Category: Research Discoveries

‘BPA-Free’ Chemicals Plus BPA Disrupt Lab-Grown Breast Tissue

A drug that new mothers sometimes take for a simple reason, to dry up breast milk they no longer need, may come with an unexpected second payoff: sharply lower odds of breast cancer in the years after childbirth. In a combined analysis of two large European studies, women who received cabergoline shortly after giving birth were about 69% less likely to develop breast cancer than women who didn’t.

Breast cancer that shows up in the years right after pregnancy tends to be more aggressive and harder to treat than cancer diagnosed at other times. Scientists have long known that having a baby early offers long-term protection against breast cancer, but the months right after childbirth actually bring a temporary spike in risk, one that hits hardest for women who had their first child later in life or who carry BRCA1 gene mutations. Until now, no specific method has protected those women during that dangerous stretch.

Researchers from institutions in Spain, Canada, Norway, the United Kingdom, Singapore and the United States, reporting in the journal Cancer Discovery, tested whether cabergoline, already approved to stop lactation, could close that gap. In mice bred to carry a high-risk breast cancer mutation, a single dose of the drug given right after weaning sharply delayed and reduced tumors, a clue that helped explain the pattern researchers later found in women.

How a Single Dose of Cabergoline Cut Breast Cancer in Mice

To test the idea, researchers used mice bred without working copies of two genes that normally guard against cancer: BRCA1 and a second gene called Trp53. Female mice that went through two full rounds of pregnancy, breastfeeding, and the natural recovery period afterward developed tumors later, and less often, than mice that never had pups at all. Tumors appeared around day 224 in mice that had given birth, compared with day 175 in mice that hadn’t. Only 59% of the mothers developed tumors, versus nearly 89% of the childless mice.

Then the team gave a single dose of cabergoline to another group of mother mice right when breastfeeding ended. Tumors took even longer to appear, around 259 days, and only about 28% of treated mice developed tumors. Giving the same drug to mice that had never been pregnant did almost nothing to protect them, which told researchers the benefit was tied specifically to the recovery window after breastfeeding, not some general cancer-fighting effect.

So what’s actually happening inside the breast tissue during that window? After a mother stops nursing, the breast naturally shrinks back down, clearing out the milk-producing cells it no longer needs. In mice carrying the cancer-linked gene mutations, that cleanup process slowed and left behind riskier tissue, including cells with two nuclei instead of one, which are especially prone to becoming cancerous when their normal damage-control systems are broken. Cabergoline noticeably sped up that cleanup: treated breast tissue shrank faster, had fewer risky double-nuclei cells, and showed less overall tissue growth two months later.

Cabergoline also seemed to help the immune system. Breast tissue from the high-risk mice showed signs that T cells, the immune cells that normally hunt down and destroy abnormal cells, had become worn out and less effective. Cabergoline appeared to reverse that pattern. Treated tissue had more active, cancer-fighting T cells and fewer that showed signs of exhaustion. Researchers believe the combination, healthier tissue plus a stronger immune response, helps explain why treated mice developed far fewer tumors.

What Cabergoline Means for Breast Cancer in Real Women

To see whether any of this held up outside the lab, researchers examined medical records from two different European populations. The first came from a primary care database in Catalonia, Spain, covering more than 14,800 women who had their first child at age 30 or older. Of those, 780 had received cabergoline within a month of giving birth. Over an average of eight years of follow-up, only 2 of those 780 women developed breast cancer, compared to 132 cases among the more than 14,000 women who hadn’t taken the drug. After accounting for other risk factors like age, smoking, family history and income, women who’d taken cabergoline still showed roughly a 75% lower risk of developing breast cancer.

A second analysis using the same Spanish database, this time looking at all women within ten years of their first pregnancy regardless of age, told a similar story: 2 cancer cases among 1,604 treated women, compared to 125 cases among nearly 26,000 untreated women.

To make sure the pattern wasn’t unique to one country, researchers checked it against a nationwide registry in Norway covering more than 690,000 women. The results pointed in the same protective direction, though the small number of cancer cases there, 2 among treated women compared to 899 among untreated women, meant the finding didn’t clear the usual bar scientists use to call a result reliable on its own. When the team combined the data from both countries, the pooled analysis showed an estimated 69% reduction in breast cancer risk linked to cabergoline use after childbirth.

Source : https://studyfinds.com/common-lactation-drug-linked-to-sharply-lower-breast-cancer-risk/

Gut Bacteria May Send Messages to Muscles, and Yogurt Could Join the Conversation

An afternoon nap is one of the small comforts of getting older, but these findings may make many think twice about their next nap. A new study that tracked nearly 1,000 older Americans for up to a decade found that people who napped most days or every day had a 48% higher risk of developing dementia than people who rarely or never napped.

Nodding off by accident carried its own warning sign. Older adults who said at least some of their naps happened without meaning to had a 39% higher dementia risk, while people who only took planned naps showed no clear link once their health and nighttime sleep were taken into account. By the end of the study, about half of the frequent nappers had developed signs of dementia, compared with roughly 38% of people who skipped naps.

Some 6.9 million older Americans are estimated to live with dementia, a number expected to roughly double by 2060. Poor nighttime sleep is increasingly recognized as a risk factor, but research on daytime napping has produced mixed results, with some studies finding harm and others finding none or even a small benefit from short naps. This study cannot prove that napping causes dementia, since it observed people’s habits rather than changing them. Still, it puts frequent and unplanned napping on the radar as a possible early clue.

A 10-year study of napping and dementia risk in older adults

Researchers led by Johns Hopkins University drew on the National Health and Aging Trends Study, a national survey of Medicare recipients age 65 and older who have been interviewed in person every year since 2011. In 2013, 1,623 of those participants were picked to answer an extra set of sleep questions, including several about napping. After setting aside people with missing information or signs of dementia at the start, the team followed 995 participants through 2023. About 60% were women, roughly 78% were non-Hispanic white, and about 16% were Black. Statistical weights were applied so the results would better reflect older Americans as a whole.

No one received a formal dementia exam from a doctor as part of the study. Instead, the survey used a validated scoring system that combines three sources: whether a participant or family member reported a dementia diagnosis, a short questionnaire answered by a relative or caregiver, and simple tests of memory, orientation (knowing the date and who the president is), and planning skills measured by drawing a clock. People who scored poorly in one of those three thinking areas were classified as having “possible” dementia, and stronger evidence earned a “probable” label. Researchers counted both. Over a median follow-up of five years, 417 of the 995 participants, about 42%, developed possible or probable dementia.

Three ways researchers measured napping habits

Instead of a simple yes-or-no question, the team looked at napping three ways. Frequency came first: people who napped “never” or “rarely” in the past month counted as non-nappers, “some days” made someone an infrequent napper, and “most days” or “every day” made someone a frequent napper. Intention came next. Nappers who said their naps were planned were labeled intentional nappers, while those who fell asleep without meaning to, or reported a mix of planned and unplanned naps, were labeled unintentional nappers. Length was the third measure, with naps sorted into 30 minutes or less and longer than 30 minutes.

Intention matters because a scheduled rest after lunch can be a lifelong habit, while dozing off unexpectedly may point to sleepiness driven by poor nighttime sleep or other health problems. Unintentional nappers in this study fit that second pattern. Compared with non-nappers, they had more chronic health conditions, higher body weight, more symptoms of depression, a higher risk of sleep apnea (a disorder in which breathing repeatedly stops and starts during sleep), and more frequent daytime sleepiness.

Frequent and accidental napping tied to higher dementia risk

Raw numbers showed a clear gap. About 51% of frequent nappers developed possible or probable dementia, compared with 42% of infrequent nappers and 38% of non-nappers. Frequent nappers also tended to carry more weight, have more health conditions, and report more depressive symptoms, so researchers adjusted for those differences along with age, education, smoking, anxiety, nighttime sleep length, daytime sleepiness, and sleep apnea risk. After all those adjustments, frequent nappers still had a 48% higher risk than non-nappers. Infrequent napping showed no clear link.

Unintentional napping held up through every round of adjustment, ending with a 39% higher risk. Planned napping looked risky at first, but that connection faded once health and sleep factors were added to the analysis.

Nap length produced a mixed result. Naps of 30 minutes or less were linked to a 40% higher dementia risk after all adjustments. Naps longer than 30 minutes showed a similar link at first, but it weakened once nighttime sleep, daytime sleepiness, and sleep apnea risk were factored in. In the authors’ view, a possible explanation is that longer naps may be more about making up for bad nights, so their link to dementia may really reflect poor nighttime sleep.

When researchers looked at individual thinking skills, memory showed the most consistent pattern. Frequent napping, unintentional napping, and short naps were all tied to a higher risk of developing memory problems. Napping showed no link to orientation problems, and results for the clock-drawing planning test were inconsistent.

Source : https://studyfinds.com/napping-most-days-higher-dementia-risk/

For decades, one number has largely decided who gets labeled as having obesity: body mass index (BMI), a formula built from height and weight. A new study of nearly 800,000 people found that the number tells a very different story depending on age. Among adults ages 65 to 74, 52% met a newer definition of obesity that accounts for excess body fat and related health problems, far more than the 34.4% flagged by BMI.

Published in eClinicalMedicine, a journal in the Lancet family, the analysis found the pattern flips at the other end of life. Young children were less likely to qualify under the new definition than BMI alone would indicate.

That gap matters because a label steers care. Under BMI alone, many older adults with weight-related health problems may go uncounted, while some children may be labeled before any problems show up.

Clinical Obesity Requires Excess Body Fat Plus Signs of Related Health Problems

A group of international experts, the Lancet Diabetes & Endocrinology Commission, proposed the definition, called clinical obesity, in 2025. It asks two questions. First, does the person carry excess body fat, confirmed by more than BMI, such as waist size? Second, does the person have signs of related health problems, such as high blood pressure, trouble with the heart, liver, or kidneys, or difficulty with everyday tasks like bathing and getting dressed? The approach treats obesity as a chronic disease rather than only a risk factor for other illnesses. Excess fat without those signs is called preclinical obesity.

A team led by the Murdoch Children’s Research Institute in Australia applied the definition to records from 11 existing health studies in Australia, Canada, Estonia, Finland, the Netherlands, the United Kingdom, and the United States, collected between 1996 and 2023. The records covered children and adults ages 4 and older, including 97,071 children. Until now, research on clinical obesity in children amounted to a single study of 111 kids in Mexico.

Clinical Obesity Overtook BMI-Defined Obesity Starting at Ages 55 to 64

Among young children, the new definition was the stricter one. At ages 4 to 5, 3.7% met the clinical criteria versus 8.8% by BMI. BMI counted more people through middle age. At ages 35 to 44, for example, 26.3% met the BMI cutoff versus 15.1% under the clinical definition, and preclinical obesity peaked there at 27.5%. Then clinical obesity pulled ahead in the 55-to-64 group, and the gap kept widening with age, even as clinical obesity itself peaked at ages 65 to 74.

Men and women followed different paths. Men had higher rates from the late teens through their mid-40s, including 18.6% versus 13.9% for women at ages 35 to 44, and women overtook them after age 55. At ages 65 to 74, 57.1% of women met the criteria compared with 44.1% of men. The authors say survival bias (people who live longest may differ from those who do not) and gaps in the data may partly explain women’s higher late-life numbers. UK Biobank, the largest data set, included no one older than 73. Education made a smaller difference, with slightly higher rates among people with less schooling.

