homo naledi, a much younger Middle Pleistocene species discovered in South African caves. Both possess small brains, flat nasal regions, forward-positioned cheekbones, and a distinct bump at the back of the skull.
The researchers caution against reading too much into these resemblances. Vast stretches of time and thousands of kilometers separate the two fossils, and shared primitive traits do not necessarily indicate a direct evolutionary link. But the parallels add to mounting evidence that small-brained Homo populations persisted in Africa long after larger-brained forms had emerged.
One Skull, Many Questions
Only six largely complete Early Pleistocene Homo skulls have been recovered from Africa. Each new discovery reshapes the narrative, and DAN5/P1 is no exception. Here was an individual whose brow announced membership in Homo erectus while whose face and teeth belonged to an earlier inheritance, found at a site that also yielded both simple and advanced stone tools.
The fossil confirms that the emergence of Homo erectus involved considerable variation across populations. Different groups existed simultaneously in East Africa, evolving at different rates and retaining different features. The transition from early Homo to Homo erectus appears to have been gradual and uneven, with different traits shifting at different speeds in different places.
DAN5/P1 does not settle the debate over where Homo erectus originated or how it spread across Africa and into Eurasia. Some researchers have proposed a Eurasian origin based on early Homo erectus-like features appearing in Georgia. The ancestral morphology preserved in DAN5/P1, however, remains compatible with local evolution of the species in East Africa.
Google Trends, Facebook, The Conversation, CC BY-SA
In the wake of Sunday’s tragic Bondi shooting, conspiracy theories and deliberate misinformation have spread on social media.
One thing some people have latched onto is the idea Google Trends data show a spike in searches for “Naveed Akram” – the name of one of the attackers – from Tel Aviv (or other locations) before the shooting occurred. In a surprising lateral jump, this is taken to show Akram must be an Israeli agent.
Similar stories did the rounds when US right-wing activist Charlie Kirk was killed in September, and after an attack on US National Guard members in November.
So what’s going on here? Google told the ABC Google Trends may sometimes show searches when none actually happened due to “statistical noise.”
I have studied the mechanics of Google Trends extensively in my research, and I can confirm this is true – and the “noise” can lead to strange results, especially when looking at searches for unusual terms or coming from small areas.
How Does Google Trends Work?
Google Trends shows information about what users are searching for at different places and times. The data it uses are what statisticians call a “time series,” but they are unusual in a couple of ways.
First, you can very easily select different time scales, such as minute-by-minute and year-by-year.
Second is the fact the data are only a small sample of the true gigantic volume of Google searches. Time series normally contain all available data (such as these statistics on annual hospitalizations).
Statistical Noise and Rare Searches
However, my research has shown that queries related to terms that are not widely searched (such as “Naveed Akram” before the shooting) or in small geographical regions (where there are fewer people doing searches) can display a wide variation of results from one sample to the next.
Many of the misleading social media posts show Trends results from a small region (such as only the city of Tel Aviv), which exacerbates the variation. The high variation causes a very distinct pattern of zero or near-zero values with some isolated big spikes, which is very evident in the post below.
These spikes are often caused by “statistical noise” in the data – small random fluctuations that are smoothed out when we look at a larger number of events. You can see this clearly when you compare with searches that have high volume.
How Google Trends Results Change Over Time
Another misconception about the data is related to time. Some posts mention how the displayed results seem to change from one view to the next. This is, in fact, exactly what to expect with Google Trends data.
This is a combination of the time scale used and the fact Google uses only a sample of the full data. To get accurate results, one has to aggregate many samples of Google Trends data.
However, this presents a new challenge. For short-term data (such as that typically used in these social media posts), Google continually updates results in real time. For longer-term data, Google only adds one new sample per day (though we have developed methods to get around this).
What the Numbers in Google Trends Really Mean
A third misconception is that the numbers shown on Google Trends charts are the number of searches for a given term. However, the Google Trends help again explains that the values are “normalized to the time and location” and then “scaled on a range of 0 to 100.”
This means the time point in the series with the highest number of searches is set to 100, and all other points are scaled relative to that. So if the maximum number of searches was ten, it would show up as 100 – and if there were three searches at another time, this would show up as 30 (although Google does suppress very low-volume searches).
In a sense, the number for each time point represents the likelihood that a search containing the specified terms would occur in that place at that time.
So a post about search trends for the alleged killer of Charlie Kirk claiming there are “Less than 1 in 1 BILLION odds of it happening” is incorrect.
It is, in fact, highly probable: if “Tyler James Robinson” (Charlie Kirk’s alleged killer) had 30 searches, and “Lance Twiggs” (Robinson’s partner) had 40, one would see exactly this pattern (if 40 is scaled to 100; 30 is accordingly scaled to 75).
Romance and the heart have long been synonymous on a symbolic level, but modern science now indicates the connection may be literal. Researchers are calling for romantic relationships to be incorporated far more heavily in treatment programs for heart patients.
A major review published in the Canadian Journal of Cardiology analyzed how including romantic partners in cardiac care affects recovery and found that while 77% of studies showed improved medication adherence, exercise habits, and smoking cessation, only three studies measured relationship quality—and none found improvements. So, it appears romantic partnerships affect heart health through powerful biological mechanisms, yet cardiac rehabilitation programs rarely address these crucial personal relationships.
Researchers analyzed 12 clinical trials involving nearly 1,500 couples to determine whether including romantic partners in cardiac rehabilitation improves outcomes. The biological rationale for partner involvement is compelling: large population studies show that relationship quality affects heart disease risk with effect sizes comparable to quitting smoking or maintaining healthy weight. Satisfied partners show better heart rate variability, lower blood pressure, and reduced inflammatory markers, while relationship distress triggers the same stress responses that damage the cardiovascular system.
The study, conducted at the University of Ottawa Heart Institute, found that unmarried people are over 40% more likely to have cardiovascular disease and die from a myocardial infarction than married people. But the protection doesn’t come from a wedding ring. Studies tracking relationship quality over time show that marital satisfaction matters far more than marital status alone.
The Body Keeps Score of Relationship Stress
The body responds to relationship dynamics in measurable ways. During arguments about relationship problems, both partners experience elevated heart rates and surges in cortisol stress hormones. Women in distressed relationships face a nearly 10-fold increase in uncontrolled hypertension compared to satisfied women. Among satisfied couples, every unit increase in relationship support correlates with a 28% improvement in heart rate variability, a key marker of cardiovascular health.
Physical intimacy plays a direct role. On days when couples engage in more affectionate touch like hugging, cortisol levels drop measurably. This isn’t just emotional comfort translating to feeling better. The physical act of intimate connection triggers hormonal changes that protect the heart.
Chronic relationship distress mobilizes circulating lipids and increases inflammatory markers including interleukin-6 and C-reactive protein. These same inflammatory processes contribute to atherosclerosis development and cardiovascular disease progression. In observational research, the magnitude of these effects appears comparable to traditional risk factors that doctors routinely monitor and treat.
Partners in satisfying relationships engage in better health behaviors, creating a cascade of cardiovascular benefits. Men who perceive strong partner support eat more fruits and vegetables. Both sexes consume more alcohol when experiencing marital strain. A single unit increase in relationship quality over 10 years correlates with lower weight and a 22% decrease in obesity risk.
Health behaviors sync between partners. If one spouse exercises regularly, the other has a 67% higher chance of becoming active. When one partner quits smoking, the other is 48% more likely to quit successfully. This concordance works both ways. If one partner maintains unhealthy habits, the other faces major barriers to change despite good intentions.
How Including Partners Changes Outcomes
The research team reviewed interventions designed to include partners in cardiac care. Most programs involved nurses teaching couples about medication management, exercise routines, and dietary changes over three months, typically starting right after hospital discharge.
Results showed clear benefits for health behaviors. About 77% of studies measuring exercise, medication adherence, or smoking cessation found improvements when partners participated. Patients in couples programs maintained physical activity levels while those going solo let gym routines slide. Medication adherence stayed higher, and smoking quit rates improved.
Cardiovascular outcomes showed mixed results. Some studies reported improved cholesterol levels and fewer doctor visits for patients in couples programs. Others found no differences in blood pressure, cardiac events, or functional status. The inconsistency likely reflects that most studies weren’t designed or powered to detect changes in relatively rare cardiac events.
Mental health outcomes varied widely. About 63% of studies found some improvements in anxiety or depression, but which partner benefited and when differed across programs. Some helped patients feel less depressed, others helped partners cope better with caregiving stress, and several found no mental health changes at all.
The Missing Piece: Relationship Quality Itself
Despite the well-established biological links between relationship quality and heart health, only three studies actually measured relationship quality. None of those three found improvements.
This reveals a fundamental flaw in current approaches. Most programs treat partners as helpers who can remind patients to take pills and accompany them on walks. Only two studies used actual couples therapy methods that directly addressed relationship dynamics, emotional connection, and communication patterns.
Those relationship-focused programs showed promise. Patients reported reduced concerns about the future, improved self-rated health, and better coping strategies. One program using mindfulness-based couples therapy reduced patient anxiety and depression. Another using solution-focused therapy decreased depressive symptoms and improved self-rated health scores.
The majority of programs focused almost entirely on health education and behavior change while largely not addressing the relationship itself. This approach may help couples coordinate medication schedules but does little to address relationship distress that’s actively damaging cardiovascular health through elevated cortisol, increased inflammation, and poor blood pressure control.
Researchers found that roughly 30% of people with cardiovascular disease report significant distress in their romantic relationships. For these couples, standard health education programs that don’t address relationship problems may miss the primary mechanism through which the partner could help.
The biological data makes the case clearly. Relationship distress isn’t just emotionally difficult for heart patients. It’s a physiological stressor that activates cardiovascular, neuroendocrine, and immune responses in ways that directly worsen disease progression. Happy relationships aren’t just nice to have. They provide measurable protection through reduced stress hormones, better blood pressure control, lower inflammatory markers, and improved health behaviors.
What Cardiac Rehabilitation Should Do Differently
The researchers propose that cardiac rehabilitation programs start screening for relationship quality, much like they currently screen for depression and anxiety. Brief questionnaires taking just minutes could identify which couples need extra support. Programs would then offer different levels of intervention based on each couple’s specific needs.
All patients would receive basic education about how relationships affect heart health through biological mechanisms. Those experiencing mild to moderate relationship difficulties would join structured relationship enhancement programs. Couples facing serious, long-standing problems would get referrals to specialized therapists in the community.
This stepped care approach would use existing staff more efficiently. Nurses who currently deliver health education could expand their role with proper training. Allied health professionals like social workers or psychologists could provide relationship enhancement sessions within existing program structures.
The M3 (Michigan Micro Mote) computer alone, shown floating above what appears to be Lincoln’s shoulder for scale. (Photo taken at the Michigan Integrated Circuits Laboratory. Photographer: Michael Simari)
The future is now…and it’s tiny.
Robots the size of a single-celled organism can now sense their environment, make decisions, and act on them without any outside help. Researchers at the University of Pennsylvania and University of Michigan created microscopic machines measuring just 210 to 340 micrometers wide (roughly the size of a paramecium or two human hairs laid side by side) that pack in an onboard computer, temperature sensors, memory, communication systems, and propulsion.
Published in Science Robotics, the work marks the first reported demonstration of a fully integrated, task-specific onboard computer, environmental sensors, and locomotion systems in something this microscopically small. The robots operate without external control. These devices run on roughly 100 nanowatts of power, about the same energy budget as many living cells.
Previous attempts at building robots at cellular scales forced researchers to sacrifice key capabilities. Most microrobots either relied on external equipment like magnetic coils to control them, could only execute predetermined behaviors hard-coded during manufacturing, or lacked the ability to sense and respond to their surroundings. These new microrobots overcome all three limitations.
Built Like Computer Chips, Small as Cells
The research team manufactured their microrobots using the same semiconductor processes that create computer chips. About 100 robots fit on a single millimeter-scale chip that can rest on a gloved fingertip. Each individual robot contains a tiny processor, solar cells for harvesting power from light, temperature sensors, circuits for controlling movement, memory, and an optical receiver for wireless programming.
Power represents the primary constraint when working at cellular dimensions. Living cells have evolved molecular machinery to harvest and use energy efficiently at nanowatt levels. The research team had to match this biological efficiency. The processor alone consumes nearly 90% of the robot’s 100-nanowatt power budget and occupies about 25% of its body.
To work within these cellular-scale power limits, researchers designed a custom computer architecture that compresses robot actions into specialized instructions. Commands like “sense the environment” or “move for N cycles” execute in what appears to be a single operation. This compression makes meaningful tasks possible with just a few hundred bits of memory.
Temperature Tracking and Navigation
The robots demonstrated their autonomous capabilities through experiments that mirror how single-celled organisms navigate their environments. In one test, microrobots continuously measured surrounding temperature, converted readings to digital data, and transmitted results back to a base station by encoding information in their movement patterns.
When tested in a bath of gradually warming solution, the robots’ measurements matched those from standard temperature probes. The sensors achieved 0.3-degree Celsius resolution with about 0.2-degree accuracy despite their microscopic size. This performance exceeds most existing digital thermometers of comparable volume.
The second experiment tested whether robots could exhibit taxis, or directed movement toward or away from environmental stimuli that characterizes many microorganisms. Researchers programmed the microrobots to search for warmer regions when temperature dropped, then hold position when finding warmth.
Results showed responsive behavior driven by real-time sensor input. Robots initially rotated in place without an imposed gradient. When researchers cooled the local area, robots automatically switched to exploratory movements, traveling through their environment until locating warmer zones, where they resumed stationary rotation. Reversing the temperature gradient caused robots to reverse course. This showed responses to live environmental changes rather than a fixed movement script.
Moving at cellular scales requires different approaches than standard robotics. The robots use electrokinetic propulsion, passing current between oppositely charged platinum electrodes while immersed in fluid. Mobile ions surrounding the robot respond to this electric field. The ions drag fluid along, creating flow that propels the machine forward at 3 to 5 micrometers per second. Robots can travel in different directions or rotate by changing which electrodes are active.
Light-Based Programming
Getting instructions into robots the size of cells required wireless solutions. The team developed an optical communication system using light-emitting diodes to both power and program the devices. One LED wavelength provides energy that solar cells convert to electricity. A second wavelength transmits data by flashing patterns that robots interpret as binary instructions and write to onboard memory.
A graphical user interface automates the entire programming process. Researchers can define robot behaviors without writing low-level firmware code. The system can send initialization programs to configure basic functions or task programs that define operations. Once instructions load, the robots operate completely autonomously based on their internal program and sensor readings.
To prevent random light fluctuations from accidentally altering robot behavior, the communication protocol requires passcode sequences. Each robot recognizes both a global passcode common to all devices and a type-specific code for addressing particular subsets. This enables researchers to give different instructions to different robots, similar to how cells in a multicellular organism respond to different chemical signals.
Potential Medical Applications and Future Improvements
The robots’ ability to sense, process, and respond to temperature could support future applications in biological research and medical diagnostics. Operating at cellular scales, they probe thermal gradients in ways larger sensors cannot, fitting into microfluidic chambers or capillary tubes where traditional instruments fail.
The devices could potentially interface with living systems by positioning their aqueous environment near target tissues and allowing heat to flow between environments. Reading temperature without direct physical contact bypasses biocompatibility concerns that affect many implantable sensors. The current work demonstrates these capabilities in controlled laboratory conditions, not in living organisms.
The authors estimate that, at production scale, each robot could cost on the order of a penny. Combined with the simple programming system requiring only controllable light sources rather than specialized laboratory equipment, this low cost could make cellular-scale autonomous robotics accessible beyond well-funded research institutions.
The research team notes that more advanced applications will require improvements like new actuators for in-body operation or better power transfer methods. Moving to more advanced semiconductor processes would increase onboard memory about 100-fold, enabling programs approaching thousands of lines of code and supporting more sophisticated decision-making.
The monthly payment is HOW much? (Credit: Basicdog on Shutterstock)
On average, Americans will spend close to $2 million dollars on major debt payments before their life ends. That staggering figure, according to an eye-opening study, represents every car loan, mortgage payment, student loan bill, and credit card balance between age 18 and death at 78.
A new analysis by JG Wentworth concludes that the average American will pay off $1,786,810 in debt across their lifetime. That’s money tied up in monthly obligations rather than available for savings, investing, or simply having more breathing room in the budget.
The study breaks down exactly where that $1.8 million goes over 60 years of adult life. The calculation includes four major debt categories affecting most Americans: mortgages, auto loans, student debt, and credit cards. Each follows a predictable pattern, spiking at key life stages and gradually declining through years of payments. The total includes both principal and interest, though credit card interest was excluded due to variable rates.
That $1.8 million average masks enormous regional variations. Hawaiian residents will pay off $2,570,976 over their lifetime, while West Virginians face just $1,391,240. The gap between most and least expensive states spans nearly $1.2 million, driven largely by housing costs.
Debt Peaks at Two Critical Ages
In this model, debt typically starts when someone turns 18. Between a first car loan and an initial credit card, young adults begin with $20,718 in obligations. That drops to $5,764 by age 22 as they work and make payments.
College loans often come due at 23, pushing debt back up to $42,242. For many people in the analysis, debt stays relatively manageable through their late 20s and early 30s as they buy second cars and pay down student loans.
At 38, everything changes. First-time homebuyers see their debt explode from $17,139 to $320,092 overnight. That single purchase multiplies debt nearly 20-fold.
Americans spend their 40s and 50s gradually chipping away at that first mortgage. Debt declines steadily until age 61, when the typical American buys a second home. At this peak moment, total debt hits its lifetime high: $370,259.
By retirement age 67, people have reduced their burden to $212,596. From 75 to 78, only credit card debt remains at about $6,754 per year.
Your Home Consumes $1.1 Million
Housing debt alone accounts for $1,117,860—that’s 62.6% of the $1.8 million lifetime total. The analysis assumed Americans purchase two homes: a first at age 38 with a 30-year mortgage, and a second at 61 with a 15-year term.
California homebuyers face the steepest housing costs at $1,844,069 across two homes. Hawaii follows at $1,829,064, while Washington residents pay $1,635,236.
West Virginia offers the cheapest homeownership at $784,006 for two houses. Iowa and Mississippi residents also pay less than $830,000 for two homes over their lifetimes.
The enormous variation in housing costs explains why some state residents pay nearly twice as much in lifetime debt. In Hawaii, mortgage payments consume 71.1% of lifetime debt.
Cars, Credit Cards, and College Add $670,000 More
Auto financing adds $245,297 to lifetime debt totals. The average American purchases four cars over their lifetime, with the second typically bought around age 30. Alaska residents pay the most ($290,056) due to higher vehicle prices, while New Hampshire, Vermont, and Maine residents pay around $200,000.
Credit card debt costs $387,985 over 60 years. Balances start low for young adults at $3,456 annually, peak during middle age at $9,557 per year, then drop after 60. About half of credit card users carry revolving balances rather than paying in full each month. Alaskans rack up $484,620 in lifetime credit card debt, while Iowans carry just $319,740.
Student loans represent the smallest slice at $35,668 on average. The study focused on federal undergraduate borrowing, which represents the vast majority of student debt. Maryland graduates face $43,692 in student debt, while North Dakota students pay just $29,647.
One 15-Year Window of Relief
Between ages 23 and 38, many Americans experience their only sustained period of manageable debt. During these working years, they steadily pay down initial obligations without taking on massive new loans.
Then homeownership resets everything. After roughly 23 years of paying on that first 30-year mortgage, the model assumes many buyers take on a second home at age 61. That creates another 15 years of debt extending almost to death at 78.
Three decades of adult life (ages 38-67) center on paying off two houses. The $1.8 million lifetime debt total reflects how housing obligations structure finances for most Americans.
The sun sets on every life eventually, but these findings indicate mortality and old age aren’t as closely related as believed. (Photo by Johannes Plenio on Unsplash)
The ‘Hallmarks of Aging’ Framework Has A Major Problem That Nobody Talked About Until Now
The next time a death certificate lists “natural causes” or a doctor mentions someone died of “old age,” keep in mind that may not be true after all. Autopsy studies reveal that even centenarians who seemed healthy days before death succumbed to specific, identifiable diseases, not some vague process called aging.
Scientists Maryam Keshavarz and Dan Ehninger from the German Center for Neurodegenerative Diseases argue in a new review that this fundamental misunderstanding has led aging research astray for decades. Their systematic analysis, published in Genomic Psychiatry, suggests that much of what scientists thought they knew about measuring and manipulating aging may be built on flawed assumptions.
When researchers examined 2,410 autopsies, cardiovascular disease emerged as the culprit in the vast majority of deaths, including myocardial infarction (heart attacks, 39%), cardiopulmonary failure (38%), and cerebrovascular lesions (strokes, 17.9%). A study of people over 85 who died unexpectedly outside hospitals found cardiovascular events responsible for 77% of deaths. Even among centenarians perceived as healthy, autopsies revealed that 68% died from cardiovascular causes, 25% from respiratory failure, and smaller percentages from other specific organ failures. Zero died from “old age.”
Autopsy analyses are crucial for correcting misperceptions, the researchers write, noting that relatives and even physicians frequently misjudge causes of death without examining the body.
Why Each Species Dies Differently
The pattern of disease-driven mortality extends across the animal kingdom, but with a crucial twist: each species has its own vulnerable spot. While cardiovascular disease dominates in humans and nonhuman primates, causing over 60% of deaths in aging rhesus macaques, rodents tell an entirely different story.
Cancer killed between 84% and 89% of mice in one major study under normal feeding conditions. Dietary restriction reduced this to 64% in both sexes, while rapamycin treatment lowered it to 74%. Even with interventions widely considered to slow aging, cancer remained the primary cause of death in mice, just occurring at later ages. In rats, tumors accounted for roughly 63% of deaths. Dogs showed a similar pattern, with neoplasia causing nearly half of all deaths in older animals.
Move further down the evolutionary tree and the causes shift again. Fruit flies die primarily from intestinal epithelial failure, a breakdown of the gut lining that leads to bacterial infections. Roundworms succumb to pharyngeal infections or throat muscle atrophy. Each species has a different Achilles’ heel.
This creates a problem for aging research. When a drug extends mouse lifespan by preventing cancer, has it slowed aging or merely delayed one particular disease? And if humans die primarily from cardiovascular problems rather than cancer, why should we expect mouse cancer-prevention strategies to help us live longer?