Raised Blood Pressure Was a Frequent Sign of Clinical Obesity, Even in Children

Among people who met the clinical definition, raised systolic blood pressure, the top number in a reading, was common at every age and appeared in 87% of tested children ages 4 to 9. Other signs followed life stages: abnormal liver blood tests in early and middle adulthood, kidney-related findings in childhood and after age 75, and joint and muscle problems among the oldest participants.

In the adult groups with complete body measurements, nearly everyone with clinical obesity also had a waist measurement that was large relative to height. A tape measure may be a handy way to spot excess body fat, although waist size alone cannot establish clinical obesity.

Source : https://studyfinds.com/new-obesity-definition-fewer-children-more-adults/

Most people might picture ADHD as a fidgety kid who can’t sit still in class, not a 70-year-old at a memory clinic. A large new study suggests those two pictures may be more closely connected than most of us realize.

Researchers combed through the health and genetic records of more than 187,000 Americans aged 50 and older. They found that adults with an ADHD diagnosis were more than four times as likely to develop dementia or mild cognitive impairment, an early stage of memory and thinking problems. The link didn’t rest on medical charts alone. People whose DNA carried more ADHD-linked genetic variants also faced a higher risk, giving the researchers a second, independent line of evidence pointing the same way.

ADHD was long treated as a childhood condition people simply outgrow. Doctors now recognize it can last a lifetime, yet it has been studied far less in older adults than in children. This research, published in JAMA Psychiatry, adds new weight to the idea that ADHD may matter for brain health decades down the road. It doesn’t prove that ADHD causes dementia, and the numbers come with real caveats. But it raises a fair question for the millions of adults living with ADHD: should their memory be watched more closely as they age?

How Researchers Studied ADHD and Dementia in 187,000 Older Adults

Scientists used the All of Us Research Program, a large federal health database that combines medical records with genetic information from volunteers across the U.S. Everyone in this study was 50 or older at the start of the period researchers analyzed. Their health records covered about 10 years on average, drawing on data collected from 1985 through late 2023.

Of the 187,341 people included, 3,026 had an ADHD diagnosis in their records, about 1.6% of the group. To count, the condition had to show up more than once, through repeated diagnoses or medication records on separate occasions. That stricter standard makes it less likely that a single stray billing code would land someone in the ADHD group. The team then tracked who went on to develop mild cognitive impairment or full-blown dementia.

The researchers also gave everyone a genetic score for ADHD. The score adds up many small DNA differences that, on average, show up more often in people with ADHD. A high score doesn’t mean someone has ADHD; it means their genes lean in that direction. That gave the researchers a second way to test the connection, one that doesn’t depend on whether a doctor ever made a diagnosis.

Finally, the team worked to rule out other explanations. They accounted for physical and mental health conditions, education, smoking, and how often people saw a doctor. They also checked whether some ADHD diagnoses might really be early dementia symptoms mistaken for ADHD, a problem researchers call reverse causation. To test this, they required a gap of one to 10 years between an ADHD diagnosis and any later diagnosis of cognitive decline.

How Much Does ADHD Raise the Risk of Memory Problems?

Among people with ADHD, 6.7% developed cognitive impairment during the study, compared with 3.4% of those without it. Put another way, about 93 of every 100 people with ADHD did not develop memory or thinking problems during the years their records covered. The higher risk shows up clearly in the data, but it isn’t destiny.

So where does “four times” come from? The raw percentages don’t account for age. People with ADHD in the study were about four years younger on average, and younger people are less likely to develop dementia over any given stretch of time. Once researchers compared people at the same ages and adjusted for sex, race, and a well-known Alzheimer’s risk gene, people with ADHD had more than four times the risk. When the researchers looked at dementia on its own, the risk was about three times higher.

That number shrank as the team accounted for more possible explanations. ADHD often travels with depression, anxiety, substance use disorder, and bipolar disorder, and people with ADHD in this study had far higher rates of all four. Factoring in those conditions brought the risk down to roughly three times. A model that also included education, smoking, physical health conditions, and doctor visits landed in the same place. In the strictest test, each person with ADHD was matched with two similar people without it, and the risk was a little more than double. Through all of these checks, the link never disappeared.

The pattern held across men and women and across racial and ethnic groups, though its strength varied. It also showed up in people with and without APOE4, the best-known genetic risk factor for Alzheimer’s disease, and the study found no clear sign that the gene changed the strength of the link. The authors say that hints ADHD may be tied to brain health through a path at least partly separate from that gene.

The reverse causation test produced mixed news. The link shrank steadily as the required gap between diagnoses grew. With a gap of up to eight years, the link stayed statistically meaningful, though people with ADHD now had about a 44% higher risk, down from more than four times. At nine years it was no longer statistically meaningful, partly because most cases had dropped out of the analysis by then. The authors say some of the overall link could still reflect early dementia being mistaken for ADHD.

What ADHD Genes Revealed About Dementia Risk

The genetic data pointed the same way, though the effect was smaller. People whose DNA placed them in the top fifth for ADHD genetic risk had a 35% higher risk of developing cognitive impairment than those in the bottom fifth.

A 35% bump sounds modest next to “four times,” and it is. It matters for a different reason. A medical chart can be skewed by who gets diagnosed, who sees doctors often, and how carefully symptoms get written down. A genetic score sidesteps those problems, and early dementia can’t change someone’s DNA. When two very different kinds of evidence point in the same direction, scientists tend to take a link more seriously.

The authors add a word of caution, though. ADHD-linked genes overlap with genes tied to other psychiatric and developmental traits, so the score may capture more than ADHD alone. The genetic link was also clearest in people of European and African ancestry. The score was built mostly from European-ancestry data, and results in other ancestry groups were less clear.

What Life Looks Like After a Memory Diagnosis With ADHD

Life also looked harder for people who had both ADHD and memory problems. Among those who developed cognitive impairment or dementia, having ADHD was linked to about 70% higher odds of reporting subpar mental health and quality of life on a standard health survey. It was also linked to more than double the odds of reporting subpar social satisfaction.

In the year after their memory diagnosis, people with ADHD made about a third more outpatient visits than people with cognitive impairment alone. They also made about 20% more doctor visits overall, even after accounting for how often they had seen doctors beforehand. The authors suggest that a lifetime of ADHD-related struggles with planning and organization may stack on top of new memory loss, leaving this group in need of extra support.

Source : https://studyfinds.com/adhd-linked-4-times-dementia-risk-mild-cognitive-impairment/

Marijuana is supposed to mellow people out, yet for some users a hit brings dread instead of calm. A new mouse study points to why: a single dose of a cannabis-like drug made fear-related brain cells fire harder, and switching those cells off stopped the drug from driving the animals to avoid a threatening smell. Freezing in fear, though, kept happening even with those cells shut down, pointing to two separate brain pathways for two different panic responses.

Researchers at Northwestern University, writing in the journal Nature Communications, traced the effect to a small group of neurons in the central amygdala, a deep brain region built for processing threats. A cannabinoid drug weakened the natural calming signal that normally keeps these cells quiet, making the fear cells far easier to excite and setting off bursts of activity tied to approaching, fleeing and freezing behavior.

Beyond the mouse cage, the findings carry weight for people. Cannabis use has climbed sharply in recent years, and a study tracking 12 million people found that cannabis-related emergency room visits were linked to about three times the risk of a later medical visit for an anxiety disorder. This new research cannot prove cannabis causes anxiety in humans, but it lays out, cell by cell, one way the drug could push a calm high toward sudden panic.

How Scientists Linked Cannabis and Anxiety in the Lab

To study this, the team used a lab-made drug called CP55940, which activates the same brain receptor as THC, the main mind-altering chemical in marijuana. Mice received different doses of the drug or a plain control solution, then were exposed to a chemical that mimics predator odor, a standard way to trigger natural fear in rodents without using an actual predator. Researchers tested both male and female mice, with roughly 18 to 22 animals per dose.

Researchers tracked how much the mice moved, whether they froze, and how much time they spent avoiding the area with the strongest smell. A low dose made the mice slightly more active, while the highest dose slowed them down. Higher doses increased freezing and avoidance across the board. Even so, the animals largely kept their ability to move, so the extra freezing and avoidance weren’t simply the drug slowing them down.

Fear Cells Light Up After Cannabis Exposure

A closer look came next. Researchers used a tiny camera mounted on each mouse’s head, letting them watch individual brain cells fire in real time while the animal moved freely. They focused on cells in the brain’s fear center that release a signaling chemical called somatostatin, nicknamed SOM cells, which earlier work had already tied to fear, avoidance, and freezing.

After the mice got the cannabinoid drug, these SOM cells fired in stronger bursts, and at the highest dose, more of them switched on overall. These cells also stopped acting in sync, splitting into competing activity patterns rather than firing as one unit.

When the mice were then exposed to the predator smell, these same cells showed busier, more layered responses tied to approaching, fleeing, and freezing. A computer model trained on this brain activity could predict, just by watching the cells fire, whether a mouse had taken the drug, especially as it approached the smell. These cells also began tracking more information at once, such as the mouse’s location combined with whether it was moving, and this effect grew stronger at higher doses.

How Cannabis Loosens the Brain’s Natural Brake

To confirm these fear cells were driving the behavior, not just along for the ride, researchers used a tool that blocks these SOM cells from sending signals, then compared those mice with a control group.

With those cells silenced, the cannabinoid drug could no longer make mice avoid the smell more. But freezing told a different story: the drug still increased freezing even with the cells switched off. That split points to more than one brain route for processing a threat. The drug appears to boost avoidance through this group of cells, while its effect on freezing seems to run through other brain circuits.

Lab experiments on thin slices of brain tissue revealed how. Normally, these fear cells receive a steady calming signal from neighboring cells, carried by a brain chemical called GABA, which acts like a built-in brake and keeps them from firing too easily. The cannabinoid drug weakened that brake. With less resistance holding them back, the fear cells became easier to excite. When researchers blocked the GABA brake directly with a separate chemical, they saw the same jump in cell activity that the cannabinoid drug produced, and combining both treatments didn’t push activity any higher than either one alone, pointing to that same natural brake as the route behind the drug’s effect.

Source : https://studyfinds.com/how-cannabis-can-flip-brains-calm-into-sudden-panic-new-study-shows/

 

Crack. One sharp pop from a pulled finger, and someone nearby is bound to issue the old warning: keep doing that and you’ll end up with arthritis. A sound that loud seems like it must be doing damage.

Doctors who studied the habit in 1990 wrote that the arthritis link had long been considered “an old wives’ tale” with no experimental support behind it. Starting with their study of 300 patients, researchers have tested the idea several ways. They have compared hand X-rays of crackers and non-crackers, measured grip strength and swelling with examiners kept unaware of who cracked, and watched a knuckle crack inside an MRI scanner.

None of the human studies has found that habitual cracking raises the risk of hand arthritis. One older finding, that crackers had weaker grips and more hand swelling, was not reproduced in a smaller, blinded study. And imaging suggests the pop itself comes from a pocket of gas forming in the joint fluid.

Does Cracking Actually Lead To Arthritis?

No, based on the available human evidence. Most of that research has looked at osteoarthritis in the hands, the most common type of arthritis, rather than every disease that falls under the broad label “arthritis.”

You’ve probably heard that the sharp pop is a sign of joint damage. If that were true, people who crack their knuckles for decades should have more arthritis than people who don’t. Studies have not found that pattern.

In 1990, Jorge Castellanos and David Axelrod of Mount Carmel Mercy Hospital in Detroit examined 300 patients ages 45 and older for Annals of the Rheumatic Diseases. Of those patients, 74 had cracked their knuckles habitually, on average for 35 years, and 226 had not. Based on medical histories and physical exams, hand arthritis was no more common among the crackers.

A 2011 study in the Journal of the American Board of Family Medicine took a different approach. Researchers surveyed 215 people ages 50 to 89 who had hand X-rays on file. Some had osteoarthritis visible on those X-rays and some did not. Participants described how often and for how long they had cracked their knuckles. Neither the number of years someone had cracked nor their total cracking exposure (how often per day, multiplied by years) was significantly linked to osteoarthritis in the joints they cracked.

Both of these were observational studies. Researchers looked at people’s existing habits and health rather than assigning anyone to crack their knuckles. A 2018 review in Clinical Anatomy summed up the field this way: the evidence on knuckle cracking and osteoarthritis comes mainly from observational studies, and those studies have failed to show a link.

What Is Making That Popping Sound?

A pocket of gas forming inside the joint, according to a 2015 MRI study in PLOS One. A University of Alberta-led team put one adult man’s fingers, one at a time, into a finger trap attached to a cable. Inside an MRI scanner, the cable slowly pulled on each of 10 knuckles until it cracked, while the scanner recorded what happened inside the joint.

At the moment of each crack, the joint surfaces separated quickly and a dark, gas-filled space appeared in the fluid between them. That space was still visible after the sound. The researchers said this fits a process called tribonucleation. Two surfaces coated in fluid cling together until enough force pulls them apart all at once. The pressure in the joint fluid drops, and dissolved gas comes out of the fluid. The findings challenged the older idea that the crack comes from a bubble collapsing.

The question is not fully settled. The 2018 Clinical Anatomy review found agreement that a bubble forms, but said it is still unclear how the bubble forms and what produces the sound. And because the MRI study involved one person, it offers an explanation for the noise, not evidence about long-term health effects. The Alberta team also noted a puzzle in the research. The energy released by a crack has been thought to exceed the level that can damage joints, yet habitual knuckle cracking has not been shown to increase joint degeneration.

The pop is also a different event from osteoarthritis. The National Institute of Arthritis and Musculoskeletal and Skin Diseases describes osteoarthritis as a joint disease that happens when the tissues in a joint break down over time.

Could The Habit Cause Other Problems?

Possibly, but the two studies that looked most closely disagree. In the 1990 Detroit study, habitual crackers were more likely to have hand swelling and lower grip strength. The authors concluded that the habit “results in functional hand impairment.” But the crackers in that study were also more likely to do manual labor, bite their nails, smoke and drink alcohol. That makes it hard to tell whether cracking itself caused the difference.

A 2017 study in Clinical Orthopaedics and Related Research, led by researchers at the University of California, Davis, tested those findings more directly. The team examined 400 knuckle joints in 40 adults with no hand symptoms. Thirty cracked their knuckles daily and 10 did not. Two orthopedic surgeons who did not know which participants were crackers checked grip strength, swelling and range of motion before and after participants tried to crack their knuckles. Everyone also filled out a standard questionnaire about arm, shoulder and hand problems.

Source : https://studyfinds.com/does-cracking-knuckles-cause-arthritis-the-research-2180/

 

Who comes to mind when you think of someone emotionally intelligent? Someone who can read a room, defuse an argument, and who knows exactly what to say when a friend is struggling? For many people, that person is a woman. It’s such a widely held belief that popular psychology treats it as fact.

We decided to put that assumption to the test. Our new study reviewed nearly three decades of research, from 1995 to 2023, across 76 countries and more than 600,000 people. We wanted to answer a simple question: are women really more emotionally intelligent than men? The headline answer is yes, on average, women score higher.

But the more useful finding is the type of emotional intelligence women seem to excel at, and what it potentially costs the people who have it.

Emotional intelligence is the ability to recognize, understand and regulate emotions in yourself and in others. When we looked at each element of emotional intelligence, the female advantage turned out to be concentrated in the “others’ feelings” half of the equation.

This means recognizing what someone else is feeling, understanding why, and helping them manage it. A child has a meltdown, a colleague goes quiet after their idea gets dismissed in a meeting, a negotiation gets tense. Plenty of men are excellent at this too, and plenty of women aren’t; these are averages across hundreds of thousands of people, not predictions about any one person in the room.

Is that gap simply biology? We can’t rule biological or hormonal factors out entirely. But two patterns in our data point elsewhere. The female advantage is far smaller in children than in adults, and this gap has been narrowing across the three decades our data spans. That’s not what you’d expect from something fixed at birth. Although the data in our study cannot tell us the exact reasons these differences emerge, this pattern aligns with what you’d expect from something shaped through practice.

There’s a plausible source for that practice, too. Other research has found that parents use a wider vocabulary of emotion words with daughters than sons, and more often encourage girls to reflect on and articulate their feelings.

Boys, meanwhile, are more often steered toward managing emotions by suppressing them. Their sisters are encouraged to work through it with other people – exactly the kind of social and emotional skill our data shows women excel at.

Put simply, girls appear to get more practice reading and responding to other people’s emotions, starting early in life. Like any skill built through repetition, whether it’s learning a new language or picking up a new instrument, the more you practice, the more natural it becomes.

In fact a 2019 meta-analysis of 58 studies found that emotional intelligence can be trained. Gender didn’t seem to impact the effectiveness of learning how to be more emotionally intelligent.

That’s good news. If emotional intelligence is a trainable skill rather than a fixed trait, the gap isn’t destiny. That means men can benefit from these skills too, including in negotiations and at work.

But there’s a less comfortable implication, too. If women’s advantage here goes unrecognised as a skill and gets treated instead as “how women are”, it becomes very easy to take for granted. The colleague who’s good at defusing tension becomes the one who’s always expected to do so. A capability quietly turns into an obligation: unpaid and unrewarded.

This plays out in the workplace every day. Organizations benefit when employees manage team tension, support stressed colleagues and smooth over conflict. It is work that keeps a team functioning but almost never shows up in a performance review.

Source : https://studyfinds.com/women-more-emotionally-intelligent-than-men-and-thats-problem-landmark-study/

The study identified two ways to reduce the environmental impact of medical devices: improving product design and making their use more efficient.

Medical e-waste is emerging as a global challenge, with much of it not being recycled due to concerns over contamination, according to a study by the Waste Electrical and Electronic Equipment (WEEE) Forum.

Electronic devices are increasingly used in healthcare, from diabetes sensors and blood pressure monitors to wearable drug-delivery systems.

Globally, 6.2 crore tonnes of e-waste is generated annually, a figure expected to rise to 8.2 crore tonnes in the next five years, according to the United Nations.

The study, Digital Health in Circular Economy, noted that medical devices contain electronics, batteries, metals and other valuable materials that could be recovered. However, much medical e-waste is incinerated, limiting opportunities to recover materials or reuse components.

Researchers assessed five devices across their life cycles, including manufacturing, packaging, transportation and end-of-life. For three devices, they also examined their wider healthcare use.

In the case of an endocutter, a surgical stapling device used to cut and seal tissue, printed circuit boards accounted for 92% of the mineral and metal resources used. The study said redesigning such devices for use across multiple procedures could significantly reduce waste.

The study identified two ways to reduce the environmental impact of medical devices: improving product design and making their use more efficient.

For ECG lead sets attached to patients, 200 monitoring procedures using single-use sets resulted in a climate impact equivalent to 97 kg of carbon dioxide. Plastics, metals and cable insulation were the main material contributors. Moving from single use to any form of reuse could reduce environmental impacts by 81% to 94%, the study found.

Source : https://www.deccanherald.com/environment/medical-devices-need-redesign-for-reuse-recycling-study-4175821

Air Quality Plans Focused on Tailpipes May Be Missing Summer Pollution Sources

Yeast From Invading Fruit Flies Gives Off Scents That Beat a Known Pest Repellent

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Going Remote Is Making Many Workers More Sedentary, Study Suggests

On the days hybrid workers stay home instead of going into the office, they sit for about 44 extra minutes and get roughly 58 fewer minutes of light and moderate-to-vigorous activity combined, according to research published in the International Journal of Behavioral Nutrition and Physical Activity. The study puts hard numbers on something many remote workers have long suspected: working from home quietly drains movement out of the day.

Researchers tracked 97 university employees who split their weeks between office and remote work, having each person wear a small sensor on the thigh for seven days to track sitting, standing, walking, and other activity, while participants separately logged when they went to bed and woke up. Because the same people were compared against themselves on different types of days, the study could isolate what changes when someone swaps an office desk for a home setup, rather than relying on guesses about how active people felt they had been.

A consistent pattern emerged: remote days brought more sitting, less standing and light movement, and less harder exercise, along with just a small bump in time spent resting or in bed.

Thigh-Worn Sensors Captured a Week of Real Movement
Instead of asking people to fill out surveys about their habits after the fact, the research team had participants wear a small motion-tracking device on the thigh for a full week. The device could tell the difference between sitting, standing, walking, and harder movement based on the angle and motion of the leg. Participants reported their own bedtimes and wake times separately, since the sensor couldn’t capture sleep on its own.

Each person logged a mix of office and remote workdays over the week, averaging a little more than two of each, enough to make a solid comparison. The group was mostly women in their early forties, all employed at a university where hybrid schedules had become common.

A full day always adds up to 24 hours no matter how that time gets divided between sitting, sleeping, standing, or moving. To account for that, the researchers used a statistical method built for exactly this kind of back-and-forth data. Rather than comparing single numbers, like total minutes of exercise, the method looks at how all the different activities balance against each other, since more time spent on one behavior always means less time for something else.

Remote Workdays Tipped the Balance Toward Sitting
Clearest of all was the difference in the balance between active behaviors, meaning light movement and harder exercise, and passive ones, meaning sitting and lying down. That balance tipped toward passivity on remote workdays. A typical office day included roughly 10.6 hours of sitting and 49 minutes of more vigorous activity. Remote days brought extra sitting, less light movement, and less vigorous activity, along with a modest bump in rest time.

Sitting and lying down in bed, by contrast, didn’t shift in any meaningful way between the two types of days. It was the shift from standing and moving to sitting still that stood out. The researchers pointed out that this pattern likely reflects the built-in structure of an office day, where commuting, meetings, and other routine interruptions break up long stretches of sitting in ways a home office often doesn’t.

A follow-up look at the data hinted that people who normally bike or walk to work felt the change more sharply. Outside of work hours on remote days, that group’s sedentary time crept up by roughly half an hour, more than four times the shift seen in people who usually drive or take transit, while their vigorous activity dropped by about 18 minutes. Losing a regular bike commute, in other words, may leave a bigger hole in the day than losing a drive.

Small Changes Could Help Offset the Lost Movement
Sitting less isn’t just an abstract wellness talking point. This study did not measure health outcomes directly, but the researchers point to earlier research showing benefits from breaking up sedentary time with physical activity, and note that more sitting and less activity during remote work could be tied to less favorable metabolic effects over time. The extra time in bed recorded on remote days was modest compared with the drop in movement, though the study wasn’t designed to determine whether that trade-off ultimately helps or harms health.

None of this means remote work is bad for health. It does suggest that hybrid workers may want to be deliberate about building movement into remote days, since it doesn’t happen as naturally as it does inside an office building. Standing during phone calls, taking a walk instead of a coffee break, or scheduling short movement breaks could help close the gap. The takeaway is simple: the ease of working from home comes with a quiet trade-off in daily movement, one that hybrid workers might benefit from managing on purpose rather than letting it slide.

Source: https://studyfinds.com/working-from-home-less-movement/

Six Minutes of Reading May Cut Stress by 68%, Research Review Says

People reach for a book to calm down more often than they reach for a glass of wine or a hot bath, according to a new editorial pulling together decades of research on reading and mental health. One 2015 survey found that just six minutes of reading was tied to a 68 percent drop in stress levels.