The Influential Framework Built on Questionable Evidence
The concerns grow when Keshavarz and Ehninger turn their attention to one of aging research’s most influential concepts: the “hallmarks of aging.” Introduced in 2013 as nine hallmarks and expanded to 12 in a 2023 update, this framework identifies cellular and molecular changes (from genomic instability to cellular senescence to mitochondrial dysfunction) that supposedly drive the aging process.
The hallmarks papers have been cited thousands of times and shaped research priorities across the field. Yet when the researchers systematically examined the evidence supporting each hallmark’s causal role in aging, they uncovered a widespread methodological flaw.
Between 57% and 100% of the studies supporting different hallmarks tested interventions only in old animals. This design makes it impossible to tell whether treatments genuinely slow aging or simply improve function at any age.
The distinction is critical. Imagine a drug that enhances memory equally in both young and old mice. That’s valuable, but it’s not evidence the drug slows cognitive aging. It just means the drug improves brain function generally. To claim an intervention slows aging, researchers need to show it changes the rate at which age-dependent decline occurs, not just shifts everyone’s performance upward.
When Keshavarz and Ehninger identified studies that did include young animals, they analyzed 602 age-sensitive traits across those studies. They found that 436 of these traits (72%) showed effects in both young and old age groups. The interventions were producing what the researchers call baseline effects (age-independent physiological changes) rather than genuine alterations to aging trajectories.
What Rapamycin and Fasting Studies Actually Show
The issue extends even to aging research’s success stories. Rapamycin consistently extends lifespan in mice and has become one of the field’s most studied compounds. Intermittent fasting reliably prolongs life in rodents. Genetic manipulations that reduce growth hormone signaling add months to mouse lifespans.
Yet deep phenotyping studies that measured dozens of age-sensitive traits revealed something unexpected. Most effects of these interventions appeared as baseline shifts rather than changes in aging rate. Mice showed similar improvements whether treated young (before age-related changes emerged) or old (after such changes had manifested).
A 2022 study by Xie and colleagues examined three major longevity interventions across 180 age-sensitive traits in mice. They found that 145 traits (roughly 81%) showed intervention effects in young animals equal to or greater than those in old animals. The interventions were altering physiology broadly, not specifically targeting the processes that drive age-dependent change.
Rapamycin-treated mice still died primarily from cancer, just at older ages. Intermittent fasting didn’t eliminate the diseases of aging—it postponed them. The interventions worked more like hitting a snooze button on mortality than fundamentally rewinding the aging clock.
DNA Age Tests May Not Measure What You Think
The problems extend to tools that have become wildly popular both in research and consumer markets: biological age clocks. These algorithms, particularly those based on DNA methylation patterns (chemical modifications to DNA), can predict chronological age with impressive accuracy and have spawned a cottage industry of longevity testing.
But Keshavarz and Ehninger argue these clocks share a fundamental limitation with much of aging research. They’re correlational tools that identify patterns associated with age without revealing causal mechanisms. The comparison to facial aging is apt: wrinkles predict age reliably, but treating wrinkles doesn’t make you biologically younger.
Most DNA methylation clocks rely on a surprisingly small number of genomic sites. Studies show they maintain accuracy even when many sites are removed, suggesting the remaining sites capture redundant information rather than providing comprehensive biological insight. A 2024 study using Mendelian randomization (a technique that can help distinguish correlation from causation) found that traditional aging clocks aren’t significantly enriched for sites with causal roles in aging.
The clocks remain useful for predicting health outcomes and stratifying people by risk. But they may not tell researchers whether an intervention truly slows biological aging or just shifts biomarker values in age-independent ways.
What Aging Research Needs to Change
Keshavarz and Ehninger don’t argue that aging research has been worthless. The field has identified numerous interventions that extend lifespan in model organisms and accumulated vast amounts of data about age-related changes. The problem is interpretation.
A drug that prevents cancer in mice is valuable even if it doesn’t slow aging per se. A biomarker that predicts mortality risk helps even if it doesn’t reveal aging mechanisms. But claiming these as evidence of understanding or manipulating aging itself requires more rigorous proof.
The researchers propose concrete refinements. Studies should measure diverse outcomes across multiple organ systems rather than relying on lifespan or a handful of favorite biomarkers. Interventions should be tested in both young and old subjects to distinguish rate effects from baseline effects. Researchers should explicitly acknowledge species-specific life-limiting pathologies rather than assuming mouse results translate directly to humans.
Most provocatively, they suggest the field needs to confront an uncomfortable possibility: despite decades of research and thousands of papers on aging, scientists may still lack a deep mechanistic understanding of what drives age-dependent decline. They’ve catalogued correlates of aging, identified factors that extend lifespan by postponing specific diseases, and developed predictive biomarkers. But understanding the underlying process that makes organisms more vulnerable over time may remain elusive.
This matters beyond academic debates. As longevity interventions move from mice to humans, the distinction between preventing specific diseases and genuinely slowing aging determines which treatments to pursue, how to test them, and what outcomes to measure. Getting it wrong wastes resources and, more importantly, delays finding interventions that might actually work.
Ocean temperatures warmed by human-caused climate change fed the intense rainfall that triggered deadly floods and landslides across Asia in recent weeks, according to an analysis released Wednesday. (AP Video: Aya Diab)
Ocean temperatures warmed by human-caused climate change fed the intense rainfall that triggered deadly floods and landslides across Asia in recent weeks, according to an analysis released Wednesday.
The rapid study by World Weather Attribution focused on heavy rainfall from cyclones Senyar and Ditwah in Malaysia, Thailand, Indonesia and Sri Lanka starting late last month. The analysis found that warmer sea surface temperatures over the North Indian Ocean added energy to the cyclones.
Floods and landslides triggered by the storms have killed more than 1,600 people, with hundreds more still missing. The cyclones are the latest in a series of deadly weather disasters affecting Southeast Asia this year, resulting in loss of life and property damage.
“It rains a lot here but never like this. Usually, rain stops around September but this year it has been really bad. Every region of Sri Lanka has been affected, and our region has been the worst impacted,” said Shanmugavadivu Arunachalam, a 59-year-old schoolteacher in the mountain town of Hatton in Sri Lanka’s Central Province.
Warmer sea surface temperatures
Sea surface temperatures over the North Indian Ocean were 0.2 degrees Celsius (0.3 degrees Fahrenheit) higher than the average over the past three decades, according to the WWA researchers.
Without global warming, the sea surface temperatures would have been about 1 degree Celsius (1.8 degrees Fahrenheit) colder than they were, according to the analysis. The warmer ocean temperatures provided heat and moisture to the storms.
When measuring overall temperatures, the world is currently 1.3 degrees Celsius (2.6 degrees Fahrenheit) warmer than global average during pre-industrial times in the 19th century, according to the National Oceanic and Atmospheric Administration.
“When the atmosphere warms, it can hold more moisture. As a result, it rains more in a warmer atmosphere as compared to a world without climate change,” said Mariam Zachariah, with the Centre for Environmental Policy at Imperial College London and one of the report’s authors.
Using tested methods to measure climate impacts quickly
The WWA is a collection of researchers who use peer-reviewed methods to conduct rapid studies examining how extreme weather events are linked to climate change.
“Anytime we decide to do a study, we know what is the procedure that we have to follow,” said Zachariah, who added that they review the findings in house and send some of their analysis for peer review, even after an early version is made public.
The speed at which the WWA releases their analysis helps inform the general public about the impacts of climate change, according to Zachariah.
“We want people everywhere to know about why something happened in their neighborhood,” Zachariah said. “But also be aware about the reasons behind some of the events unfurling across the world.”
The WWA often estimates how much worse climate change made a disaster using specific probabilities. In this case, though, the researchers said they could not estimate the precise contribution of climate change to the storms and ensuing heavy rains because of limitations in climate models for the affected islands.
These amphibians are all too happy to endure a few stings for a decent meal.
Japanese pond frogs can eat some of the world’s most venomous insects and apparently hop away from the meal unharmed. Research reveals these amphibians tolerate repeated stings from giant hornets carrying enough venom to kill animals many times their size.
Scientists in Japan tested how pond frogs responded to three species of hornets, including Vespa mandarinia, the Asian giant hornet notorious for its painful, potentially lethal sting. About 79% of the frogs that attacked these giant hornets successfully consumed them despite being stung multiple times.
A single sting from V. mandarinia carries enough venom to reach the LD50 dose for a 270-gram mouse. The frogs in this study ranged from just 6 to 76 grams. Some frogs were stung directly in the face, eyes, tongue, and throat yet showed no signs of injury or distress.
The hornets’ stings did not kill or harm any of the frogs, according to Shinji Sugiura, a researcher at Kobe University’s Graduate School of Agricultural Science who published the findings in the journal Ecosphere. The frogs resumed normal behavior immediately after consuming their prey.
Face to Face with Venom
The experimental setup was simple but revealing. Researchers placed hungry pond frogs (Pelophylax nigromaculatus) in plastic containers with worker hornets that had been stimulated to sting. Digital cameras recorded what happened next.
Most frogs attacked the hornets without hesitation. Video footage showed hornets repeatedly extending their stingers and jabbing the frogs during these encounters. The attacks lasted several seconds, with hornets stabbing at the frogs’ mouths and faces. Yet the frogs persisted, eventually swallowing their dangerous prey whole.
Out of 45 frogs tested, 43 attacked the hornets. Of those, 37 successfully consumed them despite the defensive stings. The frogs digested the hornets over the next few days, excreting undigested body parts in their feces.
The study tested three hornet species of increasing size and venom potency. Japanese yellow hornets (V. simillima) were consumed by 93% of attacking frogs. Yellow-vented hornets (V. analis) had an 87% consumption rate. Even the formidable Asian giant hornets were consumed by 79% of frogs that attacked them.
Built to Handle Pain
Hornet venom is a complex cocktail designed to cause maximum suffering. It contains biogenic amines like serotonin that trigger sharp, intense pain. Small peptides called vespakinins amplify the hurt. Enzymes break down tissue and can cause system-wide damage including cardiac dysfunction and blood cell destruction in sensitive animals.
These chemical weapons evolved primarily to defend hornet colonies from vertebrate predators like birds and mammals. Hornet stings cause intense, sharp pain in humans and can trigger severe allergic reactions that have caused human fatalities.
Frogs appear to tolerate both the pain and the toxicity based on their behavior. They showed no behavioral changes suggesting discomfort and tolerated both venom effects and pain in ways that set them apart from most vertebrates.
The research found that larger frogs had better success consuming hornets. This size-dependent pattern suggests bigger frogs may have proportionally greater venom tolerance, though the exact mechanism remains unknown.
Evolutionary Mismatch
Frogs and hornets cross paths frequently in Japanese wetlands. Hornet workers visit pond edges to collect water for their colonies, where they encounter hunting frogs. Previous studies have found hornet remains in the stomach contents of wild pond frogs, confirming this predator-prey relationship exists in nature.
But hornets didn’t evolve their stingers with frogs in mind. Social wasps developed venomous defenses mainly to protect their colonies from raiders trying to steal larvae and pupae. Birds and mammals pose the primary threat to hornet nests, so the venom evolved to deter warm-blooded attackers.
Frogs rarely attack hornet colonies. They prey opportunistically on individual workers foraging around water. Since hornets didn’t face strong selection pressure from frog predation, their venom may simply be ineffective against amphibian physiology.
Sticky saliva that frogs produce might offer some protection by coating their mouth and throat during attacks, though this hasn’t been tested. Frogs swallow prey whole and alive, so their digestive systems may have evolved robust linings resistant to chemical and physical damage from struggling, stinging insects.
Medical Implications
Understanding how frogs tolerate hornet venom could help scientists study pain mechanisms and venom responses. The study suggests frogs may have physiological traits that help them tolerate both the pain and the toxic effects of hornet venom, although the exact mechanism is still unknown.
Hornet stings cause serious reactions in humans each year. If scientists can identify how frog tissues resist venom damage or how their nervous systems respond to pain signals, those discoveries might eventually inform research on venom responses in other animals.
Other animals have evolved similar defenses through different paths. Horned lizards developed blood proteins that neutralize harvester ant venom. Grasshopper mice have mutations in pain receptors that make scorpion venom painless. Each species offers unique insights into how evolution solves the problem of venomous prey.
Frogs represent a particularly useful model because they’re vertebrates like humans, sharing more physiological similarities than insects or other invertebrates. Their tolerance mechanisms might translate more directly to human medicine than adaptations found in distantly related animals.
The research leaves key questions unanswered. Do frogs learn to avoid hornets after being stung, or do they continue attacking them repeatedly? Does the venom fail to penetrate frog tissues, or do frogs detoxify it rapidly? What specific proteins or cellular mechanisms provide protection?
Future studies comparing venom exposure across multiple trials could test whether frogs develop learned aversion to painful prey. Biochemical analysis of frog blood and tissues after stings might reveal detoxification pathways. Genetic studies could identify mutations in pain receptors similar to those found in grasshopper mice.
Watching Dogs Lifts Mood, But There’s a Catch for Pet Owners
Watching videos of dogs generally boosted participants’ moods regardless of whether the animals appeared happy, neutral, or upset. Indeed, according to the research published in PeerJ, even when certain pups appeared distressed, people still felt better after watching.
That’s one of the more unexpected findings from a study conducted at Arizona State University, which also uncovered a strange twist in how human emotions shape the way people perceive their canine companions.
Here’s the twist: when people were primed with happy dog images before watching the videos, they actually rated the dogs as feeling worse. Those who had just viewed upsetting images of dogs perceived the same video dogs as happier. This reversal appeared only in the experiment that used dog images as mood primes.
The finding contradicts decades of psychology research on the “emotional congruence effect,” the well-documented tendency for people in a good mood to see the world more positively and for those in a bad mood to see things more negatively. When it comes to reading dog emotions after viewing other dog imagery, the human brain appears to work backward.
Dogs on Screen Improve Human Mood
Holly G. Molinaro and Clive D.L. Wynne conducted two experiments involving nearly 600 undergraduate students at Arizona State University. Participants watched videos of three dogs named Oliver, Canyon, and Henry displaying positive, neutral, or negative emotional states. By the end of the experiments, most participants reported improved moods compared to their starting states, though the pattern varied somewhat by priming condition.
Previous research has shown that physical interaction with dogs can lift human spirits. Studies have documented mood improvements from petting dogs, walking them, and participating in animal-assisted therapy programs. This study showed that even passive viewing of silent clips of dogs against a plain black background still tended to improve how people felt.
Some of the dogs in the videos were responding to things they disliked, such as vacuum cleaners or cats. These stimuli were chosen based on owner reports of what genuinely bothered each dog. Yet even with these uncomfortable moments included, human viewers generally felt better after watching the full set of clips.
How Mood Warps Your Perception of Dog Emotions
The second major finding emerged when researchers examined whether a person’s mood affected how they interpreted dog emotions. In the first experiment, participants viewed mood-inducing photographs of people, landscapes, and objects before watching the dog videos. While the photos successfully changed how participants felt, those altered moods had no effect on how they perceived the dogs’ emotional states.
The second experiment changed the priming images to photographs of dogs. Happy dog photos put people in good moods. Upsetting dog photos put people in bad moods. This time, participants’ interpretations of the dog videos shifted, but not in the expected direction.
Participants who had just viewed happy dog images rated the dogs in the videos as feeling more negative. Those who had viewed distressing dog images perceived the same video dogs as feeling more positive. Psychologists call this pattern a “contrast effect,” and it had never been documented in cross-species emotional perception before. Notably, this effect appeared only when dog images served as the mood primes, not when participants viewed images of people, landscapes, or objects.
Why the Type of Images Mattered
One puzzling aspect of the research was why general mood priming in the first experiment produced no effect, while dog-specific mood priming in the second experiment produced the opposite of what was expected.
The mood induction worked in both cases. Participants who viewed positive images reported feeling better, and those who viewed negative images reported feeling worse. The disconnect happened only when participants tried to interpret dog emotions afterward, and only when those participants had been primed with dog imagery.
The researchers speculated that viewing dog images might activate different cognitive processes than viewing images of people or objects. When participants saw distressed dogs in the priming phase and then watched video dogs displaying ambiguous behavior, they may have perceived those video dogs as better off by comparison. The reverse may have occurred for those primed with happy dog images.
Takeaways for Dog Owners and Professionals
On the positive side, dog owners struggling with stress or low mood might benefit simply from watching videos of dogs, even if they cannot be with their own pets.
On the more cautionary side, the contrast effect raises questions about how accurately people can read their dogs’ emotions after exposure to other dog-related content. Someone who has just scrolled through social media posts of happy, playful dogs might subsequently perceive their own dog as unhappier than the animal actually is. Someone who has just read news about animal cruelty might perceive their dog as more content by comparison.
Shelter workers, veterinarians, and dog trainers all rely on their ability to read canine emotions accurately. If recent exposure to dog-related imagery can skew their perception of how an animal is feeling, it could lead to mishandled situations or unmet behavioral needs.
The researchers acknowledged limitations. The study relied on undergraduate students, mostly between 18 and 21 years old, and used only nine videos featuring three individual dogs. Future studies with more diverse participants and a wider range of breeds and behaviors would help confirm whether these patterns hold up.
For dog lovers, the study offers both comfort and caution. Dogs really do tend to make people feel better, even through a screen. But what a person thinks they see in a dog’s eyes might depend on what images crossed their path moments before.
A tattoo today may increase melanoma risk years down the line. (Photo by Getty Images in collaboration with Unsplash+)
Most people consider the pain and permanence before getting a tattoo. Few think about the carcinogenic chemicals they’re injecting into their skin.
Swedish researchers identified 2,880 individuals diagnosed with melanoma and used questionnaires to gather detailed information about tattoo exposure, sun habits, and other risk factors. The population-based study published in the European Journal of Epidemiology found that tattooed individuals face a 29 percent increased risk of developing cutaneous melanoma compared to those without tattoos. Among the 1,598 cases who responded (56% response rate) and their matched controls, 22 percent of melanoma cases had tattoos before diagnosis, compared to 20 percent of controls.
The concern centers on what’s in tattoo ink. Black ink often contains high levels of polyaromatic hydrocarbons, some classified as carcinogenic by the International Agency for Research on Cancer. Colored inks rely heavily on azo pigments, which break down into carcinogenic aromatic amines when exposed to ultraviolet radiation from sun, tanning beds, or laser removal treatments. Heavy metals appear across all ink colors.
What’s in Tattoo Ink?
Researchers calculated the increased melanoma risk after adjusting for known factors like UV exposure, skin type, sunbed use, and sunburn history. The association held even after accounting for these traditional melanoma risk factors, suggesting tattoo exposure may represent an additional risk factor.
Tattoos containing both black and colored ink showed a 38 percent increased risk compared to non-tattooed individuals. People tattooed for 10 to 15 years faced the highest melanoma risk, with a 67 percent increase. Shorter exposure duration of under five years also showed elevated risk at 60 percent, though confidence intervals were wider.
Only 30 percent of melanomas developed at the tattoo site. This finding surprised researchers, who note that the systemic nature of the risk points to tattoo ink components potentially affecting the immune system rather than causing localized skin changes alone. Studies in firefighters and petroleum workers exposed to similar chemicals show increased melanoma risk despite systemic rather than localized exposure.
Regulation Failures and Fraudulent Labeling
The European Union implemented regulations in January 2022 limiting 4,000 chemicals in tattoo ink. European regulatory authorities have found through market surveillance that many inks still contain toxic chemicals above permitted levels. Fraudulent labeling compounds the problem, with banned pigments masked by listing legal alternatives.
Subgroup analysis revealed increased risk for both in-situ melanomas (33 percent increase) and invasive melanomas (25 percent rise). Superficial spreading melanoma risk increased 40 percent, while melanocytic nevus with severe atypia showed a 39 percent increase.
When researchers excluded cases with previous melanoma diagnoses to focus only on first-time cases, tattooed individuals still showed a 23 percent increased risk. Excluding individuals taking immunosuppressive medications raised the risk estimate to 32 percent, which researchers note aligns with the hypothesis that tattoo ink could affect immune function, though this requires further investigation.
Study Demographics and Tattoo Patterns
The study population consisted of individuals aged 20 to 60 years diagnosed with melanoma in 2017. Sweden provided an ideal setting with comprehensive national cancer registry data covering over 99 percent of skin cancers. Participants reported tattoo details including size, color, number of sessions, and duration of exposure.
Most tattooed participants received their first tattoo around age 24 or 25. Professional tattoo artists in Sweden performed 90 percent of tattoos, though 7 to 8 percent came from non-professionals. Decorative tattoos were most common, followed by cosmetic applications like permanent makeup.
Study Reveals A ‘Friends-and-Neighbors Effect’ That Distorts Tax Preferences
Most people think the psychology of taxes is fairly straightforward and almost always tied to one’s personal bank account. Interestingly, researchers report something much more nuanced is at play. It isn’t so much about how much money someone has, but who they see every day.
Published in PNAS Nexus, the research uncovered that for most people, their social circles hide the extent of societal inequality so well that they do not see the true state of wealth distribution. This often leads to tax decisions that nonsensically go against one’s own financial interests, as well as society’s best interests as a whole. Even in an idealized direct democracy, redistribution can fail to close the gap.
Researchers from the London School of Economics and the Santa Fe Institute ran an experiment with 1,440 Americans who voted on tax rates in artificial societies. Crucially, they controlled who could see whose wealth. The structure of social networks created blind spots that sabotaged rational decision-making, even when voters would have benefited from redistribution.
“If people do not observe inequality on a daily basis, they underestimate the severity of the problem and their own standing, and consequently do not take the due political stance and action,” the researchers write.
How Social Circles Shape Tax Votes
The experiment randomly assigned participants to be either rich (starting with about 200 points) or poor (starting with about 20 points). Groups of 24 people then voted on a tax rate between 0% and 100%. The tax revenue would be collected and redistributed equally to everyone in the group.
Each person could only see the wealth of eight others in their group—and the researchers carefully controlled which eight. Some people saw mostly others with similar wealth. Some saw a representative sample. Others saw mostly rich people, or mostly poor people, or were completely segregated by wealth.
Networks that mirror real life — where people tend to befriend others with similar incomes — produced the lowest tax rates. In segregated networks, where the rich only saw other rich people and the poor only saw other poor people, taxes dropped even lower.
Both groups agreed on low taxes for different reasons. Poor participants thought there wasn’t much money to redistribute because everyone they saw was poor like them. Rich participants figured few people needed help because everyone they saw was doing fine. Both made rational calculations based on systematically biased information.