Published in the journal Psychological Medicine, the editorial comes from researchers at the University of Cambridge and The Queen’s Reading Room. Rather than running a new experiment, the authors combined survey findings, brain scans, and long-term health studies to argue that reading for pleasure may be more than a hobby, and could function as a low-cost habit that supports well-being.

Their conclusion goes beyond stress relief. People who read regularly for enjoyment tend to report more empathy and less loneliness, and older adults who keep reading appear to face a lower risk of memory decline. Some of these patterns held up regardless of income or education level, though the authors are careful to note that most of this evidence shows associations rather than proof that reading directly causes the outcomes.

Decades of Surveys and Brain Scans Build the Case for Reading
That case draws on survey data, memory and attention tests, brain scans comparing readers with non-readers, and studies that tracked the same groups of people for years or decades.

One survey of more than 4,000 adults asked about reading habits and well-being. Another followed close to 2,000 people in a shared reading program. Several studies gave cognitive tests to adults over 55, and a few tracked groups for a decade or more to see whether early reading habits predicted health later in life.

Reading and Mental Health Findings Beat Wine for Stress Relief
In the survey behind the 68 percent figure, reading ranked as the most popular way people said they relax, with 38 percent picking books as their go-to method for unwinding. More people in that survey said they turned to books for comfort (35 percent) than to a glass of wine (31 percent) or a hot bath (10 percent).

Reading also appeared tied to empathy and emotional steadiness. Nearly two-thirds of readers said reading helped them better understand other people’s feelings, compared with fewer than half of non-readers, and half said books made them more open to beliefs different from their own. Loneliness came up too: in a separate reading-group survey, nearly three-quarters of participants said reading helped their overall well-being, and more than 40 percent felt more connected to others.

Reading and Brain Health Improve With Age, Long-Term Studies Show
Several long-term studies followed groups of older adults for years, checking their mental sharpness against how often they read. One study that followed 801 people 65 and older for four and a half years found that engaging in activities such as reading newspapers, magazines, and books was associated with a 33 percent lower risk of Alzheimer’s disease. A separate study of 469 people 75 and older found that reading specifically was linked to a 35 percent lower risk of dementia over about five years.

More recent work suggests reading may also help narrow some of the cognitive differences associated with education. In a study of nearly 2,000 adults over 64 followed across 14 years, frequent reading was linked to a slower rate of decline across all education levels. Picking up a book regularly might help offset some of the disadvantages tied to having less schooling.

Early Reading Habits Shape Kids’ Attention and Well-Being
Using data from more than 10,000 adolescents in a major long-term study, researchers found that just over half had read for pleasure from an early age. Compared with peers who read less, these early readers showed fewer mental health problems, better attention, and improved behavior by early adolescence, along with more sleep and less screen time.

Brain scans backed this up. Kids who read early showed differences in brain regions tied to language, emotional control, and decision-making. Those patterns remained even after researchers accounted for family income, parental education, and several other factors.

Still, the editorial points to a troubling trend: reading among children and teenagers is declining, possibly to its lowest point since records began, with boys 11 to 16 showing an especially steep drop. Kids said they were most likely to pick up a book when it connected to a favorite movie or matched a personal interest, pointing to one possible way to draw young readers back.

Reading for pleasure will not replace medicine or therapy, and most of the evidence here shows links rather than proof of cause and effect. Still, the range of findings, from stress surveys to dementia studies to brain scans of children, points in a consistent direction: something as accessible as opening a book is tied to a calmer mind, a more connected life, and possibly a brain that ages more slowly, a pattern the editorial’s authors say is worth investigating further.

Source: https://studyfinds.com/reading-linked-lower-stress-better-brain-health/

That recurring middle-of-the-night wake-up may feel like a sign that something is off. Yet researchers say it can also be a surprisingly ordinary result of what happens in the body before dawn. It has sparked a larger debate over whether our ancestors once treated nighttime wakefulness as normal.

Is There Actually Something Special About Waking Up At 3 A.M.?
Not one specific clock minute, no. Sleep isn’t a flat, uniform state across the night, and the second half is structurally more fragile than the first. According to a sleep physiology overview hosted by the National Institutes of Health’s NCBI Bookshelf, deep slow-wave sleep dominates earlier in the night while REM sleep’s share of each cycle grows later on, and brief arousals cluster around transitions into and out of REM.

In young, healthy sleepers those arousals are usually minor enough to go unremembered. As that buffer weakens with age or stress, the same ordinary transition is more likely to fully wake someone, which is why a 3 a.m. eye-opening moment can feel oddly specific even though the mechanism is about sleep-cycle structure, not a fixed hour.

What Do Body Temperature And Cortisol Have To Do With It?
Two circadian signals are also moving overnight. Core body temperature reaches its daily low point, or nadir, in the early morning. It’s generally cited as occurring around 4 to 6 a.m. in a circadian rhythms overview compiled by the CDC.

Around the same window, cortisol, the hormone most tied to alertness, begins climbing toward the sharp rise researchers call the cortisol awakening response, detailed in expert consensus guidelines published in Psychoneuroendocrinology in 2016. Neither rhythm is precisely timed to 3 a.m.; the exact hour depends on chronotype and sleep schedule. But for people on conventional hours, those overlapping shifts often land in the pre-dawn window, nudging sleep lighter right when it’s already more fragile.

Could This Be An Old, Deeply Normal Human Pattern?
There’s a genuinely interesting, if contested, historical thread here. Virginia Tech historian Roger Ekirch documented more than 500 pre-industrial references to a “first sleep” and “second sleep” bridged by an hour or more of wakefulness, a pattern that largely disappeared after artificial lighting spread. In the early 1990s, NIMH researcher Thomas Wehr tested whether this had a biological basis: 16 participants, mostly men in their 20s and 30s, were confined to 14 hours of darkness nightly for a month, mimicking a natural winter night. By the fourth week, as reported by Scientific American, participants had settled into two roughly four-hour sleep bouts separated by one to three hours of quiet wakefulness.

That finding hasn’t gone unchallenged. A 2023 reassessment in the peer-reviewed journal Medical History argued that the historical and scientific evidence for segmented sleep as the dominant pre-industrial pattern is more selective than commonly presented. The paper notes a 2013 study that put campers under natural light and firelight for two weeks without reproducing Wehr’s biphasic pattern.

A 2010 European survey published in The Journal of Psychosomatic Research found 31.2% of adults already report waking at least three nights a week. The report suggests that broken sleep is simply common, not evidence of a lost ancestral rhythm.

The honest summary: middle-of-the-night waking has a plausible, unproven biological precedent, but isn’t settled science.

What Should You Actually Do About It?
Sleep specialists consistently give unglamorous, practical advice: don’t check the clock or a phone screen, since light exposure suppresses melatonin and makes it harder to drift back off. Keep the room dark and skip bright lights for a bathroom trip. If the pattern comes with daytime fatigue, loud snoring, gasping, or racing thoughts, it’s worth mentioning to a doctor, since those can point to sleep apnea, anxiety, or another treatable condition rather than ordinary sleep architecture doing what it normally does.

Source: https://studyfinds.com/why-you-keep-waking-up-3am-2180/

Einstein’s Gravity Rule Faces Its Toughest Test Yet, Thanks to a Super-Chilled Atom Beam

Six Minutes of Reading May Cut Stress by 68%, Research Review Says

Dirty Air Linked To Higher Glaucoma and Cataract Risk, Large Study Finds

People with autism who rely on Medicaid live to an average age of just 64.9 years, nearly six years shorter than other Medicaid enrollees and almost 14 years shorter than the average American. That’s the central finding of a new analysis of more than two million Medicaid beneficiaries with autism, and it shows just how much shorter life can be for autistic people who depend on Medicaid. The new study, published in the journal JAMA Network Open, set out to close that gap.”

Researchers from Columbia University and the University of Colorado combed through two decades of Medicaid records to answer a question nobody had nailed down before: how long do autistic people actually live, and what is cutting their lives short? Earlier research showed that people with autism die at higher rates than everyone else, but no one had calculated an actual life expectancy number for this group, mostly because the data needed to do it didn’t exist in one place.

Many of those lost years trace back to causes that hit this group far harder than expected. Flu deaths among autistic Medicaid beneficiaries occurred at more than ten times the rate seen in the wider Medicaid population, one of several outsized gaps involving illnesses and accidents that are often preventable or treatable.

How Researchers Measured Autism Life Expectancy

To answer that, the team pulled records from a national Medicaid database that tracks health coverage and links to a federal death registry, so it also captures actual death outcomes. They analyzed Medicaid records covering beneficiaries across all 50 states and Washington, D.C. from 2000 through 2020. Within that pool, they identified 2,048,046 people who had an autism diagnosis on record. Most, about 76%, were male, while roughly 24% were female. The group was racially and ethnically mixed: close to half were white, about 17% were Hispanic, nearly 15% were Black, and the rest identified with other racial or ethnic backgrounds.

Using the same statistical methods insurance companies and demographers use to estimate how long people will live, the researchers calculated life expectancy for autistic Medicaid beneficiaries and compared it with the broader Medicaid population and the general U.S. public. They also compared death rates for specific causes among autistic beneficiaries to what would be expected if they died at the same rate as the general Medicaid population, a way of showing how much more often certain causes of death struck this group.

Inside the Autism Life Expectancy Gap

Life expectancy at birth for autistic Medicaid beneficiaries came out to 64.9 years. The wider Medicaid population lived 5.6 years longer on average, and the general U.S. population lived nearly 14 years longer.

Sex made little difference within the autistic Medicaid group itself. Autistic men lived to about 64.6 years and autistic women to about 65, a small gap. But when researchers compared each group to same-sex peers outside the autistic population, a starker pattern showed up. Autistic women lost about 8.2 years compared to other Medicaid women and 16 years compared to women in the general U.S. population. Autistic men, while still worse off, lost less ground: about 1.9 years compared to other Medicaid men and 11.6 years compared to men generally. Being autistic appears to cost women more years of life relative to their peers than it does men, a disparity the study’s authors said may stem from higher rates of mental health conditions that occur alongside autism in women.

Progress appeared over time. Between the early 2000s and the late 2010s, life expectancy for autistic Medicaid beneficiaries climbed by 1.7 years, from 63.9 to 65.6. The gap with everyone else never closed, though. Then came 2020. Life expectancy dropped for every group that year as the COVID-19 pandemic swept through the country, but autistic Medicaid beneficiaries took the hardest hit of the three groups studied, losing 4.1 years compared to the previous five-year period.

What’s Driving the Higher Death Rates

Autistic Medicaid beneficiaries had a 44% higher risk of death than other Medicaid enrollees. That extra risk wasn’t concentrated in one or two diseases. It showed up almost everywhere researchers looked, though some causes stood out.

Death from flu was more than ten times as common among autistic beneficiaries as would be expected. Malnutrition killed people at nearly eight times the expected rate. A lung condition caused by inhaling food, liquid, or vomit into the airways showed nearly seven times the expected death rate. Accidents unrelated to traffic occurred at more than four times the expected rate, and accidental drowning happened at more than three times the expected rate. Pneumonia deaths were roughly three times higher than expected as well.

These numbers point to something beyond biology alone. Several of the causes with the largest gaps, including flu, malnutrition, pneumonia, and drowning, are often preventable or treatable. Study authors say the findings could guide targeted efforts to cut preventable deaths among autistic people, one of the country’s most at-risk populations.