Why Democratic Voting Doesn’t Fix Inequality
This finding helps solve a puzzle that has frustrated economists for decades. In theory, democratic countries with high inequality should naturally vote for more redistribution. The median voter (the person whose preferences determine the outcome) typically has less than the average wealth. They should always vote to tax the rich and share the proceeds.
Yet inequality has been rising in many democracies for 40 years. Income and wealth disparities in the United States, United Kingdom, Canada, and Australia have grown larger, not smaller, despite regular elections.
Political scientists usually blame broken institutions: corrupt elites, wealthy lobbyists, voter suppression, bundled party platforms. All of these factors matter. But the new research points to something more basic: people can’t demand redistribution they don’t know they need.
The experiment tested this directly by creating a stripped-down, idealized democracy inside the lab. No lobbyists. No political parties. No corrupt officials. Just pure majority rule, where the median vote wins and gets immediately implemented. Even under these controlled conditions, certain network structures—particularly those where people mostly see similar others—led to persistently low redistribution and high inequality.
Segregation Keeps the Poor Content With Less
Perhaps most troubling, segregation by wealth didn’t just reduce redistribution. It also kept people satisfied with unfair outcomes.
At the end of the experiment, participants rated their satisfaction with their final score and whether they thought the distribution in their group was fair. Poor people in segregated networks—who ended up with the least money—reported being the most satisfied. Poor people who saw many wealthy neighbors ended up with more money but felt worse about it.
“Segregation keeps the poor poorest but satisfied, while observing the rich makes them dissatisfied despite becoming better off,” the researchers note.
This aligns with decades of research showing that people judge their economic situation relative to those around them, not in absolute terms. A person earning $30,000 surrounded by others making the same feels richer than someone earning $40,000 surrounded by millionaires.
The political consequences are serious. If social networks keep poor people content with less, they won’t agitate for change. They won’t protest. They won’t vote for redistribution. They’ll accept their position because everyone they know occupies a similar one.
The Tradeoff Between Equality and Harmony
The experiment did find one network structure that produced high redistribution: when everyone, rich and poor alike, could see mostly wealthy people. In these networks, poor participants voted for tax rates approaching 100%, and their high numbers carried the vote.
But this came at a steep cost. These networks showed the highest levels of disagreement—the poor and rich voted for wildly different tax rates. Poor participants in these networks also reported feeling the least satisfied and judged the outcomes as most unfair, despite ending up relatively better off financially.
Over the three rounds of voting, this division intensified. Poor people who saw wealthy neighbors radicalized, with many eventually voting for 100% taxation. The rich never budged from their low-tax preferences. In contrast, when people saw mostly similar others, votes stayed moderate and agreement remained high—but so did inequality.
This exposes an uncomfortable choice at the heart of democratic redistribution: the social structures that make people demand more equality also make them more divided and dissatisfied. The structures that create harmony keep inequality entrenched.
Why Most People Underestimate Inequality
The experimental findings match survey research showing that people habitually underestimate inequality in their society. Americans tend to think wealth is distributed far more evenly than it actually is. They also misjudge their own position, with wealthy people often thinking they’re middle class.
The primary reason? Social circles aren’t random samples of society. They’re clustered by income, education, geography, and profession. A software engineer in San Francisco knows other software engineers making similar salaries. A retail worker in rural Ohio knows other retail and service workers. Neither group encounters the full spectrum of wealth distribution in their daily lives.
The mathematical properties of income distributions make this worse. Because wealth follows a right-skewed pattern, that is, most people have little while a few people have enormous amounts, the typical person is poorer than average. But in most social networks, people encounter others slightly richer than themselves, creating an upward bias.
The researchers’ computational model shows that even small amounts of clustering by similar income dramatically reduces perceived inequality. When the rich see other rich people and the poor see other poor people, both groups underestimate the gaps between them.
Taxes and Cultural Beliefs
The experiment also showed that voting on redistribution isn’t purely about self-interest. Participants clearly cared about more than just maximizing their own score. In post-experiment surveys, many mentioned concerns about equality, fairness, and balance, not just personal gain.
Many participants brought strong preexisting beliefs about taxation to the experiment. Most votes gravitated toward 20-25%, or roughly the effective tax rate many Americans actually pay, regardless of whether higher taxes would benefit them in the game. Political orientation mattered: conservatives voted for lower taxes, while those who perceived themselves as lower income voted for higher taxes.
Women assigned to be poor voted for lower taxes than men in identical situations, contradicting survey research showing women generally support higher redistribution. The researchers suggest women may have had more difficulty understanding the experimental instructions or felt more pressure to conform to prevailing anti-tax norms.
What This Means for Policy
The research carries clear recommendations. If political leaders want to build support for redistribution, they should increase the visibility of extreme wealth. News coverage of billionaires, political discourse about wealth concentration, social media discussions of inequality — all of these can counter the blind spots created by segregated social networks.
But this strategy risks increasing division and conflict. When poor people see the wealth they’re excluded from, they demand more; but they also grow angrier and less satisfied, even when redistribution succeeds.
There may be no perfect solution. Social networks appear to create an unavoidable choice: either maintain harmony through separation while inequality persists, or increase visibility of disparities while accepting greater division.
The study focused on wealth and redistribution, but the same dynamics likely apply to other forms of inequality. Gender pay gaps, racial wealth disparities, geographic divides — all of these become invisible when people cluster with similar others. And what people can’t see, they can’t fix, even in a functioning democracy.
The Burtele Foot with its elements in the anatomical position. (Photo by Yohannes Haile-Selassie/ASU)
A mysterious fossil foot discovered in Ethiopia more than a decade ago has now been linked to its most likely owner, and the revelation adds an important twist to the story of how our ancient relatives lived.
The foot probably belonged to Australopithecus deyiremeda, a 3.4-million-year-old human ancestor that shared the East African region with the famous “Lucy” species. But unlike Lucy’s kind, which was evolving toward more human-like walking, this species kept its tree-climbing abilities, new research reveals.
Scientists from Arizona State University’s Institute of Human Origins spent years searching for the missing pieces of this evolutionary puzzle. When they discovered the peculiar foot bones in 2012 at the Woranso-Mille site in Ethiopia, they knew they had something special. The foot had long, curved toes built for grasping branches and a flexible structure that looked very different from the rigid, arched feet of Lucy’s species, Australopithecus afarensis.
But there was a problem. Without teeth or jaw bones from the same individual, researchers couldn’t definitively identify which species the foot belonged to. The puzzle deepened because the foot came from the same geological layers that had produced fossils of A. deyiremeda, a species named just three years earlier, but the connection couldn’t be proven.
Now, newly discovered fossils have provided strong evidence for the connection. A juvenile jawbone with nearly intact baby and adult teeth, along with several isolated teeth from different individuals, all show the distinctive dental features of A. deyiremeda. These specimens came from the exact same ancient riverbed deposits as the foot, giving scientists solid reasons to link the two.
Curved Toes and Grasping Feet Suggest Tree-Climbing Lifestyle
The findings, published in Nature, show the story of human evolution was never as simple as textbooks made it seem. While Lucy’s species was developing feet adapted for efficient walking on the ground, A. deyiremeda took a different path, keeping features that made it comfortable in the trees as well as on the ground.
The foot bones tell the story. Long toe bones curve from front to back like those of modern apes. The second metatarsal bone (one of the long bones in the middle of the foot) shows unusual twisting and curvature. Most telling of all, the big toe bone is gracile and curved in ways that would have allowed A. deyiremeda to grasp tree branches.
“The foot displays morphological features that suggest a greater ability for grasping than modern humans and most fossil hominins,” the researchers write. The foot structure shows clear adaptations for climbing that simply aren’t present in A. afarensis fossils from the same time period.
The partial foot also lacks the rigid arch structure that makes human feet efficient for walking. Instead, it retains flexibility in the midfoot region, useful for wrapping around branches but less ideal for the kind of obligate bipedality that characterized Lucy’s kind.
Ancient Teeth Solve Decade-Old Mystery
Connecting the foot to A. deyiremeda required detective work spanning more than a decade. The breakthrough came with specimen BRT-VP-2/135, a juvenile jaw discovered about 300 meters from where the foot had been found. The jaw preserves both baby teeth and adult teeth still forming inside the bone, offering a wealth of diagnostic information.
Using micro-CT scanning technology, researchers could examine teeth that weren’t visible from the outside, still tucked away in their developmental crypts within the jawbone. The scans revealed features distinctive to A. deyiremeda that don’t appear in A. afarensis.
The canine teeth lack the prominent vertical ridge on the inner surface that characterizes A. afarensis canines. The premolars have a more primitive shape with cusps positioned more centrally and oriented at different angles than those of Lucy’s species. The upper canines and first molars are smaller than any other australopith species measured, and the molars are much narrower from side to side.
The jaw itself was missing the lateral hollow (an indentation on the outer surface) that’s diagnostic of A. afarensis jaws. Every detail pointed to A. deyiremeda.
Additional isolated teeth from the same geological horizon showed the same distinctive features. With multiple specimens all displaying the diagnostic traits of A. deyiremeda and coming from the exact location and time period as the mysterious foot, researchers had strong evidence to make the connection.
Chemical Analysis Shows Forest Diet Different from Lucy’s
Chemical analysis of tooth enamel provided a window into what A. deyiremeda ate millions of years ago. The research team drilled tiny samples of enamel powder from eight fossil teeth and analyzed their carbon isotopes. Plants use different photosynthetic pathways that leave distinct chemical signatures, and these signatures get locked into tooth enamel as it forms.
The results showed A. deyiremeda ate primarily what scientists call C3 foods, which come from forests and woodlands. These include fruits, leaves, seeds, and underground storage organs like roots and tubers. The isotope values (ranging from -12.4 to -8.8 per mil) matched those of earlier human ancestors like Ardipithecus ramidus and early Australopithecus anamensis, both of which lived in wooded environments.
By contrast, A. afarensis living at nearby sites during the same time period had much more variable isotope values. Lucy’s species ate from both forest plants and grasses from more open habitats, showing dietary flexibility that A. deyiremeda apparently lacked or didn’t need.
The dietary evidence fits well with the foot anatomy. A species spending significant time in trees would naturally have better access to forest foods. The combination of climbing-adapted feet and forest-food diet creates a coherent picture of A. deyiremeda‘s lifestyle.
Early Humans Took Multiple Paths to Walking Upright
For decades, the story of Lucy’s species dominated discussions about how our ancestors transitioned from living in trees to walking upright on the ground. But A. deyiremeda shows there wasn’t just one path.
Both species walked on two legs at least some of the time. But while A. afarensis was evolving rigid feet with arches that made walking more efficient, A. deyiremeda kept feet that could do double duty, handling both ground-based walking and tree climbing.
Study authors point out that large grinding teeth evolved before obligate human-like bipedality. A. deyiremeda had big molars adapted for processing tough plant foods, but it hadn’t given up its climbing adaptations. The package of features didn’t evolve as a unit, the way simple evolutionary narratives might suggest.
This mosaic evolution, where different body parts evolve at different rates and in different directions, appears to have been common among mid-Pliocene human ancestors. Multiple species coexisted, each experimenting with different combinations of primitive and derived features.
The juvenile jaw that helped solve the mystery belonged to an individual who died around 4.5 years old, based on tooth development patterns. The child still had baby teeth in place alongside emerging permanent teeth. The developmental pattern looked more like a chimpanzee’s than a modern human child’s, with incisors delayed in their formation relative to the first molars.
The research team worked at the Woranso-Mille site in Ethiopia’s Afar region, where erosion exposes layers of ancient sediments. The fossils came from sandstone deposits above a volcanic ash layer dated to 3.469 million years ago. Twenty-five hominin specimens have been recovered from the Burtele localities so far.
The evidence joins a growing body of research showing that human evolution wasn’t a simple progression from tree-dwelling apes to ground-walking humans. Instead, the mid-Pliocene saw multiple species coexisting in East Africa, each experimenting with different strategies for moving, eating, and surviving. A. deyiremeda kept its climbing abilities while also walking on two legs, while A. afarensis went further down the path toward obligate bipedality.
Moai statues under a blue sky at Rano Raraku on Easter Island. (Photo by Aeonian Photography on Shutterstock)
Easter Island’s famous stone heads have puzzled researchers for decades, but not for the reasons most people think. The real mystery wasn’t how ancient Polynesians carved and moved these massive sculptures across a remote Pacific island. Instead, scientists have long pondered how a society with no clear island-wide government managed to produce more than 1,000 giant statues.
Now, research using drone technology and 3D modeling has answered that question by mapping the primary quarry where these statues, called moai, were carved. Multiple small groups, likely family clans of around 15 to 25 people each, worked simultaneously in separate areas of the quarry without any boss coordinating their efforts. Each group had its own workspace, used different carving techniques, and operated independently while somehow maintaining a shared artistic vision.
The study, published in PLOS ONE, upends assumptions about what it takes to build monuments. Researchers had long debated whether Easter Island, known locally as Rapa Nui, was ruled by a centralized authority that controlled statue production. After all, coordinating the creation of over 1,000 multi-ton sculptures sounds like it would require serious organizational muscle.
The evidence points to something more interesting: a decentralized network of semi-autonomous communities that competed while cooperating, maintained distinct identities while sharing cultural practices, and built monuments without building a bureaucracy.
11,000 Drone Photos Reveal Hidden Patterns
Researchers from Binghamton University and the University of Arizona spent months flying drones over Rano Raraku, the volcanic crater that served as Easter Island’s primary statue factory. They captured 11,686 photographs and used software to stitch them into the first comprehensive 3D model of the quarry.
The level of detail was extraordinary. The model captured individual chisel marks, unfinished statues still attached to bedrock, and even the exact angles at which carvers approached the volcanic rock. This allowed researchers to see patterns that traditional ground surveys had missed.
The analysis revealed 426 moai in various stages of completion, 341 trenches cut to outline blocks for carving, and 133 empty spaces where statues had been successfully removed. More crucially, it showed 30 distinct workshop areas distributed across the crater, each separated by unworked bedrock or natural boundaries.
Each workshop contained the full toolkit of production features: trenches, partially carved statues, and the voids left by completed figures. This redundancy is telling. If production had been centrally organized, researchers would expect to see specialized areas, some for roughing out shapes and others for detailed work. Instead, each zone functioned as a complete, self-contained operation.
Competing Clans Used Different Carving Methods
The carvers didn’t even use standardized techniques. Researchers identified at least three distinct approaches to quarrying. The most common method, found in 143 cases, involved carving facial details first before outlining the head and body. In 120 instances, workers cut complete outlines of rectangular blocks before adding any decorative details. Five statues were carved sideways into near-vertical cliff faces, a completely different approach dictated by local geology.
The variation shows that different groups adapted to their specific locations in the quarry rather than following instructions from a central authority. Yet despite these technical differences, the statues themselves remained remarkably uniform in style. All featured the characteristic elongated heads, pronounced brows, and straight backs that define Rapa Nui’s aesthetic.
This combination of technical diversity and stylistic consistency points to information sharing between independent groups. Families or clans apparently communicated about artistic standards while maintaining autonomy over production methods.
The physical constraints of the workshops also reveal the scale of operations. Each workspace could accommodate perhaps four to six active carvers at a time, with another 10 to 20 people supporting them by making tools, preparing ropes, or providing food. These are kin-group numbers, not the massive labor forces that centralized projects would require.
Previous experiments have shown that teams of 15 to 50 people could “walk” even the largest moai across the island using ropes and coordinated rocking motions. Placing the cylindrical red stone “hats” atop finished statues required only about 15 people. The entire production chain, from quarrying to transport to final installation, operated at a scale consistent with extended family groups rather than island-wide mobilization.
How Competition Fueled Easter Island’s Monument Building
This decentralized pattern matches other recent findings about Easter Island’s social organization. Analysis of settlement patterns shows spatially discrete communities with their own ceremonial platforms and redundant architectural features. Studies of obsidian tools reveal highly localized material culture with limited sharing between communities. Road systems radiating from the quarry follow separate paths rather than forming an integrated network.
Historical accounts from the island’s first European visitors consistently described a society organized into competing mata, or clans, each with its own territory and chiefs. These clans maintained distinct identities and sometimes fought, but they also shared a common culture and language. The quarry evidence now extends this pattern to the island’s most labor-intensive and symbolically important activity.
Competition between clans could be fierce. While the spiritual and cultural significance of moai remained central, competition over status and resources likely fed into the statue building as groups sought to demonstrate their clan’s prestige through larger and more numerous monuments.
The research team notes that this decentralized system may have offered advantages beyond simply getting statues carved. Shared control over the quarry may have helped prevent any one group from monopolizing this resource or overusing the volcanic stone. Allowing multiple groups to develop their own techniques enabled flexible responses to geological challenges.
The finding has broader reach for understanding how societies build monumental architecture. The assumption that pyramids, cathedrals, or giant statues require kings, pharaohs, or centralized states turns out to be just that: an assumption. Rapa Nui demonstrates that communities can coordinate complex projects through horizontal social networks rather than vertical chains of command.
The study also provides a baseline for heritage management. The comprehensive 3D model documents the quarry’s current condition in unprecedented detail, creating a reference point for monitoring erosion, climate impacts, and tourism effects on this UNESCO World Heritage site. The publicly accessible model enables future researchers to test new hypotheses without conducting their own field surveys.
Easter Island’s statues have long symbolized both human ambition and environmental limits. The new findings add another layer. Monumentality doesn’t require monarchy, coordination can emerge from cooperation rather than coercion, and some of history’s most impressive achievements may have been bottom-up efforts rather than top-down projects.
Professional Santas across America describe their work in terms that sound less like a seasonal gig and more like something they were meant to do. They talk about being “called” to the role, experiencing life-changing moments when they first don the red suit, and feeling a profound sense of purpose that extends far beyond spreading holiday cheer.
A study published in the Academy of Management Journal reveals that professional Santa work operates as a calling rather than simply a job, with Santas reporting the role provides deep personal, moral, or social significance. Researchers interviewed 53 professional Santas and drew on nearly 1,300 survey responses collected across several studies to understand how workers navigate a calling when they don’t perfectly match society’s expectations for the role.
To protect their identities, researchers assigned each Santa a pseudonym based on constellations and galaxies, reflecting both the professional Santa tradition of being addressed as “Santa” and the magical, otherworldly nature of the work.
Santa Apus, a Black professional Santa, described the moment he knew this was his path. After leaving a voicemail for a major retailer, the hiring manager gushed about his voice and presence. But when she learned he was African American, her tone shifted completely. “Are you African American? Are you Black?” she asked. When he confirmed, she told him, “We don’t hire any Black Santas or Hispanic Santas. We aren’t ready for that.”
The rejection stung, but it didn’t extinguish his sense of purpose. He saw Santa work as part of his ministry, explaining: “I want to make this part of my ministry. To help bring people closer to Christ and to help us celebrate Christ’s birthday.”
The research identified three distinct groups of professional Santas based on how closely they match the culturally embedded Santa prototype: white, male, white-haired, real-bearded, overweight, extroverted, able-bodied, heterosexual, and Christian. Those who naturally fit this mold described feeling confident about stepping into the role. Those who partially matched it struggled with feelings of inadequacy. And those who deviated significantly sometimes faced rejection or pushback from parts of the Santa community.
The Identity Struggle Behind the Beard
Santa Hercules, who identifies as introverted, described the internal tension of sitting in the chair during a mall visit. Kids would wave and call out to him, but inside he wrestled with doubt: “You’re sitting in the chair, and you’re in there. But at the same time, inside I’m going, ‘What the heck, man? You’re just Hercules, man. What the heck?’”
Santas who partially matched the prototype developed creative backstories to explain their deviations. A skinny Santa told parents he was a “healthy Santa,” joking with children about why he looked different: “What, how do you think I would look after I have been around to 4,978,296,485 homes and eaten their cookies?” A hearing-impaired Santa would point to his cochlear implant and tell children: “Well, that’s a microphone to the North Pole. Bernard, the head elf, is listening to what you’re talking about, because he doesn’t want Santa to make any mistakes.”
Another Santa who had lost 192 pounds worried about no longer fitting the part but reframed his transformation: “I’m more fit as Santa instead of fitting the part.”
These explanations helped bridge the gap between their actual characteristics and what people expected.
The Physical and Emotional Transformation
Many Santas described extensive preparation to embody the role. They bleach their beards multiple times in the weeks before their first booking, invest in expensive custom suits, and practice their “ho, ho, ho” laugh until it becomes natural. One Santa worked so hard on his laugh that it became automatic. He explained how he asked another professional Santa about his authentic-sounding laugh: “He goes, ‘I had to teach myself to laugh like that, so that it’s natural. It’s not a, “Ho, ho, ho.” That’s how I sound when I laugh.‘ So I really worked at [it]. Now that’s how I laugh.”
For some, the transformation felt almost spiritual. Santa Phoenix described the experience: “I’m not putting something fake on. It is me and I have to really become that person, or let that person become me, and let it flow through me.”
Female Santas face unique challenges in a role defined by masculinity. Santa Lynx described the physical toll of appearing male: “I actually have either a binder or I have trans-tape… I try to make the girls go into my spine, which I think I still have a bruise from January, but anyway, you have to make sure…because Santa doesn’t have them double-Ds.” She spends up to 90 minutes applying her beard and makeup, compared to the five to 10 minutes it takes naturally bearded Santas to prepare.
Despite receiving hate mail and being denied entrance to Santa school because of her gender, she persists. She recalled being told: “You can’t be in the Santa school.” When she asked why, the response was: “Well, the men and I were talking, and we figured it’d be distracting to you [to learn in a group full of men].” The organizer suggested: “We can enroll you in the Mrs. Claus school or you can have your elf come and take our elf courses.” But Santa Lynx believes Santa embodies something more universal: “Santa can embody that acceptance and joy and love and understanding.”
Two Paths: Year-Round Santa or Seasonal Role
The researchers discovered that professional Santas split into two camps when the season ends. Some live as Santa 365 days a year, wearing red daily, driving cars with Santa-themed license plates, and carrying Santa coins to hand out to well-behaved children they encounter.
One Santa explained his year-round commitment: “That’s where my heart is. And, that’s why, eight years ago, I decided I’d live this way year-round, because that is who I am.” Another described the constant visibility: “You’re never off. You’re never not Santa. And you lose a little bit of your identity because you can’t let your hair down and be yourself and do all that because you don’t know who’s watching you.”
Santa Cygnus described how the role has merged with his identity: “And now my circle of friends know that I do Santa. So, you asked to start with, ‘Should I call you Cygnus, Santa Cygnus, whatever?’ I’m accustomed to being called Santa Cygnus now, because people just do it. It’s kind of become part of me.”
Other Santas carefully compartmentalize the role. They enjoy the work tremendously during the season but return to being themselves for most of the year. One explained his boundary: “Personally, I don’t want to be Santa 24/7, and I also just think that there’s so much about me that I want to live me. I don’t want to live a character.”
Another Santa described the seasonal nature of his work: “I can work [Santa jobs] four months out of the year…I’m more Santa when I’m at work [portraying Santa Claus]. When you put the suit on, that’s when you have to be that person.”
The study found that how much Santas identify with the role determines whether they practice continuous or episodic calling enactment. Those who strongly identify with being Santa integrate it into every aspect of their lives. Those with lower identification enjoy the seasonal nature of the work and use the off-season to honor other parts of themselves.
Breaking Traditional Santa Stereotypes
Santas who significantly deviate from the traditional prototype often reinterpret what Santa represents. They focus on higher-order values like kindness, generosity, and unconditional love rather than specific physical characteristics.
Santa Reticulum, who is gay, argued that people often view Santa through too narrow a lens: “I think you also exclude a lot of people if you are just being Santa for Christians.” He worries that treating Santa as strictly Christian leaves people out and prefers to see Santa as someone who accepts everyone without judgment.
Santa Lepus, who is Jewish, described how he views the role: “Santa is a guy who is truly accepting of the world and not judgmental.” He sees Santa as transcending religious boundaries and focuses on universal values of acceptance.
Atheist Santas in the study described staying away from religious aspects entirely. Santa Equuleus explained his perspective: “All of the things I like about Santa Claus are not religious. It’s this idea of being kind to people with no expectation of anything in return, except maybe cookies and milk, and even that is not a requirement. It’s just you’re kind to people for the sake of being kind.”
Despite facing rejection and having to downplay certain characteristics, these non-traditional Santas uniformly described living the role year-round. They found that once they connected with Santa’s core values, they could fully identify with the role even while looking different from what society expects.
Inside the Professional Santa Community
The Santa world includes training schools, professional associations, and local networks. Organizations like the Fraternal Order of Real Bearded Santas and the International Brotherhood of Real Bearded Santas set standards for membership, though some have begun relaxing requirements. The IBRBS now accepts fake-bearded Santas as associate members, though only real-bearded Santas can become full voting members.
These communities provide support, training, and job referrals. One Santa described the camaraderie: “We meet once a month for lunch and we all dress up as summertime Santas and we go out with our red shirts and our red tennis shoes and our full beards and we have a luncheon. We get together and we share stories, especially with the younger ones that are coming in, the newer Santas to give them insight about this.”
Several mentioned attending multiple Santa schools to improve their craft, with one Santa earning what he called a “Master’s degree at SantaClausology.”
However, the community also enforces boundaries about who counts as a legitimate Santa. Some Santas described colleagues who use scooters or wheelchairs as “bad Santas” who should retire. Female Santas reported receiving pushback from multiple directions within the community.
H5N1 bird flu has infected growing numbers of people worldwide in recent years, but this week saw something new: the first recorded human case of an H5N5 avian influenza virus. What is this virus and how concerned about it should we be?
What Happened?
In early November, a resident of Grays Harbor, a county on the south-west Pacific coast of Washington state about 100 miles from Seattle, became severely unwell with flu-like symptoms including high fever, respiratory distress and confusion.
They were admitted to hospital, and on November 14 officials confirmed that tests showed infection with an H5N5 avian influenza virus. The patient, an older adult with underlying conditions, was treated in hospital, but sadly they died on November 21.
This was the first reported human infection with an H5N5 influenza virus.
What is H5N5 Influenza Virus?
H5N5 influenza viruses are a type of avian influenza (bird flu) – an influenza A virus that infects birds.
Bird flu viruses are classified as either “high pathogenicity” or “low pathogenicity” based on the severity of symptoms they cause in poultry. (Their severity also varies in other bird species.) This H5N5 strain, like the widespread and much-reported-on H5N1 strain, is one of the high pathogenicity forms.
Where Did it Come From?
This hasn’t yet been formally confirmed. However, the patient kept a flock of backyard poultry that were exposed to wild birds, which suggests how they might have caught the virus.
H5N5 is found in wild birds around the world, and it is relatively common for it to pass from them into flocks of poultry. This is, however, the first time an H5N5 influenza virus has been found to go one step further and infect a human.
What Does the Name Mean? Is it Similar to H5N1?
Influenza A viruses are one of the major branches of the influenza virus family, and are divided into subtypes based on differences in the two proteins that form spikes on the surface of virus particles: haemagglutinin (HA) and neuraminidase (NA).
Both proteins are good targets for the immune system’s antibodies. The proteins rapidly mutate as the virus evolves to evade these antibodies, and the different forms that result are used to categorize influenza A viruses.
The bird flu viruses H5N1 and H5N5 both have HA proteins of the same H5 subtype (though recognizably distinct from each other), but have NA proteins of different subtypes. Just as humans can be infected by different influenza A virus subtypes during the same winter season (H1N1 and H3N2), genetic studies show us this H5N5 virus is distinct from the dominant H5N1 strain that is also circulating in birds worldwide.
Should We Be Worried About What Happens Next?
H5N5 is an ecological and agricultural threat. Although bird flu vaccines exist, at the moment, political and economic factors make it hard to use them in US poultry. Instead, the virus must be controlled by surveillance, housing poultry indoors, increasing farm biosecurity and, as a last resort, by mass culling of infected poultry.
This is challenging enough, but bird flu also demands our attention because the virus is a potential cause of new pandemics.
In the long run, this risk is very significant. However, it is worth remembering that, although influenza is better at changing its host species and creating pandemics than any other virus, that is still an incredibly hard thing for the virus to do.
The vast majority of “spillover” infections of bird flu into humans are one-off events. They can vary unpredictably in their effects. Most are quite mild (for example, causing conjunctivitis), but some can be very severe, as was the case in this first recorded case of H5N5. But after infecting one human, most avian influenza viruses go no further.
Scientists will watch for several warning signs that a virus may be adapting to humans, especially any hint of person-to-person spread. There is no sign that this has happened here.
The physics of coffee bubbles and volcanic eruptions are surprisingly similar. (Credit: andy0man on Shutterstock)
Your morning coffee may help scientists better predict future volcanic eruptions.
Like a dormant volcano, plenty of people just can’t get going in the morning without some coffee. Surprisingly, the physics of java and lava are actually quite similar, at least when it comes to bubbles.
Scientists have discovered that bubble formation in rising magma follows some of the same physics as bubbles in stirred coffee or shaken champagne. The finding expands the standard model of volcanic bubble formation that has guided volcanology since the 1950s and could improve eruption forecasting.
For the first time, researchers at the Université Clermont Auvergne and ETH Zurich have demonstrated that in gas-supersaturated magma, the physical act of flowing and swirling through underground channels can trigger bubble formation through mechanical stress—even without further pressure decrease. This shear-induced nucleation occurs when viscous liquids experience mechanical forces from movement itself.
The scientists demonstrate that it’s essentially the same physics at work. When magma rises through volcanic conduits, the liquid experiences intense shearing forces as it flows past rock walls and swirls around obstacles. Those mechanical forces provide enough energy to trigger bubble formation in magma already loaded with dissolved gases like water vapor and carbon dioxide, similar to how stirring creates bubbles in carbonated beverages.
When Rotation Creates Eruption
The discovery emerged from laboratory experiments using a heated polymer liquid saturated with carbon dioxide. Researchers placed the liquid on a rotating platform inside a rheometer, a device that precisely controls and measures viscous flow. As they gradually increased the rotation speed, bubbles suddenly appeared in the outer regions where shear stress was highest.
Multiple types of bubbles formed at different stress levels, with some appearing in the liquid itself and others forming on solid surfaces or near previously formed bubbles. The pattern was consistent: higher initial carbon dioxide supersaturation required lower shear stress to trigger nucleation.
What makes this finding notable is its departure from the conventional focus. Since the 1950s, volcanologists have primarily understood bubble formation through the lens of decreasing pressure. As magma rises toward the surface, reduced pressure causes dissolved gases to come out of solution, forming bubbles. Scientists have used this framework to interpret volcanic rock textures and estimate how fast magma ascended before erupting.
But the new experiments reveal that mechanical energy from flowing magma also contributes substantially to bubble formation. The researchers developed a mathematical model showing that shear stress and pressure changes contribute nearly equally to overcoming the energy barrier required for bubble nucleation in their experimental system.
Why Bubbles Matter for Volcanic Behavior
The practical consequences are substantial. Bubble formation and growth fundamentally control magma behavior during eruptions. More bubbles mean lower density, which affects how buoyantly magma rises. Bubbles also dramatically change magma viscosity and determine whether gases escape gradually or accumulate to explosive levels.
Current methods for estimating magma ascent rates rely on counting bubbles in volcanic rock samples. Scientists assume those bubbles formed only because of pressure decrease, then calculate how rapidly pressure must have dropped to produce the observed bubble numbers. But if shear stress also triggers bubble formation, those calculations could be significantly off.
The study, published in Science, report that bubble number density should reflect the combined effects of both shear stress and decompression. They also note that the contribution of shear could help explain why some explosive eruptions appear to record unrealistically high decompression rates when scientists estimate magma ascent speed by counting bubbles in erupted rock.
To understand where this shear-induced nucleation occurs in volcanic systems, the team developed a dimensionless parameter called the Poiseuille number, which relates shear stress to ambient pressure. Their calculations indicate that volcanic conduits easily exceed the threshold for shear-induced nucleation, but magma chambers likely don’t.
Explaining the Obsidian Puzzle
This finding may help explain a long-standing puzzle in volcanology. Some highly viscous, gas-rich magmas somehow erupt gently as obsidian flows instead of exploding catastrophically. Efficient bubble formation from shear in the lower conduit, followed by bubble growth and coalescence, could allow these volatile-rich magmas to outgas before reaching explosive fragmentation depths.
The research also questions the role of tiny crystals called nanolites in bubble formation. Recent studies have proposed that these iron oxide crystals, smaller than one micrometer, provide nucleation sites for bubbles. But if shear alone can trigger widespread bubble formation in conduits, nanolites may be less critical than previously thought, or they may form as a consequence of bubbles rather than causing them.
The experimental approach combined multiple techniques. After saturating the polymer liquid with carbon dioxide under pressure, researchers slowly released the pressure without triggering nucleation, then immediately transferred the supersaturated liquid to the rheometer. Video cameras captured bubble formation as shear increased, allowing precise measurements of the stress required for nucleation at different supersaturation levels.
Computer simulations using molecular dynamics confirmed the experimental observations. When researchers modeled a mixture of particles representing liquid and dissolved gas under shear, small gas-rich regions percolated and coalesced to form irregularly shaped nuclei surrounded by an envelope of volatile-rich liquid.
The team also conducted complementary experiments showing that other forms of mechanical energy trigger nucleation. Suddenly compressing the liquid or abruptly stopping the rotation both caused bubbles to form on the metal surface, demonstrating that various mechanical disturbances can overcome the energy barrier to nucleation.
While the experiments used a polymer-carbon dioxide system rather than actual magma, the researchers carefully scaled their results to volcanic conditions. The supersaturation pressures in their experiments correspond to realistic values for magmas at depths of two to ten kilometers.
Looking beyond volcanoes, shear-induced nucleation likely influences other natural and industrial processes. The phenomenon is known to affect foam formation in synthetic materials. It could also play roles in earthquake-triggered bubble formation, planetary outgassing, and thermal volatile release in hydrothermal systems.
Better models of how magma moves and bubbles form could translate to more accurate forecasts of whether a restless volcano will erupt explosively or effusively. Just as understanding that shaking creates bubbles in soda bottles helps predict whether opening the cap will cause a gentle hiss or a sticky explosion, recognizing that flowing magma creates its own bubbles through mechanical stress could help scientists better anticipate volcanic behavior.
Screen time shouldn’t be an all-the-time activity for kids. (Credit: Ana Portal on Shutterstock)
Children with more screen time showed cortical thinning in brain regions involved in memory, planning, and impulse control.
What happens inside a child’s brain after thousands of hours in front of screens?
A study of nearly 10,000 American kids offers some answers. Researchers tracking children from ages 9-10 through 11-12 found that heavier screen time was associated with measurable differences in brain structure. More specifically, reduced thickness in areas controlling attention, memory, and impulse control.
MRI scans revealed the differences weren’t random. They showed up in the same brain regions that function differently in children with ADHD. Screen time also correlated with smaller volume in the brain’s reward center and less gray matter overall, and these structural differences aligned with increases in ADHD symptoms over the two-year period.
Researchers from the University of Fukui in Japan analyzed data from the Adolescent Brain Cognitive Development study. Their work comes as children spend more hours than ever in front of screens, particularly since the COVID-19 pandemic accelerated digital device use.
While previous research had hinted at links between screen time and brain structure, most studies were snapshots rather than tracking actual developmental changes. This investigation, published in Translational Psychiatry, followed real brain growth patterns alongside behavioral shifts, giving researchers a clearer picture of how screen use lines up with changes in the developing brain over time.
Measuring Brain Changes From Screen Time in Nearly 8,000 Children
The research team analyzed data from 10,116 children at baseline and 7,880 at a two-year follow-up. Parents reported ADHD symptoms using the Child Behavior Checklist, while screen time calculations included all device use—video games, television, smartphones—averaged across weekdays and weekends.
Brain measurements came from high-resolution MRI scans processed using specialized software that maps cortical regions and quantifies both volume and thickness down to millimeters. Researchers controlled for numerous factors including age, sex, race, household income, parental education, sleep duration, and physical activity levels.
The sample size and longitudinal design set this work apart. Most earlier investigations examined smaller groups or looked at a single moment rather than following kids as their brains actually developed.
Cortical Thinning in Attention and Memory Centers
After two years, children with higher baseline screen time showed measurably thinner cortex in three specific regions. The right temporal pole, involved in social cognition and language, showed reduced thickness associated with screen exposure. So did the left superior frontal gyrus, which handles working memory and attention control, and the left rostral middle frontal gyrus, tied to cognitive flexibility and decision-making.
These aren’t arbitrary brain areas. They’re precisely the regions that support the kinds of cognitive functions that weaken in ADHD—sustained attention, impulse control, working memory, and planning ahead.
At the study’s start, longer screen time had already linked to smaller volume in the right putamen. This almond-sized structure sits deep in the brain and plays a key role in reward processing. When it functions differently, children may develop preferences for immediate gratification over delayed rewards—a hallmark of impulsive behavior.
Screen-based activities deliver instant rewards and rapid stimulation. Gaming achievements, video auto-play, and endless scrolling all provide quick hits of satisfaction. Some researchers think that constant instant rewards could train young brains to chase quick payoffs, which might help explain why heavy screen users sometimes look more impulsive. This study did not test that idea directly.
More ADHD-Like Symptoms
Perhaps the most revealing finding involved total cortical volume—the overall amount of gray matter in the brain’s outer layer. Children with more screen time had smaller cortical volume, and this difference partially explained why they also showed more ADHD symptoms.
The pattern offers a possible chain: screen exposure relates to smaller cortical development, which then correlates with attention and behavioral problems. Children with ADHD have been shown in other research to exhibit delayed cortical maturation compared to peers without the disorder.
If screen time does interfere with typical cortical growth, it could nudge some children’s brain development off its usual track. The study cannot confirm that, but it raises the possibility. The cortex is where the brain’s executive functions live—the mental processes that help kids focus, plan, and control impulses. Changes to its development could affect behavior and attention.
Interestingly, the specific regions that thinned over two years didn’t statistically explain the screen time-ADHD relationship. Researchers noted this might mean that functional brain networks or microstructural properties, rather than just size measurements, play a role in longer-term impacts.
Beyond brain changes, the study found behavioral effects. Children with higher screen time at baseline showed increased ADHD symptoms two years later, even after accounting for their starting symptom levels.
The effect remained statistically significant but modest in size. This raises questions about whether individual children should worry, versus whether the finding matters for population-level health guidance. Small statistical associations don’t always translate to noticeable real-world impacts on individual kids.
The connection between screens and ADHD-like behaviors has sparked debate for years. Some studies find only weak links, while others report stronger associations. This research indicates the relationship persists and potentially intensifies over developmental time, though the effect was small enough that experts caution against alarm.
One complication: kids with existing attention difficulties might naturally gravitate toward screens, rather than screens causing the problems. Disentangling cause and effect remains difficult without experimental studies, which would be unethical to conduct by deliberately exposing children to excess screen time.
What the Research Means for Parents
The study design prevents concluding definitively that screens cause brain differences or ADHD symptoms. While screen time preceded both brain changes and symptom increases, other unmeasured factors could be driving the associations.
Screen time was self-reported, which can introduce inaccuracy. The study also didn’t account for what kids were watching or how they used devices. Watching educational programming differs substantially from playing fast-paced video games. Screen size, lighting conditions, and whether screen time replaced other activities all matter but weren’t captured.
Effect sizes throughout the study were small enough that clinical significance remains uncertain for any individual child. A statistically detectable difference in cortical thickness doesn’t necessarily mean a child will struggle academically or socially.
However, the findings do offer evidence that screen exposure during a critical developmental window may correlate with measurable differences in brain structure. Adolescence is when both biological and environmental factors shape long-term cognitive patterns. The brain undergoes massive rewiring during this period, pruning unnecessary connections while strengthening others based on experience.
Researchers recommend future investigations should examine causal mechanisms more directly and include measures of functional brain connectivity—how different regions communicate—rather than just structural size. Understanding whether certain types of screen content or usage patterns are more problematic than others would also help parents make informed decisions.
The structural differences were real and measurable, even if small. They showed up in brain areas involved in attention and self-control. Whether those differences prove meaningful for individual children’s lives remains an open question that will require more research to answer.
Europe, much like the rest of the world, is getting hotter and hotter on average. (Credit: Shahbaz Hussain Shah on Shutterstock)
If Europe sees another heat wave like the summer of 2003, over 30,000 people could die in the span of a single week. That’s the sobering conclusion drawn from a research project highlighting just how much hotter average temperatures have become since then.
When August 2003’s heat wave baked across Europe, it killed an estimated 70,000 people over the course of the entire summer. Now, research warns that if similar weather patterns return during the world’s recent temperature spike of 1.5°C above pre-industrial levels, a single week could claim 17,800 lives across the continent. At 3°C of warming, that number jumps to 32,000 deaths in seven days, rivaling the deadliest weeks of the COVID-19 pandemic.
Scientists at Stanford University used machine learning to reconstruct five historic European heat waves under different levels of global warming, then calculated the death toll using mortality data from 924 regions across Europe. Their findings, published in Nature Climate Change, show that mass casualty events from extreme heat are not only possible at temperatures the world is approaching but remain plausible at near-future temperatures despite current adaptations to heat.
Historic Heat Waves Get Deadlier With Each Degree of Warming
The research team, led by Christopher Callahan, took weather patterns from five major European heat events between 1994 and 2023 and asked: How deadly would these same meteorological conditions be if they occurred during hotter years?
Using neural networks trained on climate models, the researchers predicted temperatures that would result from historical atmospheric pressure patterns and soil moisture levels at various global temperature increases. They combined these projections with empirical data linking temperature to mortality rates across hundreds of European districts from 2015 to 2019.
August 2003 emerged as the deadliest scenario. At 2°C of global warming, those weather conditions would generate roughly 24,700 excess deaths in one week. At 4°C—a level still possible under gradual decarbonization scenarios—the toll reaches 45,100 deaths.
Other events also showed high death tolls. July 1994 weather patterns, which produced only moderate temperature increases when they actually occurred, would kill around 25,000 people in a week at 3°C of warming. July 2006 conditions would claim 25,600 lives, while the more recent June 2019 and August 2023 patterns would each produce between 18,000 and 21,000 weekly deaths at the same temperature threshold.
Current Adaptation Measures Barely Make a Dent
The most concerning finding involves adaptation. European countries undertook heat action measures following previous extreme events, and the study’s mortality data from 2015-2019 captures these more recent adaptations. The researchers modeled additional future adaptation by assuming regions would continue adjusting as their climates warm.
When they incorporated this assumption, mortality dropped by only 10% on average. For the 2003-type event at 3°C, deaths would decline from 32,000 to about 28,800.
“While mitigating further global warming can reduce heat mortality, mass mortality events remain plausible at near-future temperatures despite current adaptations to heat,”study authors write.
The relationship between temperature and mortality shows why adaptation struggles. Warmer regions have higher temperature thresholds before mortality increases, suggesting successful adaptation. However, once temperatures exceed those thresholds, deaths rise even more steeply than in cooler regions. Extreme heat still kills even where people have adapted to generally hotter conditions.
Heat Events Could Overwhelm Hospitals Like COVID Did
To put these numbers in context, the researchers compared their projections to weekly COVID-19 deaths across the same European regions. During the pandemic’s worst 10% of weeks, between 27,900 and 34,100 confirmed COVID deaths occurred across Europe. A 2003-style heat wave at 3°C would land squarely in that range. At 4°C, the 1994, 2003, and 2006 weather patterns would each exceed even the single deadliest week of COVID-19 in Europe.
The comparison extends beyond raw numbers. Like COVID-19 surges, these heat events would strain hospital capacity and emergency services, but they would arrive with little warning and peak within days rather than weeks. Healthcare systems prepare for average heat impacts but may lack surge capacity for extreme events that compress thousands of deaths into a few days.
Heat mortality doesn’t distribute evenly. Under 1994-like conditions, Germany, Poland, and Eastern Europe see the highest death rates. Under 2023 conditions, Spain, Italy, and the Balkans suffer most. The spatial variation reflects both where temperatures climb highest and regional differences in vulnerability.
Climate Change Already Accounts for Most Heat Deaths
Comparing each event to a baseline without global warming or heat waves reveals climate change’s contribution. For the 2003-type event at 3°C, anthropogenic warming accounts for about 23,000 of the 32,000 peak weekly deaths, or roughly 72%. Without human-caused climate change, the same weather pattern would still produce 9,000 excess deaths, but global warming more than triples the toll.
This attribution holds across the other events as well. At higher temperature increases, 70-80% of heat deaths trace directly to climate change intensifying what the weather pattern would have produced naturally.
The work differs from typical climate impact studies. Rather than projecting how often certain conditions might occur, it asks: What happens if weather patterns that have already produced heat waves return when the world is hotter? This “storyline” approach acknowledges that the short observational record makes it difficult to assess probabilities of the rarest events.