Source : https://studyfinds.com/autistic-adults-on-medicaid-are-dying-14-years-too-soon-study-finds/

Scroll through TikTok or Instagram for five minutes and there’s a good chance a creator will explain exactly what to eat to look the way they do. A flat stomach. Toned arms. That “glowy” skin. The pitch always sounds simple: copy the creator’s diet, get the creator’s body.

New research suggests that pitch is not only oversimplified but often flat-out wrong, and that it tends to come from people with no business dispensing health advice. A team of Australian researchers, writing in the Journal of Technology in Behavioral Science, analyzed 300 videos tagged with popular healthy-eating hashtags on TikTok and Instagram and found that more than two-thirds contained misleading or deceptive information. Most of that content came from influencers with no dietitian training, nutrition degree, or health credential of any kind, while the small slice of videos made by actual qualified professionals, like dietitians, was far more likely to be accurate.

Researchers weren’t just counting up bad advice for its own sake. They were hunting for patterns connected to orthorexia nervosa, a condition marked by an unhealthy obsession with eating only foods considered “pure” or “clean,” rigid food rules, and distress when those rules are broken. What they found describes a social media world filled with many of the same themes tied to that kind of thinking, hashtag by hashtag, whether the person posting means to or not.

Inside the TikTok and Instagram Diet Advice Study
A research team from Flinders University in Australia searched TikTok and Instagram for the hashtags #healthylifestyle, #nutrition, and #cleaneating between May 25 and 27, 2025. For each hashtag on each platform, they pulled the first 50 videos that came up, skipping duplicates, which added up to 300 total videos: 150 from TikTok and 150 from Instagram Reels. Videos ran about 26 seconds on average on both platforms, so length wasn’t a factor separating the two.

Women were the focus for a reason. They make up a large share of the user base on both apps and face a higher risk of eating disorders, so the researchers zeroed in on content aimed at and featuring women.

Researchers coded all 300 videos against a detailed checklist built to capture signs linked to orthorexia: things like moral language around food (“good” versus “bad” foods), body-focused messaging, restrictive eating rules, exercise habits, and whether the information shared was accurate. Creators were then looked up on Google or LinkedIn to check whether they held any real qualification in nutrition, dietetics, or exercise science, a detail kept hidden during the initial coding so it wouldn’t sway the ratings. To confirm the scoring held up, a second reviewer independently coded a fifth of the videos, and agreement between the two came out very high.

What the Videos Actually Showed
Food and people appeared together in nearly three out of four videos, a format that visually ties eating habits directly to how someone looks. About 36% of videos pushed a specific eating pattern, and 67% emphasized “clean” or “healthy” eating as a core message. Supplements or so-called superfoods showed up in about 75% of videos, and roughly half turned healthy eating into a kind of lifestyle trend, presenting food more like a brand than something to actually eat.

Nearly one in three videos imposed actual food rules or restrictions, telling viewers to hit specific protein targets, cut out entire food groups, or follow rigid patterns like always pairing dinner with a protein source. Moralizing language, the kind that frames food choices as reflections of a person’s character or worth, showed up in about 20% of videos. One creator in the study put it directly: “I eat high-quality foods because I’m a high-quality person.”

Body objectification appeared in 63% of all videos studied, but Instagram was noticeably more intense on this front, hitting 78% compared with 48% on TikTok. Instagram also zoomed in on specific body parts more often and was far more likely to show people with lean, muscular bodies, 70.7% of the time versus 47.3% on TikTok. On Instagram, about one in three videos had creators directly crediting their physique to a specific diet choice, compared with 16% on TikTok. Exercise followed a similar split: Instagram leaned toward strength training and framed workouts around appearance more often, while TikTok leaned toward cardio and framed health in more general wellness terms. Across both platforms, roughly 10% of videos showed exercise that was compensatory or excessive.

Who’s Really Giving the Diet Advice
Perhaps the most telling numbers in the study concern who’s doing the talking. Unqualified influencers made up the vast majority of creators in the sample, a status verified by checking public bios and LinkedIn profiles.

That imbalance mattered for accuracy. Across the full sample, 68% of nutrition and exercise information was rated misleading or deceitful. Qualified creators were far more trustworthy: 45.5% of their content was rated accurate, compared with just 4.7% of content from unqualified influencers. Unqualified influencers were also far more likely to post content rated as misleading, 75.2% versus 40.9% for qualified creators, or outright harmful. One example flagged as harmful showed a creator eating a tiny portion of food captioned “I am so proud of myself when I control what I eat.” Another video, titled “How I lost 2kgs in 7 days,” featured a food diary consisting mostly of liquids and portions as small as one date and eight slices of cucumber for an entire lunch.

Qualified creators, meanwhile, were more likely to post under the straightforward #nutrition hashtag rather than the more lifestyle-branded #healthylifestyle or #cleaneating tags. That means the people best equipped to give sound advice were the least visible under the hashtags most associated with idealized, aesthetic content.

Source: https://studyfinds.com/nearly-70-of-diet-advice-on-tiktok-and-instagram-is-misleading/

This Blood Molecule Predicts How Fast ALS Will Progress

Losing weight can help a struggling liver, but a new study suggests the number on the scale isn’t the whole story. Two people can lose the exact same amount of weight and walk away with very different livers, depending on what they ate to get there.

That’s the takeaway from a new clinical trial that pitted three popular diets against each other: a very-low-carbohydrate ketogenic diet, a Mediterranean diet, and a very-low-fat, plant-forward diet. Researchers had 42 adults with obesity, prediabetes, and fatty liver disease lose about 10 percent of their body weight on one of the three eating plans. Researchers provided all the food directly to participants to ensure they stuck to their assigned diet. The results, published in Cell Metabolism, show that when it comes to a struggling liver, not all weight loss delivers the same drop in liver fat.

All three diets improved how well muscle handled insulin by about the same amount. But the keto diet pulled far ahead for the liver, cutting stored fat and improving blood sugar control by a wider margin than the other two plans. The results point past pounds lost, toward what happens inside the body once the weight is gone, and why the food on someone’s plate might decide how much the liver recovers.

How the Keto Diet Study Worked

Researchers at Washington University School of Medicine recruited 55 adults with what the study calls “metabolically unhealthy obesity,” meaning they carried excess weight along with prediabetes and a buildup of fat in the liver. Of those, 42 people completed the study: 14 on the ketogenic diet, 14 on the Mediterranean diet, and 14 on the low-fat, plant-forward diet. Participants were on average in their early 40s, and each group included nine women and five men.

To ensure people followed their assigned diet instead of just reporting what they ate, the research team’s kitchen prepared and delivered every meal and snack. Participants met weekly with a dietitian, and people stuck to their assigned diet more than 95 percent of the time in every group. That level of control is rare in nutrition research, which usually relies on people accurately remembering and reporting their own eating habits.

In this trial, the ketogenic diet got about 4 percent of its calories from carbs, 73 percent from fat, and 23 percent from protein. The Mediterranean diet ran about 50 percent carbs, 35 percent fat, and 15 percent protein. The low-fat, plant-forward diet was roughly 70 percent carbs, 15 percent fat, and 15 percent protein. Each participant stayed on their assigned diet until they lost close to 10 percent of their starting weight, which took roughly four to five months depending on the group. Their weight was then held steady for a few weeks before final testing.

To measure how well the body handled insulin, researchers used a test that infuses small, controlled amounts of insulin and sugar into the bloodstream while closely tracking blood levels. Researchers measured liver fat with a specialized MRI scan. Researchers also drew blood every hour for a full day, both before and after weight loss, to track how sugar, fat, and hormone levels moved throughout the day, including after meals.

What the Keto Diet Did to the Liver and Blood Sugar

Muscle responded the same way no matter the diet. All three plans improved how well muscle tissue used insulin by about the same amount, roughly 50 percent. Had the study stopped there, it might have looked like any weight-loss diet works equally well.

But the liver told a different story. The ketogenic diet produced a much bigger improvement in how well the liver responded to insulin than the other two diets. Liver fat fell from around 19 percent to about 6 percent in the keto group, a drop of roughly two-thirds. The Mediterranean and low-fat groups also improved, dropping to roughly 10 percent and 9.6 percent, but the change was smaller.

Blood sugar markers moved in the same direction. A long-term blood sugar marker that reflects average levels over three months dropped by 0.6 percentage points in the keto group, compared with a smaller 0.1-point drop in the Mediterranean group and a 0.4-point drop in the low-fat group. Fasting insulin fell more sharply in the keto group, too. Over a full day, the keto group showed a 20 percent drop in blood sugar exposure, compared with an 8 percent drop in the other two groups, and insulin exposure fell by 74 percent in the keto group compared with 44 percent and 27 percent in the Mediterranean and low-fat groups.

Prediabetes went away entirely, meaning blood sugar returned to a normal range, in half of the keto group, compared with 29 percent of the Mediterranean group and just 7 percent of the low-fat group.

Not everything favored the keto diet, however. Levels of “bad” cholesterol (LDL) and a similar marker that tracks cholesterol-carrying particles in the blood did not differ meaningfully between the three diets. Blood pressure improvements were also similar across groups. Even though the keto diet in this study contained a lot of saturated fat, it didn’t produce worse cholesterol numbers than the other diets, and it actually showed advantages in a few markers linked to heart disease risk, including certain fat particles in the blood and a marker tied to blood clot risk.

Researchers said the shift in insulin and glucagon could help explain some of the liver benefits. On the ketogenic diet, a hormone called glucagon rose while insulin fell sharply, changing the balance between the two. That shift is believed to slow the liver’s own fat production and push it to burn fat instead of storing it. On the higher-carbohydrate diets, that hormone shift didn’t happen the same way.

Source : https://studyfinds.com/keto-diet-beats-mediterranean-and-low-fat-diets-reducing-liver-fat-study-finds/

Breakfast is widely considered one of the most important parts of a child’s day. A new national poll finds that nearly all school-age kids are eating something in the morning before class. For many families, though, getting a nutritious meal on the table is a daily struggle, shaped by picky eaters, rushed mornings, and kids who are calling their own shots at the breakfast table.

A nationally representative poll conducted for C.S. Mott Children’s Hospital found that 96% of parents say their child between the ages of 6 and 12 usually eats breakfast on a school day. That sounds like a win. But dig into what kids are actually eating, and the picture gets more complicated. About one in five parents say their child’s breakfast rarely meets the report’s marks for a balanced meal, meaning protein and fiber with little added sugar.

Mornings with school-age kids are notoriously chaotic, and this poll captures that reality in hard numbers. One in three parents say their child has 15 minutes or less to eat. Three out of four report at least one obstacle to getting their child a healthy meal. About half say their child decides what ends up in the bowl.

A Poll Built on Real Family Breakfast Data

Findings come from the C.S. Mott Children’s Hospital National Poll on Children’s Health, conducted in July 2026 by Ipsos Public Affairs. Researchers surveyed a nationally representative, randomly selected sample of adults who were parents of at least one child between ages 0 and 18 living in their household. The final analysis focused on responses from 1,037 parents who had at least one child between ages 6 and 12. The margin of error for these results is plus or minus 1 to 4 percentage points.

Parents were asked about where their child eats breakfast, how much time they have to eat, who decides what they eat, what factors go into choosing breakfast foods, and what barriers get in the way of a healthy morning meal.

Where Kids Eat Breakfast, and How Little Time They Get

Most children, about 68%, eat breakfast at home on a typical school day. Another 23% eat at school, and 5% eat on the way to school. Only 4% of parents say their child usually skips breakfast altogether.

Eating at home doesn’t mean eating leisurely, though. Nearly half of parents, 47%, say their child has between 15 and 25 minutes to eat, and only 19% have 30 minutes or more. That kind of time pressure shapes everything from what gets made to whether anyone sits down together. About 16% of parents say their child eats breakfast alone, with no sibling or parent at the table, while most kids eat with a sibling (66%) or a parent (49%).

Who Decides What Kids Eat for Breakfast

Among parents whose children eat breakfast at home or on the way to school, 53% say the child usually picks what they eat. Parents largely support that arrangement, with 69% saying it is very important to offer something their child actually likes. Convenience also ranks high, with 37% calling it very important to choose foods that are quick and easy, and 25% saying it matters that the child can prepare the food themselves.

When it comes to buying breakfast cereal specifically, 65% of parents say their child’s preference influences the choice. Nutritional factors like protein or fiber come in close behind at 60%, followed by calories or added sugar at 37%, cost at 34%, and artificial coloring at 23%.

Handing kids the wheel comes with a tradeoff. Parents who say their child usually picks breakfast report fewer days per week where the meal includes protein, fiber, fruit, or stays low in added sugar. Across all families surveyed, the report card is mixed. Asked how often their child’s breakfast includes protein, 39% of parents said most days, meaning four to five days a week, while 43% said some days and 18% said rarely. For fiber, 37% said most days, 43% some days, and 20% rarely. For whole or cut fruit, 36% said most days, 38% some days, and 26% rarely. For keeping added sugar low, 34% said most days, 46% some days, and 19% rarely. Taken together, the results point to a meaningful share of children not regularly getting the mix of protein, fiber, fruit, and lower added sugar that the report ties to a healthier breakfast.

Source : https://studyfinds.com/96-of-kids-eat-breakfast-but-1-in-5-meals-miss-the-basics/

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For anyone with asthma who has ever felt too intimidated or too worn out to start a formal exercise program, a new study offers a welcome shortcut. Getting people to walk more and sit less, with coaching and a fitness tracker, worked about as well as structured treadmill workouts for controlling asthma symptoms.

Researchers in Brazil put 52 adults with moderate to severe, poorly controlled asthma through one of two eight-week programs, according to findings published in the journal Pulmonology. One group did supervised treadmill training twice a week. The other met with a health coach once a week and used a wearable activity tracker to nudge them into moving more throughout the day, without any formal exercise sessions. Both groups ended up breathing easier, feeling less anxious, and reporting a better quality of life, and those gains mostly held up four months later.

That result matters because starting an exercise routine can feel like a tall order for someone who struggles to catch their breath climbing stairs. Many people with asthma avoid physical activity altogether because they fear triggering symptoms, and that inactivity itself has been linked to worse disease control. There is more than one path to feeling better here, and patients do not have to choose the toughest one.

Setting Up the Asthma Control Study

Researchers recruited adults between 18 and 65 who had moderate to severe asthma that was not well controlled, based on their medication needs and symptom scores. Participants also had to be physically inactive at the start, getting less than the recommended amount of moderate to vigorous activity each week, as measured by a small motion-tracking device worn on the body.

Fifty-two people were randomly split into two groups. Twenty-seven were assigned to treadmill training, working out twice a week for 45 minutes a session over eight weeks, at an intensity set by an individual fitness test. The other 25 were assigned to a coaching program, meeting with a health professional once a week for up to 90 minutes. Instead of formal workouts, that group focused on building daily habits: they wore a commercial fitness tracker set to buzz when they hit a step goal or when they had been sitting still for an hour, and reviewed their progress with a coach who helped them set realistic goals and work through obstacles.

Both groups also attended an asthma education session, and everyone kept taking their prescribed asthma medications throughout. Researchers checked in three times: before the programs started, right after the eight weeks ended, and again four months later. They measured asthma symptom control using a standard questionnaire, along with quality of life, anxiety and depression symptoms, sleep, body composition, and how much people actually moved during the day.

Nearly 9 in 10 participants were women. A typical participant was carrying extra weight, dealing with multiple health conditions, and showing signs of anxiety or depression along with a lower quality of life. That combination lines up with what other research has found about who tends to struggle most with uncontrolled asthma.

What Researchers Found About Asthma Control

Both groups saw meaningful drops in their asthma symptom scores by the end of the eight weeks, large enough by standard scoring guidelines to count as a real improvement in day-to-day symptoms. That improvement held up four months later in both groups, with no meaningful gap between the treadmill group and the coaching group. Roughly two-thirds of participants in each group still showed a clinically meaningful improvement at the four-month mark.

Quality of life scores climbed in both groups too, again by an amount considered clinically meaningful, and those gains also stuck around at follow-up. Anxiety and depression symptoms eased in both groups as well. Neither group showed changes in sleep quality or body composition.

A couple of results ran counter to expectations. Aerobic training usually lifts a person’s peak fitness, but the treadmill group saw no such bump, which the researchers tied to participants already having fairly well-preserved lung and heart fitness at the start, or to the program running only eight weeks. The coaching group’s daily step counts did climb over the eight weeks, though the researchers felt the gains fell short of what earlier behavioral programs have produced and pointed to that group’s higher body weight, which other studies have linked to a weaker response. Either way, both groups logged more weekly minutes of moderate to vigorous activity, the kind that gets the heart working.

Both groups also reported fewer personal and everyday barriers to being active after their programs, such as feeling too tired or not having a safe place to exercise, and those improvements remained at follow-up.

Source : https://studyfinds.com/skipping-the-gym-walking-more-controlled-asthma-about-as-well-as-treadmill-workouts/

Blood Vessels, Ovaries, and Prostates Don’t Age on the Same Clock

What 300,000 People’s Diets Reveal About Preventing High Blood Pressure

Masculine, Still Image-Conscious: Appearance Concerns Pushed Men To Diet More Than Health Scares

A toddler finds a gummy on the coffee table. It looks like candy. It smells sweet. Before anyone notices, the child has swallowed it. That gummy might contain marijuana, and it might not be the only edible drug parents now have to worry about vanishing off counters and out of purses.

A new study published in BMC Public Health looked at more than two decades of calls to United States poison centers and found something startling: the rate at which young children accidentally swallowed recreational drugs jumped by 3,307% between 2000 and 2024. That is not a typo. What started as roughly one ingestion per 100,000 children in 2000 climbed to nearly 36 per 100,000 by 2024, with the sharpest climb kicking off around 2013.

A research team led by Nationwide Children’s Hospital analyzed data from the National Poison Data System, which collects information from poison centers across the country. They zeroed in on children younger than 6 who accidentally swallowed drugs like marijuana, cocaine, methamphetamine, psychedelic mushrooms, and opioids such as fentanyl and heroin. The goal was to figure out who these kids were, what they swallowed, and how badly it hurt them.

How Many Kids Are Swallowing Recreational Drugs?

Across the 24 years, researchers reviewed 41,612 cases of children under 6 who swallowed a recreational drug and were reported to poison centers. Most of these kids, 57.6%, were younger than 3. That tracks with how toddlers explore the world: everything goes in the mouth, and anything left on a low table or in an open purse is fair game.

Nearly all of the cases, 96.4%, happened at home, and 95.9% involved just one drug rather than a mix. Marijuana and related products made up the overwhelming share of ingestions at 84.7%. Cocaine and methamphetamine accounted for 8.4%, psilocybin mushrooms for 3.5%, opioids for 2.8%, and ketamine and similar drugs for 0.6%.

About half of the children (50.6%) had no effect or only mild symptoms. Another 30.8% had moderate effects, and 5% suffered what poison centers call a major effect, meaning symptoms were life-threatening or caused lasting harm. Six children died during the study period, and all six were younger than 3.

Age made a real difference in how badly a child was hurt. Kids under 3 were about 54% more likely to suffer a major effect than kids aged 3 to 5, and about 23% more likely to end up in intensive care. Study authors suggest younger kids weigh less, so the same amount of a drug may hit them harder relative to their size. Toddlers also struggle to tell adults something is wrong, which can delay treatment.

Marijuana Edibles Are Driving the Recreational Drugs Surge

Edible forms of marijuana like gummies and baked goods accounted for nearly half of all cases in the study, 47.9%. Edible cases began appearing in the study data in 2013 and grew fast, eventually overtaking other forms of marijuana around 2019.

Researchers tie this rise to the wave of state laws legalizing marijuana and the growing number of edible products showing up in people’s homes. Oddly, edible marijuana ingestions were actually less likely than other drugs to cause a major health effect or land a child in intensive care. But there were so many cases that these products still accounted for a large share of hospital admissions.

Opioids, Stimulants, and Mushrooms: Fewer Cases, Rougher Outcomes

Opioids made up a small slice of the total cases, just 2.8%, but their impact was outsized. Ingestions involving opioids were about 2.6 times more likely to be linked to an intensive care stay compared with other drugs combined. Fentanyl stood out most: it was involved in almost two-thirds of opioid cases and was roughly 7.7 times more likely to be linked to a major effect than all other substances combined. Four of the six deaths in the study were linked to fentanyl.

Cocaine and methamphetamine told a similar story. They accounted for 8.4% of cases but were about twice as likely to be linked to an intensive care stay or a major effect compared with other drugs combined. Two of the six deaths involved cocaine. Dissociative drugs, a category that includes ketamine and PCP-related substances that can cause hallucinations and a sense of detachment from reality, made up less than 1% of cases but were about 1.6 times more likely to be linked to intensive care admission than the other drug categories combined.

Psilocybin, the psychoactive compound in certain mushrooms, produced one of the more unexpected findings. Ingestions involving psilocybin mushroom products rose sharply starting around 2018, climbing more than 1,400% by 2024. By the last two years of the study, psychedelic ingestions had grown to outpace every other drug category except marijuana.

Researchers suspect this jump tracks with psilocybin’s expanding legal status for therapy and its growing popularity as a recreational drug. They also flagged a separate problem: independent testing of some mushroom-branded gummies and chocolates has found inconsistent labeling, meaning products marketed as psilocybin may actually contain other substances entirely. That makes it harder to know exactly what children are being exposed to.

Source : https://studyfinds.com/toddlers-poisoned-by-marijuana-gummies-at-record-rates-study-warns/

Results Show The Average American Is Out Of Energy Before 3 P.M.

Coconut oil has long had a place in kitchens and beauty products, but researchers are now making a serious case for putting it in jet engines. New research found that aviation biofuel made from coconut oil can power a small jet engine about as efficiently as traditional jet fuel, with lower unburned hydrocarbon emissions, though the blends burn more fuel and emit slightly more carbon monoxide.

Aviation accounts for a meaningful share of global carbon dioxide emissions, and pressure on the industry to find cleaner fuel options has intensified in recent years. The International Civil Aviation Organization has identified sustainable aviation fuel, commonly called SAF, as the single most effective strategy available for cutting aviation’s carbon footprint. But many current methods for producing SAF are themselves energy-hungry and costly, which chips away at the environmental benefit. The new study, published in the journal Fuel, zeroes in on a production approach designed to sidestep that problem entirely, using a technique that requires far less energy to make the fuel in the first place.

Researchers at Osaka Metropolitan University tested biofuels made from coconut oil through what they call a “co-solvent method,” a process that mixes acetone with alcohol and coconut oil to produce high-purity biofuel without the intense heat and pressure required by conventional production methods. Rather than stopping at production, the team took the next step and burned the fuel in a small jet engine, measuring both engine performance and exhaust emissions.