By learning from climate models how atmospheric patterns translate into surface temperatures at different global warming levels, the machine learning system can project realistic scenarios without requiring those exact conditions to appear in lengthy model runs. Each counterfactual event uses meteorological conditions from reanalysis data, ensuring physical consistency.
The mortality calculations use a regression approach that isolates the causal effect of temperature while controlling for seasonal patterns and trends. Because the analysis uses mortality data from 2015-2019, it captures recent adaptation, including changes made after 2003.
The study acknowledges several limitations. It uses all-age mortality rather than age-stratified rates, though the researchers found nearly identical exposure-response functions for people over 65, who dominate heat deaths. Future population aging could increase vulnerability by 1-3%, a small effect relative to the temperature changes examined.
The projections also depend on whether historical weather patterns recur. If those atmospheric configurations never repeat, these events won’t happen. However, the short observational record means even more extreme patterns likely exist that haven’t yet been witnessed.
Why pay a human to take a poll when a bot comes 97% cheaper – and will answer however you want. (Credit: Andrey_Popov on Shutterstock)
Dartmouth Study Reveals How Easily Artificial Intelligence Can Manipulate Online Polls
A single survey completion costs about five cents when powered by artificial intelligence, according to an eye-opening study from Dartmouth College. The typical payout to a real human, meanwhile, is around $1.50. That 97% profit margin has created a gold rush for fraudsters, and researcher Sean J. Westwood warns it poses a potential existential threat to the infrastructure of online research.
Westwood has shown that AI language models can produce survey responses so convincing they pass standard quality checks designed to weed out bots and inattentive humans. The consequences stretch far beyond academic integrity, reaching into public health decisions, political campaigns, and policy-making that relies on understanding what people actually think.
AI Bots Pass Every Standard Quality Check
Westwood’s autonomous system can complete entire surveys while maintaining a coherent demographic persona, remembering previous answers, and calibrating writing style to match an assigned education level. Across 6,000 trials of common attention checks, including instruction-following tasks, logic puzzles, and questions written to detect non-human actors, the AI passed 99.8% of them.
That near-perfect success rate turns survey fraud from a labor-intensive cottage industry into a scalable, automated business model. With open-weight models, the marginal operating cost approaches zero. Even paid APIs can price out to pennies per completion.
Research Defender estimates that 31% of raw survey responses contain some form of fraud, not all of it AI. A 2024 sample found that more than one third of respondents admitted using AI to help answer open-ended survey questions, though this represents human-assisted use rather than the fully autonomous bots Westwood created.
How Westwood’s AI Mimics Human Responses
The complexity of these synthetic respondents makes detection difficult using current methods. When asked directly whether it was human or artificial, Westwood’s AI chose the human response every time. Seven out of nine other models tested did the same.
The system does more than pass basic checks. It shows human-like reasoning. Housing costs in the AI-generated data scaled realistically with income and location. Time reported at children’s sporting events peaked for middle-aged personas and dropped to zero for elderly respondents whose children would be adults.
Psychology scales did not trip it up. The AI handled reverse-scored items, which are questions worded in the opposite direction to catch inattentive respondents, and it produced consistent responses across trait measures. It did show one limitation when asked to endorse socially undesirable, chaos-seeking items, which the model declined. That refusal can still look plausible for some profiles.
When presented with questions designed to catch superhuman abilities, such as solving complex calculus or writing code in obscure languages, the AI strategically declined 97.7% of the time. It imitated human limits to avoid detection while still looking like a genuine, if sometimes uncooperative, respondent.
The Economics of Survey Fraud at Scale
Westwood demonstrated that synthetic respondents can be instructed to bias results in specific directions while maintaining cover. A single instructional sentence shifted answers to a question about America’s primary military adversary, moving mentions of China from 86.3% to 11.7% in his experiments.
For actors motivated by ideology rather than profit, the return on investment is even more attractive. In Westwood’s analysis of seven major national polls from the 2024 presidential election, injecting just 10 to 52 synthetic respondents could flip which candidate appears to be leading. Pushing results outside the margin of error required only 55 to 97 fraudulent responses in those polls, which averaged about 1,600 participants each.
Westwood’s modeling also showed that contaminating half the surveys in a ten-poll average, the kind media outlets use to smooth out individual poll quirks, required fewer than 30 biased responses per targeted survey. That modest investment could erase a candidate’s lead in the polling average and create a false story about momentum.
Why Current Survey Panels Can’t Stop the Threat
Current survey panels vary in their security practices, but many use river sampling, which means open enrollment with low barriers to join. This maximizes participation and speed but makes infiltration easier.
Panel providers such as CloudResearch and Prolific deploy batteries of quality checks, yet Westwood’s AI cleared them. Questions about impossible biographies, such as visiting the moon or being elected president, caused no errors. The AI recorded zero incorrect answers on these traps across trials.
A deeper risk comes from what researchers call demand effects, where study participants alter their behavior to match what they think investigators want to find. When the AI encountered common experimental designs, it often inferred the researcher’s hypothesis and then biased its answers to confirm that hypothesis while maintaining realistic variation. That pattern can corrupt findings from within because it tells investigators exactly what they expect to see.
The breadth of vulnerable research is wide. Public health relies on self-reports of symptoms and behaviors. Economics depends on consumer surveys. Political science tracks attitudes and voting intentions. Psychology measures personality and mental health. Marketing tests product preferences. All of these fields have adopted online surveys for speed and cost. All now face the same potential vulnerability.
Unlike older forms of survey fraud that added random noise, AI-generated responses can introduce targeted bias. They can inflate treatment effects, confirm researcher expectations, or push opinion measures in chosen directions. Even careful teams may miss the problem because data that “fits” a hypothesis can look especially credible.
Westwood tested nine different large language models, including both commercial and open-weight systems. The ability to generate convincing survey responses while hiding non-human identity appears to be a general property of modern AI, not a quirk of one platform.
Westwood argues that an arms race of trick questions is the wrong fix. More clever checks may filter out legitimate human respondents, especially people with less formal education or non-native English speakers, which creates a new kind of bias.
Instead, the field needs changes in how panels operate. Researchers should ask for transparency on identity verification, limits on how many surveys a panelist can complete, quality-check histories, and location verification. Panels that cannot provide this information should be treated as high risk.
The community may also need to rethink its reliance on low-barrier online convenience samples. Address-based sampling, deeply vetted longitudinal panels, and face-to-face interviews cost more and take longer, yet they are more resistant to automated fraud. Some studies may require accepting those trade-offs.
The financial incentives behind this threat are not going away. As long as surveys pay human-level compensation for work that AI can complete for pennies, the profit motive will attract bad actors.
What is at stake is more than academic integrity. Public opinion polling informs policy choices, shapes campaign strategy, and supports democratic accountability by measuring what citizens want. If that measurement system is corrupted by synthetic responses that push specific narratives, a tool meant to understand the public becomes a tool that manipulates it.
Westwood’s findings show the capability exists today and the economic incentives are in place. While the tools to create such fraud are readily available and affordable, the extent to which autonomous bot attacks have already occurred at scale remains unknown. The question Westwood poses is whether research methods can adapt quickly enough to address this emerging threat before it becomes widespread.
In the ever-evolving world of beauty trends, few have sparked as much debate – and discomfort – as “menstrual masking.” This is the practice of applying menstrual blood to the skin, usually the face, as a form of DIY skincare.
Popularized on social media, hashtags such as #periodfacemask have amassed billions of views. In most videos, users apply menstrual blood for a few minutes before rinsing it off. There’s no clear agreement on how much blood to use or how long to leave it on. Some call the practice healing or empowering, describing it as a spiritual ritual that connects them to their bodies and ancestral femininity. But what does the science say?
Advocates of menstrual masking often argue that period blood contains stem cells, cytokines and proteins that could rejuvenate the skin. There is currently no clinical evidence to support using menstrual blood as a topical skincare treatment. However, its biological composition has shown potential in medical research.
A study found that plasma derived from menstrual fluid could significantly enhance wound healing. In laboratory tests, wounds treated with menstrual plasma showed 100% repair within 24 hours compared with 40% using regular blood plasma. This remarkable regeneration is thought to be linked to the unique proteins and bioactive molecules in menstrual fluid: the same substances that allow the uterus to rebuild itself every month.
Researchers are now exploring whether synthetic menstrual fluid could help treat chronic wounds.
Stem cell research has also turned attention to menstrual blood–derived stem cells, or MenSCs. These cells grow easily and can develop into many different cell types. Studies show that mesenchymal stem cells (MSCs) from various sources can help heal skin by boosting collagen, reducing wrinkles and releasing growth factors that repair damage caused by burns, UV exposure or wounds. Because they are versatile and appear safe, MenSCs are seen as a promising option for developing medical treatments to regenerate skin and slow photoaging: the premature aging caused by long-term sun exposure.
Menstrual Masking Not The Same As A ‘Vampire Facial’
Some menstrual masking advocates liken the practice to the so-called “vampire facial”: a cosmetic procedure popularised by celebrities such as Kim Kardashian. Vampire facials use platelet-rich plasma (PRP) extracted from a patient’s own blood and injected into the face.
But experts caution against comparing PRP with menstrual blood. Menstrual fluid is a complex mixture of blood, sloughed-off endometrial tissue (the uterine lining), vaginal secretions, hormones and proteins. As it passes through the vaginal canal, it can pick up bacteria and fungi, including Staphylococcus aureus, a common microbe that normally lives on the skin but can cause infections if it enters cuts or pores. There’s also a risk that sexually transmitted infections (STIs) could be transferred to the skin.
PRP, by contrast, is prepared under sterile conditions. During PRP treatment, a small amount of blood is drawn and spun in a centrifuge to separate out the platelet-rich layer, which is then injected into the skin using fine needles. Some clinicians also add filler for faster cosmetic results. The procedure can cost thousands; unlike menstrual masking, which is free and easily accessible.
‘Body-Based’ Beauty
Menstrual masking isn’t the only unconventional beauty practice involving bodily fluids. “Urine therapy,” the application of urine to the skin, has roots in Ayurvedic medicine and was once believed to detoxify the body and cure ailments. Some modern advocates even claim benefits for acne or eczema, although these claims lack scientific support.
While urine does contain urea – a compound used in some moisturisers – the urea found in urine is far less concentrated and not the same as the purified, synthetic form used in skincare products. The idea that raw urine or menstrual blood could safely replace clinical-grade cosmetic ingredients is not supported by dermatological evidence.
Menstrual masking sits at the intersection of body positivity, cultural ritual and pseudoscience. For some, it’s a celebration of the menstrual cycle and a rejection of stigma. For others, it’s an unproven and potentially risky beauty trend.
The biological richness of menstrual blood is undeniable, but its safe and effective use belongs in controlled medical research – not in DIY skincare routines. As with many viral health trends, it’s vital to distinguish between symbolism and science. Menstrual masking may feel empowering, but from a dermatological perspective, it’s a practice best left to personal belief rather than the bathroom mirror.
This breakthrough sets the stage for more ambitious clinical trials moving forward. (Credit: Inside Creative House on Shutterstock)
A genetically modified pig kidney has survived and functioned in a human recipient for 61 days, setting a record for this type of procedure and offering new hope to the nearly one million Americans living with end-stage kidney disease. The study, conducted at NYU Langone Health, showed that a pig organ with just a single genetic modification could sustain life-supporting kidney functions for over two months, even bouncing back from a serious rejection crisis.
Only about 3% of patients with end-stage kidney disease receive transplants each year. Many die before receiving an organ. Pig kidneys, capable of being produced on demand, represent one potential path forward.
Scientists transplanted a kidney from a 199-day-old female pig into a 57-year-old brain-dead man in July 2023. The pig had been genetically modified to remove alpha-Gal, a sugar molecule that humans lost millions of years ago during evolution. The human immune system now attacks alpha-Gal as foreign. Rather than using pigs with dozens of genetic changes, researchers opted for this simpler approach with just one gene edit.
A Month Of Success After Pig Kidney Transplant
Within hours of transplantation, the pig kidney began producing urine and filtering waste from the blood. A blood test measuring creatinine showed the organ was working very well. Creatinine is a waste product that builds up when kidneys fail. The recipient’s creatinine level dropped from 1.0 mg/dL before surgery to just 0.32 mg/dL within 12 days. For comparison, normal human kidneys maintain creatinine between 1.0 and 1.5 mg/dL.
For nearly a month, the transplanted kidney performed better than many human donor kidneys. It filtered blood at a rate of about 125 mL per minute per 1.73 m² of body surface.
Then on day 33, trouble struck. The kidney experienced antibody-mediated rejection, where the immune system mounts an attack against the foreign organ. The recipient’s kidney function declined as antibodies surged and immune cells swarmed into the organ. Microscope examination of tissue samples revealed inflammation in the tiny blood vessels and filtering structures, along with deposits of antibodies and immune proteins coating the kidney’s inner surfaces.
Doctors responded with treatments already approved for human organ transplants. They used plasma exchange, a process similar to dialysis that removes harmful antibodies from the blood. They added drugs that suppress the immune system and block complement, a component of immune defense that amplifies attacks on foreign tissue. The combination worked, and kidney function climbed back to normal levels. By day 60, the organ was filtering at well over 100 mL per minute per 1.73 m², similar to a healthy human kidney.
Tissue analysis on day 49 showed rejection had returned with immune cells now attacking blood vessel walls. Researchers added another round of plasma exchange and a powerful drug called rabbit anti-thymocyte globulin that eliminates T cells, a type of white blood cell that coordinates immune attacks. Once again, the kidney recovered. When removed at the planned end of the 61-day study, tissue samples showed no signs of rejection, no antibody deposits, and no damage to the filtering structures essential for kidney function.
T Cells Present Before Surgery Multiplied and Attacked Transplant
Researchers used sophisticated genetic sequencing to track immune cells throughout the study. They uncovered a troubling pattern: T cells capable of recognizing pig tissue as foreign were already present in the recipient’s blood before surgery. After transplantation, these cells multiplied explosively.
Before surgery, the five fastest-growing types of these pig-recognizing T cells made up just 3% of all circulating T cells. By day 49, they accounted for more than 30%. One particular T cell type ballooned from less than 0.1% to over 20% of the total population. These expanding cells transformed into activated killers, turning on genes that produce toxic proteins designed to punch holes in target cells.
When researchers examined kidney tissue samples taken during rejection, they found these activated T cells had infiltrated the organ alongside natural killer cells and other immune cells that amplify attacks. The finding suggests that simply suppressing the immune system after transplant may not be enough. Strategies to eliminate or control these pre-existing pig-reactive immune cells before surgery might be necessary.
Antibodies driving the rejection targeted an unknown pig protein found on blood vessel cells. Strangely, these antibodies attacked vessels from both minimally modified pigs and pigs with 10 genetic changes designed to eliminate foreign molecules that previous research had identified as problematic. The discovery means scientists still don’t know which pig molecules need to be modified or masked to prevent this type of immune attack.
Most Kidney Functions Worked, Some Didn’t
Beyond just surviving, the pig kidney needed to perform the complex chemical balancing act that kidneys carry out every moment. Researchers monitored whether the organ could respond to human hormones, regulate electrolytes, filter drugs, and handle the intricate calcium-phosphate system that keeps bones healthy. Most functions worked well, though not perfectly.
The pig kidney responded correctly to vasopressin, a human hormone that signals kidneys to conserve water. This was not guaranteed to work because pigs produce a slightly different version of the hormone. When researchers briefly stopped the vasopressin being used to manage the brain-dead recipient’s water balance issues, urine output shot up to over 1,000 mL per hour, sodium levels climbed, and urine became watery. Restarting the hormone quickly reversed everything, proving cross-species hormone signaling could work.
Blood levels of sodium, potassium, and magnesium stayed relatively stable throughout the study with only occasional need for supplements. The kidney filtered and cleared drugs appropriately, including the antibiotic vancomycin. Calcium and phosphate levels were managed, though the kidney held onto more phosphate than expected, requiring medications to bind excess phosphate in the digestive tract.
One hormonal system didn’t work as expected. The kidney’s part of the renin-angiotensin-aldosterone system, which regulates blood pressure and salt balance, appeared nonfunctional. No pig renin enzyme could be detected in the recipient’s blood. Previous lab studies had shown pig renin doesn’t work well on human proteins, so this mismatch was somewhat expected. Yet blood pressure remained normal for over two months with only standard care, suggesting the body found workarounds.
The pig kidney also didn’t produce erythropoietin, a hormone that tells bone marrow to make red blood cells. Blood transfusions were needed to keep red cell counts adequate, though lab tests showed the bone marrow was trying to compensate by producing immature red cells at elevated rates.
Despite these limitations, the kidney’s core filtering function remained intact. No excess protein leaked into the urine throughout the study, and microscope images showed the delicate cellular structures responsible for filtering blood stayed healthy even after two rejection episodes.
No Dangerous Pig Viruses In Patient
A major safety question about using pig organs has been whether viruses that naturally infect pigs might jump to humans and potentially spread to others. Researchers tested extensively for known pig viruses throughout the 61 days, examining blood, the transplanted kidney, and various tissues.
Porcine endogenous retroviruses, which are permanently embedded in pig DNA, showed up in some blood samples from the recipient. However, these viruses appeared only when pig mitochondrial DNA was also present, pointing to the presence of a few circulating pig cells rather than actual infection of human cells. No pig viruses were replicating in human tissues.
The heavy immunosuppression needed to prevent organ rejection did allow some human viruses to flourish. The recipient developed norovirus and showed rising antibody levels against Epstein-Barr virus. Tissue from the removed kidney showed signs of post-transplant lymphoproliferative disorder, an abnormal immune cell proliferation that sometimes happens when transplant patients take strong immunosuppressive drugs.
Hope For Solving The Organ Shortage
Researchers included pig thymus tissue attached to the kidney as an experimental approach. In animal studies, donor thymus tissue can train the recipient’s immune system to tolerate foreign organs. Human immune cells were developing in the pig thymus when examined at study’s end, and lab tests showed recipient T cells responded less vigorously to pig cells by day 49 compared to day 28. But the explosive expansion of pre-existing pig-reactive T cells suggests more aggressive strategies will be needed to control immune responses that exist before surgery.
The success with minimal genetic modification defies earlier expectations. Primate studies had suggested more extensive changes might be necessary. The pig used here, with just one gene knocked out, lacked human genes for proteins thought important for preventing rejection. Yet it performed well for two months. Single-gene-edit pigs can be bred normally rather than cloned individually, making them more practical for producing organs at scale.
Brain-dead recipients offer both advantages and limitations as test subjects. Unlike primate studies, researchers can use the full range of treatments available for humans, including plasma exchange and sophisticated molecular monitoring difficult to perform in animals. Brain-dead individuals maintain working immune systems and normal physiology. But the model can’t show what would happen in living patients with kidney disease, who face different immune challenges and medical complications.
Timing breaths between strikes helps woodpeckers generate maximum pecking power. (Credit: LABETAA Andre on Shutterstock)
Woodpeckers have adopted the same breathing technique used by professional tennis players. Both exhale through the moment of impact. Research reveals these birds forcefully breathe out with every strike of their bill against wood, using a respiratory pattern that likely stabilizes their core during forceful pecking.
Scientists at Brown University discovered that downy woodpeckers maintain airflow while drilling. They coordinate exhalation with each peck in a pattern remarkably similar to the grunting athletes use when serving a tennis ball or lifting heavy weights. This respiratory strategy increases air pressure inside the body, stiffening the torso and potentially creating a more stable platform for forceful strikes.
The finding challenges assumptions about how woodpeckers manage hammering trees. Rather than bracing against impact by closing their airways, these birds keep air flowing while contracting their abdominal muscles to spike internal pressure at precisely the right moment.
The Science Behind the Woodpecker Grunt
Nicholas Antonson, lead author of the study published in the Journal of Experimental Biology, used electromyography to measure muscle activity in eight downy woodpeckers as they drilled wood. His team recorded changes in air-sac pressure and breathing patterns, syncing these measurements with high-speed video to capture the exact timing of each behavior.
Abdominal muscles contracted in two distinct bursts during each peck. The first occurred as the bird swung its head forward toward the wood. The second happened at the moment of contact, coordinating with a rise in expiratory pressure around impact, with a brief dip exactly at contact.
This pattern mirrors what happens when tennis players grunt during a serve. They forcefully exhale while contracting their core muscles, and studies show this technique measurably increases ball velocity without raising oxygen costs. The mechanism stiffens the spine and torso to provide a more stable base for generating power.
Woodpeckers appear to use a similar principle. By exhaling forcefully at impact while pressurizing their air sacs and contracting abdominal muscles, they likely create rigidity throughout the body precisely when the bill strikes wood.
To confirm that woodpeckers maintained airflow during drilling, researchers inserted tiny thermistor probes into the trachea of two birds. These probes detected continuous airflow during drilling, proving the airways remained open during pecking. This contrasts sharply with behaviors like defecation, where woodpeckers close their airways to pressurize the thoracic cavity, similar to the Valsalva maneuver used during heavy lifting.
Mini-Breaths at Lightning Speed
The breathing strategy persisted even during rapid tapping, where birds struck wood at rates reaching up to 13 times per second. Remarkably, individuals synchronized respiration with each strike in a perfect one-to-one ratio, taking miniature breaths between successive pecks. These inspirations could be as brief as 40 milliseconds, meaning respiratory rates increased from roughly three breaths per second at rest to approximately nine breaths per second during tapping.
The mini-breath pattern closely resembles respiratory strategies in songbirds. Many bird species take quick inspirations between vocal phrases during songs, allowing them to maintain long singing bouts. The discovery that woodpeckers use similar mini-breaths during non-vocal behavior suggests this respiratory adaptation may have broader evolutionary origins than previously recognized.
A Whole-Body Hammer
Beyond breathing, the study revealed that drilling engages muscles throughout the entire woodpecker body. Eight different muscle groups spanning the head, neck, abdomen, hips and tail activated in precisely timed sequences during each peck. Neck muscles contracted to create a stiffened lever arm, hip muscles powered forward movement, and tail muscles braced against the tree.
This whole-body coordination transforms the bird into a biological hammer. The head and bill function as the hammer head, while the stiffened neck serves as the handle. Hip muscles provide the swing force, and the tail anchors the body against recoil.
The hip muscle showed particularly interesting behavior, activating more intensely during hard pecks compared to soft pecks. This suggests hips play a key role in modulating drilling power.