A Greener Way to Make Coconut Oil Jet Fuel

Most SAF production routes involve intense industrial processes, including high-temperature refining steps that drain energy out of the fuel’s lifecycle before a single flight takes place. The co-solvent method works differently. By adding acetone to a mixture of alcohol and coconut oil, normally incompatible liquids blend uniformly and react completely at relatively low temperatures, producing biofuel with purity levels exceeding 97%.

Coconut itself offers a practical advantage as a raw material. Roughly 30% of the coconut is discarded after extracting its internal moisture during processing. This study used oil from material the researchers describe as discarded and non-edible, including the large seeds and leftover flesh, so the fuel draws on parts of the crop that would otherwise go to waste. The process also produces biodiesel suitable for vehicles and marine vessels, plus high-quality glycerin as a byproduct.

Two types of biofuel were produced and tested: one made using methanol and another made using ethanol. Both are plant-based fuels commonly studied for diesel engines, but this research examined their behavior in a jet engine, a question that has received comparatively little scientific attention.

Inside the Engine: How Coconut Oil Jet Fuel Actually Performs

Researchers tested the fuel in a small commercial jet engine capable of reaching speeds up to 130,000 rotations per minute. Researchers blended the biofuels with conventional kerosene at ratios of 10%, 30%, and 50% biofuel by volume, then ran the engine across a range of speeds. Measurements included fuel consumption, engine efficiency, and exhaust concentrations of four pollutants: unburned hydrocarbons, carbon monoxide, carbon dioxide, and nitric oxide.

In terms of fuel efficiency, the biofuel blends required more fuel to produce the same amount of thrust. At 80,000 rotations per minute, a 50% methanol-based blend consumed about 16.8% more fuel than pure kerosene, while the ethanol-based version consumed about 19.6% more. This is largely because the biofuels carry less energy per kilogram than kerosene, so more must be burned to maintain the same output level.

Despite burning more fuel by weight, the blends converted heat into usable work at rates comparable to pure kerosene. At 100,000 rotations per minute, the thermal efficiency of the highest biofuel blend differed from pure kerosene by a small margin, and thrust output remained consistent across all blend ratios tested.

What Comes Out of the Exhaust

Emissions are where coconut oil-based jet fuel shows some of its most encouraging results. Increasing the proportion of biofuel in the blend consistently reduced unburned hydrocarbon emissions. At a 50% blend ratio, hydrocarbon concentrations in the exhaust dropped by roughly 5% to 40% compared to pure kerosene, depending on engine speed. Researchers said the drop was likely tied in part to fuel composition, since the coconut-derived biofuels contain none of the ring-shaped, aromatic hydrocarbon molecules present in conventional jet fuel.

Carbon dioxide emissions remained at levels consistent with pure kerosene across all blending ratios tested. While higher biofuel content increased total fuel consumption, the CO2 in the exhaust did not rise proportionally. Researchers say that pattern may point to some unburned biofuel leaving the engine, a question they flagged for future investigation.

Carbon monoxide emissions, a product of incomplete combustion, did increase modestly at higher blend ratios. A 50% blend produced roughly 3% to 17% more carbon monoxide than pure kerosene depending on engine speed. Researchers linked this to the biofuels being harder to ignite than kerosene and carrying less energy, both of which can create fuel-rich zones inside the combustion chamber where oxygen runs short.

Nitric oxide emissions, which can contribute to ozone depletion at high altitudes, were broadly comparable between the biofuel blends and pure kerosene. A 30% methanol-based blend showed nitric oxide concentrations 20% to 30% lower than pure kerosene across all operating conditions tested, a result the authors say requires further study to fully explain.

Source : https://studyfinds.com/coconut-oil-jet-fuel-matches-kerosenes-efficiency-in-engine-tests/

When a 35-year-old man went in for a cardiology appointment in 2005, thyroid trouble was the last thing on his mind. His cardiologist felt something unusual in his neck and ordered an ultrasound. That single scan set off a chain of discoveries that would later give doctors the chance to act on his children’s inherited cancer risk before either child developed the disease.

That man’s story sits at the heart of a virtual tumor board article published in CA: A Cancer Journal for Clinicians, written by specialists in endocrinology, surgery, oncology, genetics, and radiation medicine. Together, they used his 20-year medical journey to illustrate how, for this one family, a single genetic test reshaped the way a rare form of thyroid cancer called medullary thyroid carcinoma was managed across generations, allowing doctors to spot the inherited risk early and step in before it reached his children as clinical disease.

Medullary thyroid carcinoma is not the common kind of thyroid cancer that usually comes to mind. It grows from a different type of cell, does not respond to the radioactive iodine treatment used for other thyroid cancers, and in as many as one in four cases, it is inherited. Before genetic testing, hereditary forms of the disease were usually recognized only after cancer had already appeared in a family, signaled by a thyroid nodule, rising calcitonin, or a suggestive family history. A genetic test targeting the RET gene gave doctors a way to identify at-risk relatives in advance.

A Cancer Hidden in Plain Sight

When surgeons operated on that 35-year-old man in 2005, they expected to find papillary thyroid carcinoma, the most common and usually treatable form of the disease, based on a needle biopsy done beforehand. Instead, the tissue removed during surgery revealed medullary thyroid carcinoma. The cancer was present in multiple spots across both sides of his thyroid, and his blood showed sharply elevated calcitonin, a hormone produced by the specific cells where this cancer originates. His calcitonin level measured 1,160 picograms per milliliter against a reference range of less than 9.8.

Surgeons removed the thyroid and the lymph nodes from the center of his neck. All 19 removed lymph nodes came back negative for cancer. That was good news. But then came the genetic test.

Results confirmed he carried a mutation in the RET gene at a location called codon 609, a change linked to a hereditary syndrome called multiple endocrine neoplasia type 2A. That finding instantly shifted the story from one man’s cancer to his entire family’s risk.

One Genetic Test Changed Three Generations

A certified genetic counselor worked with the family to understand who else might carry the mutation, a process called cascade testing. That testing identified additional carriers across multiple generations, including the patient’s brother, son, and daughter.

What happened next shows the difference between catching this mutation early versus late. The patient’s brother, not screened until age 37, had already developed metastatic disease by the time the mutation was found in him. His preoperative calcitonin level was 2,450 picograms per milliliter. He underwent total thyroidectomy with bilateral neck dissection and now has persistent disease, currently being treated with a targeted drug called selpercatinib.

Identified only through genetic testing, the patient’s son and daughter underwent preventive thyroid removal at ages 6 and 3, respectively, and are now 25 and 22. Both have had undetectable calcitonin ever since and show no evidence of disease. According to the patient perspective section of the report, learning that his children were carriers felt initially overwhelming and painful, but the clarity provided by testing quickly transformed that fear into a sense of direction and control over the disease.

What 20 Years of Follow-Up Revealed About This Thyroid Cancer

After his initial surgery, the patient achieved undetectable calcitonin levels and stayed in that state for three years. In 2008, calcitonin began rising again, and by 2013, imaging confirmed multiple liver metastases. Even so, the disease advanced unusually slowly. From 2013 to 2025, his calcitonin rose from 850 to 1,820 picograms per milliliter, an increase of roughly 80 picograms per milliliter per year. His calcitonin doubling time, a marker doctors use to gauge how fast the cancer is progressing, stretched from about 13 months in the earliest phase to more than 24 months by the time liver metastases were found in 2013, and beyond 60 months in the years that followed.

Because this patient’s disease was progressing slowly and he had no symptoms, his medical team chose careful monitoring over immediate drug therapy rather than treating based on numbers alone. Then, in 2025, FDG-PET-CT imaging revealed new hypermetabolic lesions, and MRI confirmed bone metastases in the spine, though he remained without symptoms and without any compression of the spinal cord. As of the report, surveillance continues with bisphosphonate support to address the bone involvement.

This 20-year history is both unusual and instructive. It shows that patients with certain RET mutations can experience long periods of stable disease even after metastasis, and that knowing a patient’s genetic profile allows doctors to plan treatment deliberately rather than reactively.

How New Drugs Have Transformed Medullary Thyroid Carcinoma Treatment

For years, doctors treating advanced medullary thyroid carcinoma relied on drugs that targeted multiple cell signals at once. While those medications helped slow the disease, they carried significant side effects including high blood pressure, severe diarrhea, fatigue, and skin problems on the hands and feet. Many patients required dose reductions or had to stop the drugs entirely.

A newer class of drugs, designed to block only the RET protein specifically, has sharply improved outcomes. In two large clinical trials referenced in the paper, LIBRETTO-001 and ARROW, these targeted drugs produced response rates ranging from 69% to 79% in patients with RET-mutated medullary thyroid carcinoma, with far better tolerability than earlier treatments. A critical finding from those trials was that response rates to selective RET inhibitors were similar whether the RET mutation was inherited or acquired by the tumor, meaning the same drugs appear effective for both types of patients.

About half of sporadic MTCs carry somatic RET mutations in the tumor itself, so testing the tumor directly is needed to determine whether these targeted drugs will work for those patients.

Multiple specialists contributed to this report, including pathologists, endocrinologists, surgeons, oncologists, radiation doctors, and a medical geneticist, each examining the same patient’s case through their own lens. That structure was deliberate. No single specialty has the full picture of hereditary MTC.

Radiation therapy plays a narrow but meaningful role here. Because this cancer does not absorb radioactive iodine the way common thyroid cancers do, external radiation is reserved for specific situations: patients with high-risk features after surgery, tumors that could not be fully removed, or painful bone and spinal metastases. In this patient’s case, with bone metastases detected but no pain or neurological symptoms, the team opted to hold radiation in reserve for future need.

Studies cited in the paper show that countries where genetic screening became routine saw the average age of MTC diagnosis drop by years or even decades. In a German cohort, the average age at diagnosis decreased from 35.6 to 23.0 years after routine screening began. In a Norwegian study, the proportion of patients who achieved remission increased from 50% to 89% following the introduction of systematic genetic testing.

Source : https://studyfinds.com/gene-test-revealed-inherited-cancer-risk-across-three-generations-of-one-family/

Younger Adults With Eczema Face Surprisingly High Shingles Risk

Staying clear of diabetes, high blood pressure, and smoking through middle age may promote more than a decade of extra dementia-free years compared to peers carrying all three conditions. A large, long-running community-based study published in Neurology® Open Access and tracking 12,409 participants from four U.S. communities found that the gap in dementia-free years between the healthiest and least healthy midlife groups was 12.6 years, a number researchers say offers a clear, personal way to think about heart health and brain aging.

Dementia already looms large over American life. Roughly 42% of middle-aged adults in the U.S. may develop the condition during their lifetime, according to prior research cited in the study. Most conversations about preventing it focus on the odds of getting it at all, rather than something more personal: how many good cognitive years a person actually gets to enjoy. This study set out to answer that second question directly.

Researchers Followed 12,000 People for Nearly 30 Years

Researchers drew on data from the Atherosclerosis Risk in Communities study, a long-running project that began enrolling participants between 1987 and 1989 across four U.S. locations: Forsyth County, North Carolina; Jackson, Mississippi; the Minneapolis suburbs; and Washington County, Maryland. The team focused on 12,409 participants who were alive and free of dementia at age 55, with an average starting age of about 56. Just over half were women.

At a baseline checkup in the early 1990s, researchers noted whether each participant had diabetes, high blood pressure, or was a current smoker, then gave everyone a simple score from zero to three based on how many of those three conditions applied. From there, participants were tracked for a median of about 26 years, in some cases all the way to 2022. Over that stretch, 3,008 people developed dementia and 5,238 died without ever developing it.

Doctors did not rely on guesswork to identify dementia cases. Participants took cognitive tests in person, completed phone interviews when they could not make it to a visit, and had their hospital and death records checked continuously. An expert panel confirmed every diagnosis.