During sequences of rapid tapping, most muscles progressively increased their activation across successive strikes, likely compensating for cumulative fatigue while maintaining consistent strike force and timing. Two neck muscles, however, maintained steady activation throughout, possibly serving postural stabilization roles.
The highs and lows of pro sports fandom bring our brains back to their tribal roots. (Credit: Drazen Zigic on Shutterstock)
Ever yelled at the TV when your team’s rival scored? That rage isn’t just in your head… well, actually, it is. And scientists have uncovered exactly what’s happening in there.
Chilean researchers put dozens of die-hard soccer fans (across a range of engagement/interest levels) in brain scanners and showed them goals from matches involving their favorite teams. What they found explains a lot about why some fans lose it when things go south, and why beating your rivals feels so damn good.
The study, published in Radiology, focused on supporters of Chile’s two biggest rival football (soccer) teams. Participants watched 63 goal sequences while researchers tracked their brain activity. Some fans were casual spectators. Others were fanatics. The differences in their brains tell a fascinating story.
When The Rival Team Scores, Your Brain’s Emergency Brake Dozes Offc
When highly engaged fans watched their rivals score, a region that normally keeps emotions in check was less active. It’s sort like an emergency brake in your brain — the thing that stops you from doing something you’ll regret. In fanatics watching rival goals, that brake wasn’t working as well as usual.
This brain region connects your emotions to your decision-making. When it dims, people struggle to control aggressive impulses. The more fanatical the fan, the quieter this control center became during rival defeats.
But something else interesting happened. Less extreme soccer fans showed more activity in brain regions used for understanding other people’s thoughts and intentions. They seemed to be working harder to process what the defeat meant, rather than just reacting emotionally.
Watching Your Favorite Sports Team Win Is Like Eating Really Good Food
When fans watched their team score against rivals (compared to scoring against random teams), their brain’s reward system lit up like a Christmas tree. Same areas that activate when eating something delicious, having sex, or taking certain drugs.
This isn’t a coincidence. Evolution wired our brains to release feel-good chemicals when our tribe wins. It made sense for survival thousands of years ago. Now that same wiring makes us lose our minds over 22 people kicking a ball around.
Brain regions tied to personal identity also fired up during rival victories. Fans weren’t just happy for the players—their brains processed these wins as personal achievements. The team’s success felt like their own success.
Not All Soccer Fans Are Created Equal
The researchers recruited 60 male fans of Chile’s two biggest rival teams and put them in brain scanners. Over 26 minutes, participants watched 63 goal clips. Some showed their team scoring, some showed rivals scoring, and some showed other random teams.
The researchers compared brain activity during rival moments versus non-rival moments. This isolated what made rivalries special versus just watching any football match.
Participants in the study were sorted into three groups: spectators (casual fans), regular fans, and fanatics. On the fanaticism scale, lower scores meant more extreme fandom.
The brain patterns matched the intensity levels. More fanatical soccer fans showed bigger drops in that control region during defeats.
Goals only triggered these intense brain responses when they involved rivals. Score against a random team? The response was weaker. Score against your mortal enemy? Fireworks.
Humans evolved as tribal creatures. Our ancestors survived by sticking with their group and competing against others. Those ancient tribal instincts are still there, and football taps right into them. Your brain treats your team like your tribe and rival teams like threats, even though nobody’s actually in danger.
Why Does The Brain React This Way?
Soccer violence around the globe is real. Riots, assaults, even deaths happen around big matches. Understanding that extreme fans experience reduced activity in brain control centers could help explain why some people cross the line from passion to violence.
Stadium security usually assumes fans make rational choices about their behavior. But if someone’s brain control center is essentially offline when their rival scores, they’re not thinking rationally. That doesn’t excuse violence, but it suggests different approaches to prevention might work better.
The strong reward response might also explain obsessive fan behavior: spending thousands to travel to games, prioritizing matches over family events, or melting down over a loss for days. If your brain treats a win like hitting the jackpot, it’s easy to keep chasing that feeling.
Why Soccer Has This Power
Argentine writer Eduardo Galeano observed that football identity is non-negotiable and deeply ingrained. The neural data support this cultural observation. The patterns of brain activation involve fundamental systems of reward, identity, and social belonging rather than superficial preferences.
Football offers something most of life doesn’t: clear winners and losers, on a predictable schedule. Matches create rhythms: weekly fixtures, seasons with beginnings and endings. Your brain’s reward system loves that clarity.
Plus, watching with other fans amplifies everything. Shared highs and lows strengthen group bonds. That collective experience is part of what makes fandom so powerful and, for some, so consuming.
Every single silver strand of hair represents the successful elimination of DNA-damaged cells. (Credit: Halfpoint on Shutterstock)
Those silver strands sprouting on your head might be doing more than announcing your age. Research from the University of Tokyo shows that gray hair in mice reflects a built-in cleanup program in which the body hunts down and eliminates damaged cells capable of becoming cancer. Importantly, there are supporting signs this same mechanism is present in human skin tissue samples.
Scientists tracked what happens to the stem cells responsible for hair color when they get damaged. This led to a surprising discovery in mice. Their bodies force these damaged cells to mature and then kick them out, leaving behind gray hair.
It’s a biological trade-off that may be happening in humans too. In other words, accept some gray hairs, or allow damaged cells to persist.
Gray Hair 101: How Follicles Clear Cells Tied To Skin Cancer
The stem cells in your hair follicles act as tiny factories that produce pigment. When everything works correctly, these cells wake up during each hair growth cycle, make copies of themselves, and send some of their offspring down the hair shaft to add color. Then they go back to sleep until the next cycle.
But what happens when radiation, sun damage, or other environmental stressors break the DNA in these stem cells? Researchers Yasuaki Mohri and Emi K. Nishimura discovered something unexpected. The damaged cells don’t just die quietly. Instead, they get forced into an unusual double state: they stop dividing forever (that’s the safety brake) while simultaneously maturing into regular pigment cells (that’s the exit strategy).
The cells essentially get a one-way ticket out of the follicle. They complete one last job making pigment, then leave the protected stem cell area and get cleared away naturally. The hair follicle loses its color-making factory, and you get a gray hair. Each silver strand represents a successful elimination of cells carrying DNA damage.
The study, published in Nature Cell Biology, confirmed this in mice by studying animals lacking p53, a protein that acts as the body’s chief DNA damage detector. These mice kept their dark fur even after radiation exposure that would normally cause graying. Sounds great, right? Not exactly. Those damaged cells stayed put, raising the risk that they could eventually transform into cancer.
When Carcinogens Hijack the System
When the researchers exposed mice to cancer-causing chemicals like DMBA (a lab carcinogen used in skin-cancer models) or strong UV radiation, those substances didn’t trigger gray hair at all. Even when the cells had the same DNA breaks that radiation causes, the carcinogens somehow convinced them to keep dividing.
The trick involves a protein called KIT ligand, or KITL. Normally, cells surrounding the stem cells produce small amounts of KITL to support the stem cell population. But carcinogens cranked up KITL production dramatically, essentially shouting “keep growing!” to cells that should be getting eliminated.
At the same time, the carcinogens turned on arachidonic acid pathways inside the damaged stem cells. When researchers gave mice a prostaglandin E2-like signal (a product of this pathway), it reproduced the effect, blocking the graying response. It’s a two-pronged attack: external survival signals from the environment combined with internal changes that favor growth over elimination.
Mice treated with just a carcinogen didn’t go gray—their damaged stem cells survived and spread into the surrounding skin, forming the pigmented spots that can progress to melanoma. When researchers gave mice both radiation and a carcinogen together, the carcinogen won, blocking the protective gray hair response.
The Skin Stem Cell Niche
To test whether KITL really controls this life-or-death decision, the team created mice with reduced KITL in the cells surrounding stem cells. These mice went gray faster, even without any radiation exposure. Their stem cells couldn’t maintain themselves without enough KITL support.
More tellingly, when these low-KITL mice received both radiation and carcinogens, the carcinogens couldn’t override the protective response anymore. The mice still went gray because their environment lacked enough KITL to keep damaged stem cells alive. The experiment proved that the surrounding niche makes the critical decision about whether damaged stem cells get eliminated or allowed to persist.
The researchers also examined human melanoma samples, specifically the type caused by cumulative sun exposure over many years. In several samples, KITL was elevated not just around hair follicles but throughout the skin surrounding tumors. The cancer had essentially expanded its own support system, creating an environment where damaged cells could thrive and spread.
The Mystery of Recovering Gray Hair
Rare case reports describe a puzzling phenomenon. Patients whose gray hair appears to “come back to life” and regain color in certain scalp areas, only to receive a melanoma diagnosis in those exact spots months later. This research offers a possible explanation.
The gray hair wasn’t actually recovering. Instead, early melanoma cells spreading through the epidermis were producing their own KITL and other growth factors, supporting any remaining stem cells and their pigment-producing offspring. The darkening hair was actually a warning sign that cancer precursor cells were colonizing that area of scalp.
This reframes what looks like rejuvenation as an early danger signal—a cancerous field spreading beneath the skin surface, creating conditions that support cell growth rather than elimination.
Aging Skin and Gray Hair: Signals That Shift Skin Cancer Defenses
When the team compared young and old mice, they found that aging naturally reduces KITL and other growth factors produced by the stem cell niche. In older mice, these support signals fall and graying speeds up. Aged skin simply doesn’t support stem cell maintenance as well as young skin does.
But this decline might not be entirely bad. By reducing the signals that promote stem cell survival and growth in mice, aging skin may be tilting the balance toward elimination rather than preservation of cells that have accumulated DNA damage over time. It’s a biological guardrail that becomes more conservative with age.
Single-cell analysis of over 60,000 skin cells from young and old mice revealed that the proportion of both stem cells and melanocyte clusters dropped significantly in aged animals. The stem cell niche itself shrinks with age in mice, not just the stem cells it supports.
When Skin Cancer Mutations Take Control
To test whether cancer-driving mutations could bypass the protective response like carcinogens do, researchers created mice carrying activated versions of NRAS or BRAF — two of the most common genetic changes in human melanoma — specifically in their hair color stem cells.
These mutant mice kept their dark fur even after doses of radiation that would normally eliminate all stem cells and cause complete graying. The mutations made cells independent of external KITL signals, allowing them to survive and multiply despite DNA damage.
The team then flipped the question. Could eliminating stem cells through the protective response prevent melanoma? They irradiated cancer-prone mice before triggering the melanoma mutations. Melanoma development dropped dramatically compared to non-irradiated controls. By depleting the stem cell population first, there were simply fewer cells available to transform into cancer when the mutations hit.
What This Means for Real People
These findings don’t suggest that radiation prevents cancer. Kt clearly doesn’t, and the doses used in research mice don’t match human exposures. But the research does reveal something important about visible aging: those gray hairs represent successful quality control, not just breakdown.
People who gray early or extensively, especially in sun-exposed areas like the temples and crown, may have particularly active protective mechanisms. Each gray hair is a follicle where the body identified damage and chose elimination over risk.
Whether anti-aging treatments aimed at preventing or reversing gray hair could affect melanoma risk remains an open question for future studies. If such treatments work by keeping damaged stem cells alive and functional longer, it’s unclear what that might mean for cancer development in people with significant sun exposure or other DNA damage sources.
The research team calls the protective process “seno-differentiation,” combining cellular aging’s permanent growth arrest with the maturation and migration that clears damaged cells from stem cell homes. It’s natural quality control that doesn’t require drugs or interventions, just the body’s built-in wisdom about when to eliminate rather than repair.
The paradox is clear. Fewer stem cells (and more gray hair) can protect against cancer by limiting the pool of cells available for transformation. Visible aging in this case reflects invisible protection.
The Bigger Picture
So, should we rethink the relationship between aging and cancer? They’re often portrayed as related processes driven by accumulated DNA damage, but this work shows the body’s response to damage matters more than the damage itself.
The stem cells studied here face a fundamental choice when they acquire DNA breaks. Either undergo the protective elimination program that causes gray hair, or bypass it through carcinogen exposure or cancer mutations and risk melanoma. Individual cells make this decision based on signals from their surrounding environment, but the cumulative effects of millions of these decisions determine whether a person develops gray hair or cancer.
The surrounding niche acts as the critical decision-maker, integrating information about growth factor levels, damage signals, and metabolic status to instruct each stem cell about its fate. When carcinogens reprogram the niche to produce high KITL levels, they’re essentially rigging the decision in favor of survival over elimination.
There are easier ways to cross an ocean, but few are as slick or stylish as the remora’s whale-surfing joyride.
Scientists tracking humpbacks off the coast of Australia have captured rare footage that shows clutches of the freeloading fish peeling away from their host in what looks like a high-speed game of chicken, just moments before the whale breaches.
As the humpback plunges back below the surface the remoras, also known as sucker fish, return to the whale, sticking their landings with the timing and precision of Olympic gymnasts. It’s elegant work for a hitchhiking fish that lives upside-down and survives on dead skin flakes.
Remora australis spend their lives aboard whales or other large marine mammals, which they ride like giant cruise ships, breeding and feeding their way across stretches of ocean. The species has an adhesive plate on its head that helps to create a kind of vacuum seal, allowing the fish to grab a whale and hang on for the ride.
1 of 4 | Scientists have captured rare footage of remoras, also known as sucker fish, hitching rides on humpback whales off the coast of Australia. Remoras use an adhesive plate on their heads to cling to whales, feeding on dead skin and sea lice.
On whale cams, clingy fish steal the show
The marine scientist who recorded the accidental close-ups of the remoras’ high-speed whale surfing had placed suction-cup cameras on humpbacks during their annual migration from Antarctica to the waters off Australia’s Queensland state. Olaf Meynecke planned to study whale behavior, but his video feeds regularly filled with dozens of photobombing remoras, which rode in groups of up to 50 as they clung to the same spots where his cameras were attached.
“Whenever the whale was breaching and doing in particular fast movements it appears that the sucker fish were responding very quickly to the movements,” said Meynecke, from the Whales and Climate Research Program at Griffith University. “They knew exactly when to let go of the body of the whale before it was breaching the surface of the water and then returned to the same spot only seconds later.”
A hitchhiker with good instincts
Remoras are harmless to the 40-metric ton (44-U.S. ton) giants of the ocean, feeding on the whales’ dead skin and sea lice in a mutually beneficial arrangement — or at least that’s what scientists say. Meynecke said his footage suggested the whales found their hangers-on annoying.
“We’ve had individuals with high numbers of these remoras and they were continually breaching and there were no other whales that they were communicating with,” he said. “It appeared that they’re trying to just get rid of some of these remoras and they were checking whether they had less after they breached.”
Scientists just built a brain implant barely visible to the naked eye. At 370 micrometers long and 70 micrometers wide, it’s about as wide as three or four human hairs. These innovative, tiny devices recorded the brain activity of a group of mice for an entire year.
A neural implant developed at Cornell rests on a grain of salt. About 300 microns long and 70 microns wide, it’s the smallest neural implant capable of wirelessly transmitting brain activity data. (Credit: Sunwoo Lee/Provided)
The implant is so small that dozens could fit on a pinhead. Yet it stayed functional for 365 days, capturing everything from individual brain cells firing to coordinated activity across neural networks. Compare that to existing wireless brain implants, which can be hundreds of times larger.
“The long-term recording of neural activity could be used to understand complex behaviors and disorders,” the researchers wrote in Nature Electronics. The international team, led by Sunwoo Lee from Nanyang Technological University and colleagues from Cornell University, showed these microscopic devices could track brain signals without the tissue damage that plagues larger implants.
So how does something this small actually work?
Light Does All the Heavy Lifting
Instead of wires or radio waves, these implants use light for everything. An external red LED beam powers the device continuously. The implant sends data back using brief infrared pulses. Think of it like a conversation conducted entirely with flashlights.
This matters because traditional wired implants damage brain tissue as they shift around. Your brain actually moves slightly inside your skull during normal activity. When wires are tethered to external hardware, that movement creates friction and scarring. Wireless systems avoid this problem, but they’re typically too bulky.
The device uses a single component that pulls double duty. It harvests power from incoming light 93.4% of the time and transmits data for the remaining fraction. Inside this grain-of-sand-sized package, hundreds of tiny transistors amplify signals from nearby neurons, encode the information, and drive the light output. The whole system runs on 1 microwatt—about one-millionth the power of a typical LED bulb.
Building Something Smaller Than a Dust Mite
Getting electronics this small to work inside a living brain required some serious engineering gymnastics.
First, the team had to bond different materials together—silicon chips and light-sensitive semiconductors—without the usual residues that gum up the works. They used an ultra-low-pressure heating process at 300°C to clean and strengthen the connections.
Then came waterproofing. The body is essentially a corrosive salt bath, so the researchers built up ultra-thin protective layers totaling less than 1.5 micrometers thick. That’s about one-fifth the width of a red blood cell.
There was, however, a problem. Light leaking into the silicon electronics could generate unwanted electrical signals and scramble the brain readings. The solution? Wrap everything in a form-fitting platinum coating that simultaneously blocks light, records neural activity, and reinforces the structure.
From Beating Heart Cells to Mouse Brains
Before trying these devices in living brains, researchers tested them on lab-grown heart cells. The implants tracked the cells beating in sync, then recorded the changes when researchers applied drugs that sped up or slowed down the heartbeat. From 1.8 beats per second up to 2.0, then down to 0.8. The devices worked perfectly.
For the brain experiments, the team implanted eight devices in six mice, placing them in a region that processes whisker sensation. Using a tiny glass pipette, they inserted the implants 100 to 400 micrometers deep—about the thickness of a few sheets of paper stacked together.
Here’s where the size becomes an advantage. Researchers could load these devices into pipettes while suspended in rubbing alcohol, which sterilizes them and evaporates quickly without causing damage. Once in place, only light needed to pass through the skull window to power them and receive their signals back.
When researchers touched the mice’s whiskers with a motorized rod, the implants detected the resulting brain activity and transmitted it optically. A photodiode captured those infrared pulses, and software reconstructed what the neurons were doing.
A Full Year of Brain Recording
Four of the implanted devices captured coordinated activity from groups of neurons. Two others, placed on the brain surface, recorded broader electrical patterns. One ended up too deep to work reliably, and another got damaged during preparation.
The recordings showed clear responses to whisker stimulation that stayed detectable well past 100 days. Individual neurons firing appeared as sharp electrical spikes. Groups of neurons working together showed slower, wave-like patterns.
The signal strength varied somewhat over time, probably because the devices shifted 50 to 300 micrometers as post-surgical swelling went down during the first few weeks. This moved them slightly closer to or farther from active neurons. But the overall patterns remained stable.
On day 365—a full year later—one implant still responded to whisker touches. The signals had gotten weaker, requiring the researchers to average 30 to 40 recordings to see them clearly above background noise. But it was still working. When they removed the devices and tested them, both still lit up when exposed to light, meaning the circuits were fine. The recording electrodes had simply degraded slightly over time.
Why Brain Tissue Barely Noticed They Were There
When the researchers examined brain tissue under a microscope after six months, they found very little damage around the implant sites.
Neurons beneath the six-month-old implants looked healthy and normal, with their characteristic branching structures intact. Immune cells (which indicate inflammation) near the implants were at similar levels to control areas under the same skull window where no device had been inserted. The window itself seemed to trigger more immune response than the implants.
The real surprise came when they compared these six-month results to optical fibers implanted in other mice for just three months. Despite being in place for half as long, the fibers caused substantially more inflammation. Neurons beneath them showed signs of degeneration that were completely absent around the microscopic implants.
Why the difference? Volume. These implants displace less than a nanoliter of brain tissue. Even thin optical fibers occupy thousands of times more space. Less volume means less mechanical stress and less foreign surface area triggering immune reactions.
Solving Problems That Have Plagued Brain Implants for Years
This technology addresses issues that have limited brain recording for decades.
Wired implants cause ongoing damage because brains shift slightly inside skulls during normal activity. The wires create shearing forces that damage tissue and cause scarring.
Wireless systems avoid that problem but face a different constraint: they’re typically huge. Radio-frequency and ultrasound-based approaches need components scaled to their wavelengths. Some wireless systems approach 1% of total mouse brain volume per recording channel. For comparison, a mouse brain is about 400 cubic millimeters total.
These optical implants are orders of magnitude smaller. Researchers could theoretically implant thousands before reaching the volume of existing single-channel systems. That scalability could enable mapping neural circuits across entire brain regions—something impossible with current technology.
The optical approach also works deep in tissue. Red and near-infrared light penetrate biological tissue easily, and the light intensity stays well below levels that cause heat damage. Simulations suggest these devices could theoretically work at depths up to 6 millimeters in mouse brains—enough to reach most regions.
There are limitations, of course. The bandwidth captures signals up to about 10 kilohertz, which covers most brain activity but might miss some high-frequency events. Each device has two recording electrodes spaced 300 micrometers apart, so they can’t isolate signals from individual neurons as precisely as dense electrode arrays. And for now, mice need to remain head-fixed during measurements while connected to external optical hardware.
Beyond Brain Recording
The technology could work in places where existing tools can’t.
Brain organoids—tiny three-dimensional brain tissue cultures grown in labs—are too small and delicate for conventional electrodes. These microscopic implants could fit inside and measure electrical activity directly.
Fruit flies and roundworms are crucial research models, but their nervous systems are too tiny for traditional recording methods. These implants could enable direct electrical measurements without genetic modifications.
Related micro-devices from the same research group can sense chemical changes, suggesting a path toward monitoring metabolism in engineered tissues or detecting biomarkers in organ-on-chip systems.
Sharks are usually the hunters, but these killer whales have developed a surprising new way to enjoy a meal.
An orca swims next to a shark with a visible wound. (Image by Marco Villegas)
Off the coast of Mexico, a pod of killer whales has developed a specialized hunting technique. They flip juvenile great white sharks upside down in a way that likely triggers a trance-like paralysis, then extract their livers while discarding the rest of the carcass.
Researchers captured two attacks on video: one in August 2020 and another in August 2022, at nearly the same spot in the Gulf of California. Both times, the orcas targeted sharks about two meters long, around six and a half feet. The footage reveals a deliberate method: repeated strikes, maneuvering the young sharks belly-up in what likely induces tonic immobility, a physiological state that leaves them defenseless and unable to move.
Once the shark goes limp, the killer whales access the liver with precision. In one attack, the organ emerged intact at the surface. An adult female held it in her mouth, its distinctive two-lobed shape clearly visible. She released it to another whale. For several minutes, four pod members passed the liver between them before finally consuming it.
Researchers captured two attacks on video: one in August 2020 and another in August 2022, at nearly the same spot in the Gulf of California. Both times, the orcas targeted sharks about two meters long, around six and a half feet. The footage reveals a deliberate method: repeated strikes, maneuvering the young sharks belly-up in what likely induces tonic immobility, a physiological state that leaves them defenseless and unable to move.
Once the shark goes limp, the killer whales access the liver with precision. In one attack, the organ emerged intact at the surface. An adult female held it in her mouth, its distinctive two-lobed shape clearly visible. She released it to another whale. For several minutes, four pod members passed the liver between them before finally consuming it.
During one sequence, a California sea lion tried to grab a piece. The orcas drove it off by exhaling bubbles. The researchers noted in their study, published in Frontiers in Marine Science, that the killer whales shared the liver among pod members, including calves.
A Pod That Adapts Its Methods
Photo analysis identified at least three killer whales from the 2020 incident as members of the “Moctezuma pod,” a group documented hunting multiple shark and ray species across the Gulf of California between 2018 and 2023.
The pod adapts its technique to each prey type. When hunting Munk’s pygmy devil rays, they target stragglers at the edge of schools, grabbing them by the wingtip before repositioning to control the head. Pelagic stingrays get slammed with forceful tail strikes to stun them and avoid their venomous spines. Bull sharks require different handling altogether.
For white sharks, the flipping technique likely induces paralysis and allows access to the liver without risking a bite. A 2.5-meter white shark can generate bite forces exceeding 3,000 newtons, enough to cause serious injury and derail an attack.
This behavioral flexibility sets the pod apart. Killer whale populations worldwide tend to focus on narrow prey types, with distinct groups hunting fish, marine mammals, or sharks. The Moctezuma pod hunts at least six elasmobranch species using adapted methods for each, which points to an unusually diverse skill set.
Shark livers offer high nutritional rewards. These massive, oil-rich organs can comprise up to a third of the animal’s total weight. For an orca, it is high-calorie fuel for relatively low effort once the extraction technique is learned.
But learning that technique requires practice and coordination. The 2020 footage shows the process unfolding. One young female pushed the shark from below toward the surface while it bled from its underside. The whales took turns controlling the inverted shark, working together. After several minutes underwater, an adult female surfaced with the liver and began passing it among the pod.
Seven minutes into the video, the whales attacked a second juvenile white shark. This one was worked over repeatedly until its liver began protruding from the right side of its body, partially exposed. At eleven minutes, the shark sank motionless. Pink tissue floated at the surface.
The 2022 attack followed a similar pattern. An adult female surfaced with the shark held below, mouth open, large pectoral fins visible. The characteristic black tips on the underside of white shark pectorals can be seen in the footage. The shark bled from its gills, liver exposed on the left side. Minutes later, pieces of liver tissue appeared in the mouths of the females. The adult male and a calf fed at the surface. Seabirds including boobies, gulls, pelicans, and frigates arrived to scavenge scraps.
Scientists report the first ever clinical pregnancy aided by AI-guided sperm recovery. (Photo by Suhyeon Choi on Unsplash)
After 19 years of trying to conceive, a couple facing severe male infertility achieved their first pregnancy using an artificial intelligence system that detected sperm invisible to human examination. Reported in The Lancet, this represents, to the authors’ knowledge, the first reported clinical pregnancy resulting from AI-guided sperm recovery. It offers new hope for men whose semen appears empty on manual examination, a diagnosis where traditional methods frequently fail.
A 39-year-old man had been diagnosed with non-obstructive azoospermia, meaning sperm are absent or extremely rare in his semen. His 37-year-old partner had undergone 19 egg retrievals across four fertility centers over 11 years. Despite invasive testicular procedures and extensive manual searches, the couple had produced only one embryo suitable for transfer in nearly two decades. That attempt failed.
When doctors examined the man’s semen sample under a microscope, they found nothing. But when researchers processed the same sample through the STAR system (Sperm Tracking and Recovery), the AI identified seven sperm after analyzing 2.5 million images in about two hours.
Two of those sperm could move on their own. Both were injected directly into eggs. Both eggs became embryos. Thirteen days after transfer, the woman received her first positive pregnancy test in 19 years.
How the System Works
The STAR system combines high-speed imaging with AI trained to recognize sperm. As the sample flows through a specialized chip, a camera captures 300 frames per second, analyzing over a million images per hour.
Rather than relying on a single snapshot, the system tracks each potential sperm across roughly ten consecutive frames. It confirms detection only when the object appears as sperm in at least three frames, which helps eliminate false positives from debris or other cells.
Once confirmed, a microfluidic gate isolates the sperm for retrieval. To validate accuracy, researchers tested the system by adding known numbers of sperm to samples. The results showed excellent correlation: R²=0.99.
The system is fully enclosed to prevent contamination, and all components are single-use to ensure sterility. Both partners provided informed consent, and the research received ethical approval from Columbia University’s institutional review board.
When Standard Treatments Fall Short
Male factor infertility contributes to roughly 40 percent of all cases. Azoospermia and cryptozoospermia (extremely rare sperm) account for about 10 to 15 percent of male diagnoses.
Standard approaches include testicular sperm extraction, where surgeons remove small pieces of testicular tissue hoping to find sperm, or extended manual searches by embryologists. Both methods are invasive or time-intensive and frequently unsuccessful. Many couples are ultimately advised to consider sperm donors or adoption.
This couple had tried everything. The male partner underwent two testicular extractions with only rare sperm recovered. His partner’s hormone levels showed her egg supply was critically depleted. Her 19 egg retrievals produced consistently poor fertilization when sperm was available. Several cycles involved only egg freezing because sperm couldn’t be obtained.
The STAR system found seven sperm in a sample that appeared empty under manual examination. Small numbers, but enough for a chance.
The Results
Two of the seven sperm could move. These were injected into two eggs: one fresh, one thawed. Both became embryos.
Two additional thawed eggs were injected with non-moving sperm. Those didn’t progress. Only the motile sperm produced viable embryos.
Both embryos were transferred. Thirteen days later: positive pregnancy test. The couple’s first in nearly two decades. At eight weeks, ultrasound confirmed normal development with a heartbeat of 172 beats per minute.
While the STAR system had previously recovered sperm in other patients, this marks the first time AI-detected sperm were used immediately for fertilization and resulted in a confirmed pregnancy. That matters because it shows the system can support real-time clinical decisions, not just sperm banking.
The AI Behind the Detection
The AI model was built on the You Only Look Once architecture, trained specifically on sperm images. It divides each video frame into a grid and predicts where sperm might be in a single pass.
The model flagged sperm correctly 89 percent of the time and successfully identified 90 percent of actual sperm present. Processing at this speed required specialized computing power that would be impractical for manual examination. Even highly trained embryologists can examine only a fraction of a sample’s volume and may still miss rare sperm.
What This Means for Infertility Treatment
For men with severe male factor infertility, standard options can be uncomfortable or time-consuming without guaranteeing results. Many couples spend years cycling through repeated procedures, accumulating both financial costs and emotional exhaustion.
By automating detection and analyzing the entire sample volume, the STAR system creates opportunities where traditional methods have failed. It requires only a standard semen sample rather than surgical extraction, making it less invasive.
Larger clinical studies are underway to evaluate the system’s performance across broader patient populations. If those trials confirm consistent success, the technology could become a valuable addition to fertility clinics.
Hard workouts pay off for women. (Photo by Unsplash+ in collaboration with Getty Images)
Wearable device data from about 85,000 people suggests striking sex differences that challenge current health guidelines
Women may achieve similar heart disease protection as men with about half the weekly exercise time. That’s according to research tracking approximately 85,000 people wearing wrist accelerometers measuring moderate-to-vigorous physical activity for a week.
The study, published in Nature Cardiovascular Research, reports that women reached roughly a 30% lower coronary heart disease risk at about 250 minutes of weekly exercise, while men needed approximately 530 minutes for comparable protection. Among people who already had heart disease, the gap looked even wider: meeting activity guidelines was linked to about 70% lower overall death risk for women versus 19% for men.
Major health organizations currently recommend identical exercise targets for both sexes: at least 150 minutes of moderate-to-vigorous activity per week. Women already struggle more than men to hit these targets, yet this research suggests they may need less time to reap the same rewards.
Exercise And Gender By The Numbers
Researchers from Xiamen University analyzed UK Biobank data spanning nearly eight years. Rather than relying on people’s memories of how much they exercised (which tends to be overly optimistic), participants wore devices that objectively tracked their movement.
But despite doing less, the minutes were linked to larger cardiovascular benefits in women than in men.
Among people without heart disease at the start, women who hit the 150-minute weekly target showed 22% lower risk of developing heart problems during follow-up. Men meeting the same target? Just 17% lower risk.
For those already living with heart disease, the pattern held. Active women had death rates of 1.76% versus 9.15% for inactive women. Active men fared better than inactive men too (9.38% versus 15.13%), but the relative benefit was smaller.
Why Women’s Bodies Might Respond Differently
Scientists don’t have the complete answer yet, but they’ve got some educated guesses.
Estrogen could be key. Women naturally have much higher levels than men, and research shows estrogen boosts fat burning during exercise. Since using fat for fuel (rather than just sugar) appears to benefit heart health, this hormonal difference might partly explain why women see bigger returns on their exercise investment.
Muscle composition offers another clue. Men have more type II muscle fibers, built for quick, powerful movements but dependent on sugar metabolism. Women have more type I fibers, which excel at endurance and efficiently burn fat. These differences in how muscles work during sustained activity might translate to different heart benefits.
The researchers stress these are still theories requiring lab studies to confirm.
Showing Up Matters
The study also looked at consistency. Each extra day women squeezed in about 21 minutes of exercise was linked to 6% lower heart disease risk. For men, each active day is connected to about 4% lower risk.
Women who exercised daily saw their heart disease rates drop from 5.2% to 1.5%. Men who went from zero to seven active days weekly saw rates fall from 10.2% to 4.7%.
If these findings hold up in more diverse populations, they might reshape how we think about exercise recommendations. Right now, telling everyone to hit the same target may discourage women, who globally lag behind men in meeting activity guidelines (33.8% of women versus 28.7% of men fall short).
Knowing that women might achieve similar or better protection with less time could help narrow this gap. And with fitness trackers becoming ubiquitous, personalized targets based on sex, health status, and individual response patterns could become more common rather than one-size-fits-all advice.
Studied chimps were capable of differentiating between genuinely new information and redundant details (Patrick Rolands/Shutterstock)
Chimpanzees can weigh and rationalize conflicting information before deciding what to believe. That’s the main conclusion of research that tested whether our closest living relatives can do something scientists call “rational belief revision,” a thinking skill previously thought to set humans apart.
Researchers at UC Berkeley, the University of Portsmouth, and other institutions designed a series of clever experiments with 15 to 23 chimpanzees at Ngamba Island Chimpanzee Sanctuary in Uganda. The chimps watched as food was hidden in boxes, then received different types of clues about where to find it. Sometimes they saw the food directly through a glass window. Other times they only heard it rattling around inside a box or saw traces of it left behind.
After the chimps chose a box based on one piece of evidence, researchers gave them a second, contradictory clue pointing to a different location. The question was whether the apes would stick with their first choice or change their minds, and more importantly, whether they’d make that decision in a smart, strategic way.
The chimps didn’t flip-flop randomly as one might expect. They stayed committed to their initial belief when the first evidence was strong and the contradicting evidence was weak. But when the situation reversed and weaker evidence came first, they readily changed their minds after receiving stronger proof pointing elsewhere.
Chimpanzees Use Rational Thinking, Not Random Guessing
In one experiment, chimps heard food shaking in one box, then saw food directly in another box through a clear panel. Most switched their choice to the box where they’d seen the food, recognizing that visual proof beats auditory hints. In another version, they saw food traces near one box, then heard rattling in another. Again, they favored the stronger evidence, in this case the sound of actual food over mere leftovers.
Study authors wanted to know if chimps were truly thinking about evidence or just responding to whatever seemed flashiest. So they ran a test with three boxes: one with strong evidence, one with weak evidence, and one with no evidence at all. After showing the chimps all three options, they removed the box with strong evidence. If the animals were only paying attention to the most obvious cue, they should have chosen randomly between the two remaining boxes. Instead, they consistently picked the box supported by weak evidence over the one with none, suggesting they were tracking more than one possibility all along.
The researchers point out that changing your mind based on evidence strength requires keeping track of not just what you know, but how you know it.
Telling Real Information From Noise
Perhaps most impressively, the chimps could tell the difference between genuinely new information and redundant evidence. When researchers shook a box twice, the chimps recognized this as the same piece of evidence presented again. It didn’t make them more likely to pick that box. But when researchers dropped two separate pieces of food into a box one after another, creating two distinct sounds, the chimps treated this as accumulating evidence and were more likely to revise their choice.
The animals changed behavior when their original evidence was undercut. In one test, after a chimp chose a box where it had seen food through a window, researchers revealed that the window actually showed a picture of food, not real food. This undercut the earlier visual cue; chimps treated it as weaker and were more willing to switch boxes. When researchers revealed an empty window instead of a picture, which didn’t change anything about what they’d seen, the chimps mostly stuck with their choice.
Why This Matters for Animal Intelligence
Previous research showed that great apes could figure things out based on various types of clues. A hungry chimp might locate hidden food by listening to sounds, looking at visual hints, or noticing that food is absent from other spots. But those abilities could be explained by simpler mental shortcuts that don’t require actually reasoning about how trustworthy different sources of information are.
This study, published in Science, goes further. The chimps went beyond simply responding to evidence — they took time evaluating it. When deciding whether to stick with or abandon a belief, they compared the strength of competing pieces of information.
The research team used mathematical models to predict how a perfectly rational thinker should behave when faced with conflicting evidence of different strengths. The chimps’ behavior matched these predictions remarkably well, not just overall but for nearly every individual animal tested.
These results show that the ability to weigh evidence and change your mind accordingly likely has deep evolutionary roots among great apes.
The study also addresses a longstanding debate about whether animals can truly think about their own thinking, or if they just happen to behave in ways that look smart. Critics have argued that when chimps search for more information or skip difficult tasks, they’re not really reflecting on their own knowledge—they’re just reacting to uncertainty in ways that mimic deeper thought.
But the experiments in this study make that skeptical explanation harder to accept. Recognizing when a piece of evidence has been proven wrong by later information requires understanding the relationship between evidence and belief, not just reacting to whatever’s in front of you.
Dark chocolate may provide a notable memory boost. (Photo by Victor Moussa on Shutterstock)
Eating flavanol-rich foods like dark chocolate or berries may boost memory performance. How? By synchronizing stress hormones with the brain’s natural window for locking in new information, according to research from Japan. In mice, memory improved when flavanols were given before learning, though the timing effects in humans remain unknown.
Scientists at Shibaura Institute of Technology discovered that the bitter, astringent compounds in cocoa trigger a precisely timed release of noradrenaline in the hippocampus (the brain region that converts short-term memories into lasting ones). Mice that consumed flavanols one hour before a memory test showed a 30% improvement in recognizing new objects compared to those given plain water.
The study, published in Current Research in Food Science, offers a potential explanation for why large trials have found memory improvements in older adults who consume these compounds regularly. Rather than protecting brain cells directly, flavanols may work by hijacking the body’s stress response system at just the right moment.
The Critical Window for Memory
Lead researcher Yasuyuki Fujii and his team tested mice in a standard memory experiment. Animals explored two identical objects for 10 minutes, then returned an hour later to find one object replaced with something new. Mice given flavanols before the initial training spent significantly more time investigating the novel item, a sign they remembered the familiar one.
Mice spent more time exploring the new object, raising the discrimination index versus controls. The effect was observed when flavanols were given before the training session.
Brain imaging showed why. Noradrenaline rose quickly in the brain’s alertness network, including the locus coeruleus and nucleus accumbens, and remained elevated for about an hour. This surge coincided with the period neuroscientists call early memory consolidation, when electrical activity in the hippocampus replays recent experiences and transfers them to long-term storage.
Prior studies have shown that blocking noradrenaline receptors during this window can impair memory formation, while activating them enhances it. The flavanols appear to provide that activation naturally, through taste rather than direct drug action.
Your Brain’s Built-In Alarm System
The memory enhancement stems from how flavanols activate the locus coeruleus, a small cluster of neurons in the brainstem that acts as the brain’s alarm system. When triggered, it releases noradrenaline throughout the brain, sharpening attention and prioritizing information for storage.
Mice given flavanols showed clear signs of this activation. Urinary levels of adrenaline and noradrenaline (stress hormones secreted by the adrenal glands) increased significantly at the higher dose over 24 hours. Gene expression of corticotropin-releasing hormone, which regulates the body’s stress response, increased in the hypothalamus 30 minutes after administration.
The animals also moved more in their cages and showed increased grooming and rearing, behaviors associated with alertness. Mass spectrometry imaging revealed noradrenaline accumulation not only in the hippocampus but also in the nucleus accumbens, a region involved in motivation and reward processing.
A Sensation, Not Absorption
Flavanols barely make it into the bloodstream, a fact that has puzzled researchers for years. Studies using radioactive tracers show that only a few percent of the compounds get absorbed intact, with most breaking down in the gut or metabolized by bacteria.
The new research points to an alternative pathway. The authors propose that the astringent, mouth-puckering sensation these compounds produce activates sensory nerves in the digestive tract, which relay signals to the brainstem and then to the locus coeruleus. However, this pathway requires targeted tests to confirm.
Earlier work by the same research group showed that blocking specific sensory receptors or giving antioxidants eliminated the effects of flavanols on blood flow and nervous system activity. The reactive oxygen species that form when flavanols contact saliva or stomach acid may be what actually triggers the response.
This would explain why the effects happen so quickly. Sensory signals travel much faster than absorbed compounds, reaching the brain in seconds rather than the 30 minutes it takes for dietary substances to peak in blood. The researchers suggest the brain may be treating the astringent sensation as a signal to activate its memory-enhancement systems.
What This Means for People
The mice in the study received doses higher than typical single-serving intakes. Whether lower amounts produce the same effects remains unknown.
The experiments also only tested acute effects from a single dose. Repeated exposure to stress triggers often leads to tolerance, where the same stimulus produces a weaker response over time. Another open question involves the potential downsides of chronic stress pathway activation. Short-term stress responses can be beneficial, but prolonged elevation of stress hormones is linked to anxiety, sleep problems, and cardiovascular strain.
The research used adult male mice with small sample sizes for some brain imaging analyses (two to five animals per group), meaning the findings need replication in larger studies and eventually in humans.
However, the one-hour window offers a potential strategy for students or professionals preparing for tasks that require strong recall. Consuming flavanol-rich foods shortly before studying or attending an important meeting might enhance retention of the material.
This is the first discovery of such a phenomenon for bats located in North America. The tricky thing now, the researchers said, is figuring out why. (Credit: Andrea Piazza)
The discovery is both spooky and thought-provoking, but researchers are left with more questions than answers
A bat collected in 1922 and one caught last decade have something unexpected in common: both glow green when exposed to ultraviolet light, producing the same range of wavelengths. Scientists at the University of Georgia discovered this peculiar trait while examining museum specimens, some more than a century old. The color of their fluorescent properties hasn’t changed.
Researchers Briana Roberson, Steven Castleberry and their colleagues tested 60 preserved bat specimens ranging from 22 to 103 years since collection. They tested whether specimen age would shift the wavelength of the glow. It didn’t. A bat that’s been sitting in a museum drawer since the Roaring Twenties produces the same green emission, peaking between 520 and 552 nanometers, as bats collected in recent years.
What Makes Museum Bats Keep Glowing
This discovery goes beyond just validating museum collections for fluorescence research. It shows that whatever causes bats to glow under UV light is remarkably stable. The trait survives decades of preservation and storage. Something this consistent points to a stable biological trait with an unknown mechanism. Whether the glow comes from true fluorescence or light scattering remains unclear and requires further testing with different wavelengths of excitation light.
All six North American bat species examined displayed bright green photoluminescence on their wings, uropatagium (the membrane stretching between tail and hind legs), and limbs. The species included big brown bats, eastern red bats, Seminole bats, southeastern myotis, gray bats, and Brazilian free-tailed bats. Every specimen glowed green.
Photoluminescence describes what happens when molecules absorb photons at one wavelength and emit light at a longer wavelength. Think of it like a biological light converter. While this phenomenon has been well-documented in plants, invertebrates, and marine organisms for generations, mammals have only recently attracted attention for displaying the trait.
“It’s cool, but we don’t know why it happens,” admits Castleberry. “What is the evolutionary or adaptive function? Does it actually serve a function for the bats?”
How Scientists Measured the Glow
Researchers used a spectroradiometer to quantify the exact characteristics of emission from each bat. This instrument precisely measures light wavelengths. Before taking readings, the team had to account for all other light sources. They recorded scans with no light present and reference scans of the UV light itself, then subtracted these from specimen scans to isolate only the light produced by the bats.
Photography documented the findings separately. Researchers photographed specimens under UV light alone, then through a yellow UV-filtering lens to reduce visual noise from UV and blue wavelengths. Finally, they used a longpass filter that blocked wavelengths under 470 nanometers. This filtering technique captured the pure emission color without interference from the excitation light.
Museum specimens from the Georgia Museum of Natural History provided the raw material for the research. Bats originally came from across Georgia, South Carolina, Tennessee, Illinois, and California. Using preserved specimens offered advantages beyond their longevity. Researchers could eliminate potential confounding factors like bacteria or fungi that might naturally fluoresce on live animals.
White-nose syndrome lesions are known to be photoluminescent under ultraviolet light, as are certain bacteria common in bat skin microbiomes. Both are unlikely in well-preserved museum specimens.
Why All Six Species Glow the Same Green
The consistency of wavelengths across all six species examined points to a shared physiological mechanism. In scientific terms, the trait appears to be homologous among these species. This means it evolved once in a common ancestor rather than independently in different lineages.
Previous research has identified porphyrins as responsible for red UV-fluorescence in various mammals. Tryptophan metabolites produce other pelage fluorescence colors. The green glow in these bat species differs from both patterns.
Researchers found no differences between male and female bats in their emission characteristics. This rules out sexual selection as a likely explanation for these species. If photoluminescence helped bats attract mates, males and females would likely show different wavelengths or intensities.
The wavelengths also don’t match what would be expected if the glow provided camouflage among foliage. That would require emission peaks around 680 nanometers to align with chlorophyll fluorescence.
Social behavior varies considerably among the species examined. Myotis species, big brown bats, and Brazilian free-tailed bats form social aggregations, sometimes numbering in the thousands. Eastern red bats and Seminole bats are foliage roosters with more solitary habits. Despite these differences in lifestyle and roosting preferences, all species showed the same emission characteristics.
Can Bats Actually See Their Own Fluorescence?
The green wavelengths detected in the study fall within ranges that bat eyes can detect. Bats possess medium to long-wave sensitive vision. Other research has found that bat eye proteins (called opsins) respond most strongly to wavelengths between 536 and 560 nanometers, which overlaps with the green glow observed in this study. However, this study did not test whether the bats examined can actually perceive or respond to their own photoluminescence.
Just because bats might see these wavelengths doesn’t necessarily mean the glow serves a purpose. Several theories exist for why mammals might photoluminesce: predator evasion, communication between individuals, or improved vision in low-light conditions. Proving ecological relevance requires more than demonstrating that an animal glows in a laboratory, though.
The amount of UV light present in natural settings may not be sufficient to produce noticeable photoluminescence, especially in dark caves or hollow trees where many of these species roost. The glow was clearly visible on the undersides of wings and limbs. These are areas more visible during flight than while roosting.
What Other Bats Glow
Published in Ecology and Evolution, the study adds to growing evidence that photoluminescence in mammals is widespread. Mexican free-tailed bats sport photoluminescent bristles on their feet. Eastern tube-nosed fruit bats in Australia show glowing wings similar to what the research team found. Greater Antillean long-tongued bats display piebald spots that become more visible under UV light.
Understanding whether the trait serves a purpose requires specific types of studies. Scientists need to compare photoluminescence in live individuals with museum specimens. They need experiments testing bat responses to photoluminescent signals. And they need measurements of UV light availability in natural bat habitats during active hours.
“Bats have very unique social ecology and sensory systems, and the characteristics we found in these species differs from many other observations in nocturnal mammals,” says Roberson, lead author of the study. “It’s possible for glowing functions to be more diverse than we previously thought.”
Cancer rates, particularly gastrointestinal cancers, continue to rise among young adults. (Photo by Frame Stock Footage on Shutterstock)
If you’re reading this there’s a good chance that you, like me, are a millennial. If so, you’ve probably noticed more and more cases of friends or acquaintances with diseases that you would normally associate with later adulthood – hypertension, Type 2 diabetes or perhaps even the one that we’re all scared to name: cancer.
Millennials – people born between 1981 and 1995 – are the first generation at greater risk of developing tumors than their parents. Between 1990 and 2019, cases of early-onset cancer among people under 50 increased by 79% worldwide, and mortality by 28%.
The truth is that around 80% of cancers are “sporadic,” meaning they are not caused by hereditary mutations but by external factors that damage DNA over time. This includes what we eat and breathe, as well as our level of physical activity, rest, stress and exposure to harmful substances.
In other words, the things that make the biggest difference are the lifestyle factors that surround us every day, and not the genetics we inherit. And we know that our parents’ and grandparents’ lifestyles differed greatly from our own.
Diet’s Effect On The Body
One of the main factors behind this “new epidemic” is diet. Childhood obesity began to skyrocket in the 1980s. In 2022, more than 390 million children and adolescents aged 5 to 19 were overweight – 160 million of these were obese, according to the WHO.
This condition is not just a question of aesthetics: it is associated with insulin resistance, low-grade chronic inflammation, and hormonal changes that increase the risk of developing colorectal, breast, or endometrial cancer.
Most importantly, the effects of childhood obesity do not disappear with age. According to the Colon Cancer Foundation, a meta-analysis involving more than 4.7 million people showed that those with a high body mass index (BMI) in early life are at greater risk of colorectal cancer in adulthood: 39% higher in men and 19% higher in women compared to those who had a healthy BMI in childhood.
Changes in diet have also altered our gut microbiota. It has been shown that diets rich in ultra-processed foods reduce bacterial diversity, and increase the proportion of strains that produce pro-inflammatory metabolites.
This contributes to gastrointestinal diseases such as irritable bowel syndrome or SIBO, which often seem to be endemic among millennials – ask a group of thirty-somethings which of them suffers from gastrointestinal problems and you’ll find few hands are left unraised.
Alcohol’s Invisible Effects
The second major culprit is alcohol, as millennial gatherings often revolve around a table laden with food and drink. For years it was thought that a glass of wine was could “protect” you in some way, but today we know that there is no safe level of alcohol consumption: the International Agency for Research on Cancer classifies it as a Group 1 carcinogen, on the same level as tobacco. This is because the body converts ethanol into acetaldehyde, a compound that damages DNA.
Furthermore, consumption patterns differ between generations. While baby boomers (those born between 1946 and 1964) drink more on a daily basis, millennials tend to drink less frequently but engage in more binge drinking, which carries significant risks. This is confirmed by the Spanish Ministry of Health’s 2024 EDADES survey, which explores the different levels of risk associated with different behaviors across generations.
And, as if that weren’t enough, a recent study by Environmental Science & Technology found that many beers contain perfluoroalkyl substances (PFAS). These chemicals, also known as “forever chemicals,” are linked to higher rates of testicular and kidney cancer.
Not Enough Sleep
We sleep less and worse than previous generations. Recent surveys show that millennials and generation Z get an average of 30-45 minutes less sleep per night than baby boomers, largely due to night-time exposure to screens and social media. This artificial light disrupts the release of melatonin, an antioxidant hormone that regulates the cell cycle.
Chronic lack of sleep not only impairs DNA repair, but also reduces melatonin’s protective effects against cancer. Reduced levels of this hormone have been linked to a reduced ability to counteract oxidative DNA damage and increased cell proliferation.
Furthermore, disrupted circadian rhythms interfere with the expression of genes that are key to repairing DNA. This means mutations accumulate over time, increasing the risk of tumor-forming processes.
The Weight Of Stress
Millennials are probably the generation with the highest cortisol levels. When this “stress hormone” remains elevated for a long time, it not only promotes insulin resistance and hypertension, but also weakens the immune system.
Research reveals that chronic stress increases inflammation, hinders the body’s defenses from eliminating abnormal cells, and can even “awaken” dormant tumor cells. In fact, studies in the general population have found that people with higher stress levels are up to twice as likely to die from cancer as those who manage stress better.
The Risks Of Self-Medicating
Lastly, younger generations also resort to self-medication more than previous ones. This poses new short and long-term risks.
Frequent use of paracetamol is linked to increased liver damage and a possible increase in liver cancer. Oral contraceptives, used for very long periods due to delayed motherhood, slightly increase the risk of breast and cervical cancer, although they do protect against ovarian and endometrial cancer.
In addition, prolonged use of antacids and antibiotics has been linked to an increased risk of digestive cancer through indirect mechanisms such as carcinogenic compounds or intestinal dysbiosis (an imbalance in the gut microbiota).
What Does The Future Hold For Millennials?
The projections are worrying. It is expected that cancer cases could rise from around 20 million in 2022 to nearly 35 million in 2050 – an overall increase of almost 77%. The trend is particularly marked in digestive and gynecological tumors, which are becoming more and more common in young adults.
We are the generation of immediacy, anxiety and quick-fix pills, but all is not lost, as we can take control of many of the factors that make us ill, starting today. Adopting healthier habits can reduce risks, and improve our quality of life in a future that is not as distant as we might like to believe.
From dancing the tango to playing video games, there are countless creative ways to promote a sharper, younger mind.
Creative activities like dancing help keep the aging mind sharp. (Credit: kamira777 on Shutterstock)
Researchers have developed a method to calculate whether someone’s brain is aging faster or slower than their chronological age suggests. The technique, called a “brain clock,” works similarly to how a fitness tracker estimates your cardiovascular age based on heart rate and activity levels. But instead of measuring steps, brain clocks analyze patterns in brain activity to predict biological age.
A study published in Nature Communications used these brain clocks to examine whether creative experiences influence brain aging. The findings suggest that people who engage in creative activities, from tango dancing to playing StarCraft II, show signs of delayed brain aging compared to those without such pursuits. The research team analyzed brain data from 1,472 participants across 13 countries, making it one of the largest investigations into creativity and brain health.
The study compared experts and non-experts in four domains: tango dancing, music performance, visual arts, and real-time strategy video gaming. Across all four areas, experts showed what researchers call negative “brain age gaps,” meaning their brains appeared younger than their actual age would predict. The differences were substantial: across domains, experts’ brains looked about four to seven years younger than matched non-experts.
How Brain Clocks Work
Brain clocks rely on machine learning algorithms trained to recognize age-related patterns in brain connectivity. As people get older, certain networks in the brain become less efficient, particularly connections between the frontal and parietal regions. These changes happen predictably enough that artificial intelligence can estimate someone’s age just by looking at their brain activity patterns.
When the predicted “brain age” matches chronological age, it suggests typical aging. When the brain age is higher, it indicates accelerated aging, a pattern seen in many neurological diseases. When brain age is lower than chronological age, it suggests the brain has been preserved better than average. The brain age gap is simply the difference between predicted and actual age—values below zero indicate younger-looking brain patterns.
The research team used electroencephalography (EEG) and magnetoencephalography (MEG) to measure brain activity. These techniques track the electrical signals produced when neurons communicate. From these signals, researchers mapped how different brain regions connect and coordinate with each other. The resulting connectivity patterns served as the input for the brain age calculations.
The Creativity Connection
The researchers didn’t stop at comparing experts to non-experts. They also examined whether the degree of expertise mattered. Musicians were evaluated based on years of experience playing instruments. Gamers were assessed by their league rankings in StarCraft II, a strategy game that requires rapid decision-making and coordination. Visual artists were judged on years of university-level art education. Tango dancers reported months of formal instruction.
Across these measures, a clear pattern emerged: the more skilled someone was in their creative domain, the younger their brain appeared. This dose-response relationship suggests the brain benefits accumulate with practice rather than appearing as an all-or-nothing effect.
A separate experiment tested whether short-term learning could produce similar benefits. Non-gamers participated in 30 hours of StarCraft II training over three to four weeks. After training, their brain age gaps decreased compared to their pre-training measurements. An active control group that played a different game, Hearthstone, showed no such changes. The learners also improved on an attention task unrelated to gaming, suggesting the brain changes translated to broader cognitive benefits.
Players who showed the largest gains in actions per minute, a measure of in-game skill, also showed the greatest decreases in brain age, reinforcing the connection between skill development and brain preservation.
How Creativity Influences Brain Aging
The brain doesn’t age uniformly. Some regions decline faster than others, particularly areas in the frontal and parietal cortex that handle attention, motor control, and coordination. These age-vulnerable regions are also among the areas most affected by neurodegenerative diseases.
The study found that creative experiences particularly affected these regions. Experts showed increased connectivity in the same brain hubs that typically decline with age, suggesting creative activities may provide a protective effect precisely where the brain needs it most.
Different creative domains activated somewhat different brain networks, but all converged on similar age-vulnerable hubs. Across the expertise groups, enhanced connectivity was associated with motor control, movement, rhythm, coordination, and visual processing. The short-term learners showed different patterns, with changes primarily linked to visual perception, object recognition, and attention. Despite these variations, all groups showed enhancement in frontoparietal networks involved in executive function.
The Mechanism Behind the Benefits
The researchers didn’t just document that creative experiences correlate with younger-looking brains. They also investigated potential mechanisms using computational brain models. These models simulate how brain regions interact by incorporating both structural connections, measured through brain imaging, and functional dynamics, measured through electrical activity.
Two properties stood out. First, people with more creative experience showed higher “local efficiency” in their brain networks—tighter, faster communication among nearby regions. This suggests specialized networks have become more refined through practice, allowing quicker and more reliable information processing within expert-related circuits.
Second, long-term experts, but not short-term learners, showed changes in “global coupling,” or stronger long-range coordination across the entire brain. Increased global coupling suggests that creative expertise doesn’t just refine isolated networks but improves communication throughout the brain.
These findings align with research on neural plasticity, the brain’s ability to reorganize itself through experience. Creative activities that involve motor skills, attention, rhythm, and coordination may strengthen both local circuits and long-distance connections. The brain becomes not just more specialized but more integrated.
Comparing Short-Term Learning to Long-Term Expertise
The effects of 30 hours of video game training were smaller than the differences between lifelong experts and non-experts. This scaling makes biological sense. Neuroplasticity requires sustained practice to produce lasting structural changes. A month of training can begin the process, but years of engagement drive more substantial reorganization.
Even the smaller effects from short-term learning, however, were accompanied by measurable cognitive improvements. Learners not only got better at StarCraft II but also responded faster on an unrelated attention task, demonstrating transfer effects beyond gaming-specific skills. The control group showed no such brain age changes.
Study Limitations and Future Directions
The research team acknowledged several constraints. The cross-sectional design for the expertise comparisons prevents definitive causal conclusions—it’s possible that people with healthier brains are more likely to pursue and excel in creative activities. While the pre-post learning experiment provides stronger causal evidence, it involved only 24 participants and focused solely on video game training.
Additionally, the research measured brain age but didn’t directly assess clinical outcomes such as dementia risk or cognitive decline over time. Future studies should track participants longitudinally to determine whether delayed brain aging translates into tangible health benefits.
The use of EEG and MEG data from different studies, with varying electrode configurations and recording protocols, introduced technical challenges. However, the consistent findings across different datasets and recording methods suggest the core results are robust rather than artifacts of any particular measurement technique.
The study also couldn’t fully control for all potential confounding factors. Unmeasured factors could still play a role in the observed associations between creative expertise and brain age.
Creativity as Brain Health Intervention
The research adds to growing evidence that lifestyle factors influence brain aging. Previous studies have linked physical exercise, education, and social engagement to healthier brain aging patterns. This study extends those findings to creative and artistic pursuits.
The results may inform public health recommendations. If creative activities genuinely slow brain aging, they represent accessible interventions that many people already enjoy. Unlike pharmaceutical treatments, creative hobbies carry minimal risks and offer additional psychological benefits including stress reduction and social connection.
The cross-cultural nature of the research, spanning 13 countries across Latin America, Europe, and North America, suggests the brain benefits of creativity transcend cultural boundaries. Whether someone practices tango in Argentina or plays video games in Poland, engagement in creative activities appears to support brain health.
The inclusion of video games alongside traditional arts challenges conventional thinking about creative pursuits. Strategy games like StarCraft II require rapid problem-solving, adaptive planning, and coordination, elements that overlap with more conventional creative activities. The findings suggest that what matters for brain health may be the cognitive demands and engagement rather than the specific medium.
When Apple introduced the Retina Display in 2010, the company made a bold claim: the screen packed in so many pixels that the human eye couldn’t discern individual dots. Steve Jobs declared it had crossed a magical threshold—matching the limits of human vision itself.
Turns out, that wasn’t quite true.
A study published in Nature Communications reveals that human eyes can detect significantly more detail than tech companies have assumed. Researchers at the University of Cambridge and Meta found that eyes can perceive up to 94 pixels per degree for high-contrast content like text—roughly 50% sharper than the “Retina Display” threshold. Even Apple’s latest iPad Pro, with its Ultra Retina XDR screen, delivers only about 65 pixels per degree when held at a comfortable reading distance.
“This demonstrates that the 60-65 ppd range is not the ‘retinal resolution’ for a display,” the researchers wrote.
The gap matters. For over a decade, the display industry has operated under the assumption that 60 pixels per degree represents the ceiling of human perception. That number came from the standard eye chart test—the familiar poster with progressively smaller letters. Achieving 20/20 vision means resolving details at one arcminute of visual angle, which translates to 60 pixels per degree. But the Cambridge team discovered that younger adults with healthy vision routinely exceed this benchmark. Some participants in the study could see details as fine as 120 pixels per degree.
How Researchers Measured the True Limits of Human Vision
Measuring the true limits of vision required solving a technical puzzle. Digital displays can only reproduce images crisply at their native resolution. Trying to show intermediate resolutions demands digital resampling, which introduces artifacts that contaminate the measurements.
The research team, led by Maliha Ashraf, Alexandre Chapiro, and Rafał Mantiuk, built an inventive workaround: a 27-inch 4K monitor mounted on a motorized track. Moving the screen closer increased the pixels per degree; moving it farther decreased them. The setup was actually a high-tech remake of a 130-year-old experiment from 1894, when researcher Theodor Wertheim used wire gratings on a movable frame to study vision.
Eighteen participants sat in a dark room, watching patterns flash on the traveling display. Patterns consisted of high-contrast gratings—alternating light and dark stripes wrapped in a blurred bubble. Participants identified which of two time intervals contained the pattern, and a computer algorithm adjusted the display distance based on their answers, homing in on the threshold where they could just barely detect the stripes.
The experiment tested three types of patterns: black-and-white, red-green, and yellow-violet. Researchers also tracked how resolution limits changed when participants looked at the center of the screen versus 10 or 20 degrees to the side, simulating the difference between direct and peripheral vision. To confirm the findings applied to real content and not just test patterns, they also measured thresholds using actual text rendered in both standard and dark mode formats. Text results closely matched the pattern results.
Why Your 8K TV Might Be Overkill
Practical concerns emerge when considering display purchases. The research team built a model translating their measurements into real-world viewing scenarios, and the results challenge current industry standards.
Take 8K televisions. The International Telecommunication Union recommends viewing 8K displays from between 0.8 and 3.2 display heights away. But the Cambridge model shows those recommendations are overly conservative. According to the new data, sitting farther than 1.3 display heights from an 8K screen means most people won’t perceive any benefit from the extra resolution. For a 65-inch 8K TV, that’s about 3.5 to 4 feet. At typical couch distances of 8 to 10 feet, most viewers would not see a meaningful sharpness gain over 4K.
Desktop monitors also reveal a gap between current technology and human capability. A typical 27-inch 4K display at arm’s length hovers near 60 pixels per degree—right at the old 20/20 vision standard but well below the 94-pixel-per-degree benchmark the study identified.
Phone screens present an interesting case. At close reading distance, a modern phone like the iPhone 15 nears, but does not meet, the 94-pixel-per-degree average limit for high-contrast detail.
Virtual reality faces the biggest challenge. Most current headsets render well below the eye’s central limit, which is why vendors use foveated rendering. The new data suggests tuning color and luminance differently across the field could provide additional performance benefits.
The Hidden Problem with Video Streaming Quality
One of the study’s more technical discoveries has far-reaching consequences for video streaming and image formats. Standard practice in compression assumes human eyes are much less sensitive to color details than brightness details. Nearly every video format, from JPEG images to H.265 video, reduces color information by half based on this assumption.
The new data suggests this practice needs reconsideration, at least for red and green. The achromatic resolution limit hit 94 pixels per degree, while red-green patterns came in at 89 pixels per degree—a negligible difference. Only yellow-violet patterns showed a substantial drop to 53 pixels per degree.
Current compression algorithms typically cut resolution for all color channels equally. If the red-green channel can be perceived nearly as sharply as black-and-white, current schemes may be discarding visible information. At the same time, the yellow-violet channel could potentially be reduced more than current practice without affecting perceived quality.
Your Peripheral Vision Can’t See Color Nearly as Well
Looking straight ahead delivers the sharpest vision humans can muster. As an object moves toward the edge of the visual field, the ability to see fine details plummets. The study quantified exactly how much and revealed that the drop-off differs dramatically between brightness and color.
For black-and-white patterns, resolution declined 2.3 times between the center of vision and 10 degrees to the side. But for both red-green and yellow-violet patterns, the decline was much steeper—nearly five times at 10 degrees compared to dead center.
By 20 degrees into the periphery, participants could only detect black-and-white patterns at 21 pixels per degree, red-green at 7 pixels per degree, and yellow-violet at just 5 pixels per degree.
These measurements have practical applications for VR and AR displays, which use a technique called foveated rendering. Headsets track where users are looking and render the center of vision in high detail while reducing quality in the periphery. Most foveated rendering systems only account for brightness sensitivity. The new data shows they could save even more computing power by dialing down color resolution more aggressively away from the center of the gaze.
For consumers, the gap between current technology and perceptual limits means room remains for noticeable improvements. Displays that genuinely match human acuity would make text crisper, eliminate the faint pixel grid visible on close inspection of current screens, and remove the subtle blur that viewers might not consciously notice but that affects perceived image quality.
Whether manufacturers will invest in reaching these higher thresholds depends on costs, battery life, and whether consumers will pay for the difference. Phone makers appear closest to the target. TV manufacturers have already exceeded what most people can perceive at typical viewing distances, making 8K a solution in search of a problem for living room setups. Monitor makers and VR developers have the farthest to go.
These limits reflect high-contrast content and a relatively young sample, so real-world perception will vary. But human vision has more resolving power than the industry has given it credit for. Tech companies now have a clearer target, backed by rigorous measurement rather than marketing calculations. Whether they’ll aim for it remains to be seen.
‘It reveals that both intense radiation from around the black holes as well as the high-speed jets they emit can work together to eject gas from the centres of galaxies, potentially shutting down star formation in their central regions and regulating galactic growth.
https://www.thehindubusinessline.com/
A new study led by astronomers at the Indian Institute of Astrophysics (IIA) has found that black hole activities suppress the birth of new stars around it.
Supermassive black holes at the centres of galaxies are known to drive outflows of gas, and astronomers have long studied how feedback processes from these outflows can in turn determine the evolution of these galaxies.
However, a key puzzle has been to understand the relative influence of this gas outflow versus radiation from the central regions on the behaviour and evolution of the host galaxy.
The astronomers have uncovered key insights into these powerful forces shaping the universe. The Department of Science and Technology said that the study reveals that both intense radiation from around the black holes as well as the high-speed jets they emit can work together to eject gas from the centres of galaxies, potentially shutting down star formation in their central regions and regulating galactic growth.
Using cutting-edge archival data from international astronomical facilities like the Sloan Digital Sky Survey (SDSS) Telescope at optical wavelengths and the Very Large Array (VLA) at radio wavelengths, both located in the United States, the researchers studied over 500 relatively nearby galaxies hosting active galactic nuclei (AGN).
“AGN are energetic galaxy centres that emit copious radiation and gas, powered by matter falling onto their supermassive black holes, many millions of times more massive than our Sun,” the department said.
“We found that outflows of warm ionized gas are widespread in AGN, and while radiation from the black hole is the main driver, galaxies with radio jets show significantly faster and more energetic outflows,” said Payel Nandi, a Ph.D. student at IIA and the lead author of the study.
Their investigation further showed that such outflows, which are high-speed streams of gas pushed out from galactic centres, are more than twice as likely in galaxies detected in radio wavelengths (56%) compared to those without radio emission (25%).