The More Risk Factors, the Fewer Good Years

A clear step-down pattern emerged. People with none of the three risk factors averaged 30.1 dementia-free years between ages 55 and 95. Add one risk factor and that number dropped to 26.3. Two dropped it to 21.0. All three brought it down to 17.5, a 12.6-year difference from the healthiest group. Only 176 participants landed in that highest-risk group, a small enough sample that the exact number carries more uncertainty than the figures for the larger groups.

Here is the twist: people with all three risk factors were nearly three times as likely to develop dementia as those with none, but they were more than five times as likely to die of something else first, before dementia ever got the chance to set in. By age 75, 10% of the highest-risk group had developed dementia, compared to just 3% of the healthiest group. By age 95, those numbers had essentially flipped, with the healthiest group reaching a 42% dementia rate while the highest-risk group topped out at just 23%. That is not because bad health protects against dementia. It is because the unhealthiest participants were, tragically, dying earlier from other causes.

Race and Sex Gaps in Dementia-Free Years Are Real

More risk factors meant fewer good years for every group researchers looked at, though the numbers were not identical across the board.

Women outlived men in dementia-free years at every risk level, averaging 18.1 years versus 16.6 for men among those with all three conditions. Women also had a higher lifetime rate of dementia by age 95, 40.3% compared to 32.8% for men, likely simply because they tend to live longer, giving the disease more years in which to appear.

Black participants had shorter dementia-free years than white participants at every risk level too. Among those with all three conditions, Black participants averaged 16.0 dementia-free years compared to 19.6 for white participants. Black participants also made up 60.2% of the highest-risk group despite representing a smaller share of the overall study population. Researchers say that heavier burden of health risk likely contributes to the disparity, and that addressing the social and economic forces behind it will matter just as much as clinical treatment.

People carrying a gene variant called APOE-ε4, which is linked to higher dementia risk, had fewer dementia-free years than non-carriers at every single risk level, from zero risk factors up through all three.

Source : https://studyfinds.com/midlife-risk-factors-dementia/

 

For women trying to conceive later in life, the uterus itself can be just as much of an obstacle as egg quality. Even with the best fertility treatments available, including donor eggs from younger women, older mothers still face higher rates of failed implantation and pregnancy loss. Scientists have long suspected the aging uterus plays a major role, but the biological reasons behind it have been frustratingly hard to pin down. Now, a new study points to a surprising association that hides in plain sight: the gradual disappearance of beneficial bacteria from the uterus as women age.

Researchers from Peking University Third Hospital, writing in the journal Cell Host & Microbe, found that in this study’s cohort, as women grew older, a group of protective bacteria called Lactobacillus declined in the lining of the uterus. That loss was associated with the uterine lining becoming less hospitable to embryos. The scientists also identified a specific member of that bacterial family, Lactobacillus gasseri, and found that treating aged mice with it reduced signs of uterine cellular aging and improved embryo implantation.

Its active ingredient appears to be not the bacterium itself, but a coating-like substance the microbe secretes, called an exopolysaccharide, or EPS. In lab-grown human uterine cells and in mouse tissue, EPS reduced markers of cellular aging, and experiments using a strain engineered to lack EPS showed the substance was responsible for much of the bacterium’s benefit. Researchers describe EPS as an early-stage experimental candidate, one they suggest could eventually be worth exploring as a postbiotic approach, while emphasizing that further pharmacological and translational work would be needed before any clinical use becomes realistic.

What Researchers Found About Age-Related Fertility Decline

To build their case, the team combined human patient data, cell-based lab experiments, and mouse tests. They enrolled 149 women being seen for infertility at a single hospital in Beijing between 2021 and 2022. Participants were divided into three age groups: women under 30, women between 30 and 35, and women 35 and older. During a routine surgical procedure, small tissue samples were collected from the uterine lining of each participant.

Using genetic sequencing techniques that identify bacteria by their unique DNA signatures, the researchers mapped the microbial communities living in each woman’s uterus. They then tracked embryo transfer outcomes over the following year for the subset of women who went on to attempt in vitro fertilization.

At the broader group level, clinical pregnancy rates after embryo transfer did not differ significantly across the three age groups, coming in at 65.0%, 57.1%, and 61.3% respectively, a pattern the researchers attributed to factors such as embryo selection and the limited size of the follow-up group. But when they looked within each age group, women who became pregnant consistently showed higher levels of Lactobacillus in their uterine lining than women who did not. Women who conceived also tended to have higher levels of the species L. crispatus, while those who did not conceive more often had higher levels of L. iners and another bacterium, Gardnerella vaginalis.

Zeroing In on the Right Bacteria

With an association established between uterine bacteria and fertility outcomes, the team set out to identify which specific strain would be most therapeutically useful. They isolated five different Lactobacillus species from the reproductive tracts of healthy women and put each through a series of head-to-head tests, measuring how well each fought off harmful bacteria, how strongly it attached to uterine cells, and how effectively it neutralized the cellular damage associated with aging.

L. gasseri emerged as the strongest overall candidate across multiple measures, particularly in its ability to counteract oxidative stress, essentially the cellular equivalent of rust. Oxidative stress, caused by an accumulation of unstable molecules called free radicals, is one of the main drivers of cellular aging. L. gasseri also produced the highest amount of EPS compared to the other strains tested. The other strains were not without merit: L. delbrueckii showed strong pathogen inhibition and biofilm activity, and L. crispatus demonstrated anti-inflammatory effects in co-culture experiments with uterine cells.

To test whether L. gasseri could actually slow down uterine aging, the researchers treated older female mice with the bacteria delivered directly into the vagina over 28 days. Compared to untreated older mice, the treated animals showed significant reductions in biological markers of cellular aging in their uterine tissue. The treated mice also showed improved embryo implantation rates.

How a Bacterial Substance Appears to Turn Back the Clock

When the team stripped away the bacteria and tested purified EPS alone on lab-grown human uterine cells, the substance reproduced many of the same anti-aging effects. It reduced the proportion of cells showing signs of aging, lowered levels of an inflammatory signaling cluster associated with aging cells, and reduced oxidative stress markers.

Gene expression analysis in mouse uterine tissue pointed to a specific biological pathway as a likely explanation. A communication network inside cells called the Hippo-YAP pathway, which helps regulate how cells grow, age, and respond to stress, was found to be overactive in older uteri. L. gasseri and its EPS appeared to dial that activity back down to healthier levels in the mouse model. When the researchers blocked the key protein in this pathway, called YAP, the protective effects of both the bacteria and their EPS were eliminated, showing that YAP is required for these effects and that Hippo-YAP signaling is at least part of the mechanism at work.

To confirm the link between EPS and these effects, the team also engineered a version of L. gasseri that could not produce EPS. That modified strain lost much of its protective power in mice. When EPS was added back externally, the beneficial effects were largely restored.

Source : https://studyfinds.com/an-aging-uterus-loses-protective-bacteria-lab-tested-byproduct-could-help-reverse-damage/

Some people can stand outside on a summer evening and walk back in without a single bite. Others get absolutely devoured. It turns out this isn’t bad luck or imagination. Mosquitoes appear to be responding to different chemical and microbial cues on each person’s skin. A new study tested 119 people against three different disease-carrying mosquito species, Aedes aegypti, Aedes albopictus, and Culex quinquefasciatus, and found something that could reshape how scientists think about mosquito repellents: each species ranked participants differently in the lab, so the person who acts as a magnet for one type may barely register with another.

For years, researchers have known that body odor plays a role in mosquito attraction. Most previous work, though, focused on a single mosquito species at a time, leaving a big question unanswered: do all mosquitoes prefer the same people? According to the research, published in the journal iScience, the answer is mostly no. Different species ranked the same group of people in very different orders of preference, meaning a person who is highly attractive to one species is not necessarily on the menu for another. Among the 119 participants, no one was a top target for all three species, and no one was at the bottom of the list for all three either.

One sex-based difference also stood out. One of the three species, Aedes aegypti, the mosquito that spreads dengue, Zika, and yellow fever, showed a slight but statistically significant preference for male participants over female ones, a pattern the other two species did not share.

Who Was Tested and How

Researchers at Florida International University, in collaboration with scientists at the University of Zürich, recruited 119 volunteers from Miami, Florida, aged 18 to 59. Participants were racially and ethnically diverse, and the group was split nearly evenly by sex, with 61 males and 58 females. To keep the results clean, participants were told not to shower the night before their visit and to skip deodorants, perfumes, or scented skin products.

Each volunteer stuck their left forearm into a specially built device, essentially a sealed tube that allowed mosquitoes to respond to a person’s natural scent without any physical contact. For two of the mosquito species, live arms were used. For the third species, Culex quinquefasciatus, a night-biting mosquito that also transmits West Nile virus, participants wore a thin nylon sleeve over their arms for 12 to 16 hours to capture their scent, since those mosquitoes were tested separately under low-light conditions that mimic nighttime.

Three species were tested in total: Aedes aegypti, which primarily targets humans and spreads dengue and Zika; Aedes albopictus, a related species with a broader diet that spreads similar viruses; and Culex quinquefasciatus, the night-biting species associated with West Nile virus. Across all 119 participants, Aedes aegypti showed the highest average attraction rate at about 89%, Culex quinquefasciatus came in around 43%, and Aedes albopictus had the lowest average at about 27%. These differences in overall enthusiasm for humans may reflect how deeply each species has evolved to rely on human blood, though the study’s design does not directly establish that connection.

What Mosquitoes Are Actually Smelling

To figure out what made certain people more or less attractive, the research team collected the invisible cloud of chemicals coming off each participant’s arm and analyzed it to identify individual compounds. At the same time, they swabbed participants’ forearms to study the bacteria on their skin, cataloging 246 distinct bacterial taxa across the 119 participants.

Only one of those taxa appeared in every participant, a notable result given how much the skin’s microbial makeup varies from person to person. That variability, the researchers argue, is a key part of why mosquitoes respond so differently to different people.

For Aedes aegypti, the dengue-and Zika-spreading species, high attraction was closely linked to Staphylococcus bacteria on the skin, a pattern specific to this species and consistent with earlier research. People who were least attractive to this species tended to have more Pseudomonas bacteria on their arms, a pattern previously associated with reduced mosquito attraction. When it came to airborne chemicals, high attraction for this species was tied to the absence of certain compounds rather than the presence of appealing ones, hinting that these mosquitoes may home in on people who simply lack natural deterrents.

For Aedes albopictus, the broader-diet species, the pattern flipped. High attraction was linked to the presence of specific appealing chemicals, including one compound previously tied to how mosquitoes evolved a preference for humans in the first place. Researchers found 13 volatiles were more common among people who scored highly on attraction to this species, compared with just one such chemical for Aedes aegypti. That broader set of appealing odors aligns with this mosquito’s more opportunistic nature, since it feeds on a wider range of animals rather than specializing on humans.

For Culex quinquefasciatus, the night-biting, West Nile-associated species, high attraction was again tied more to the absence of certain compounds than to the presence of appealing ones. No bacterial species were significantly linked to high attraction here, though bacteria in the Actinomyces group were associated with low attraction.

Source : https://studyfinds.com/why-some-people-attract-more-mosquitoes-than-others/

Standing on one leg for up to 30 seconds sounds like a party trick. In a study of more than 13,000 older adults, better performance on that simple balance test was associated with a lower risk of dying over the following seven years.

Researchers followed 13,423 community-dwelling adults aged 65 and older in Taiwan for a median of seven years, measuring their physical fitness through a battery of practical tests. Older adults who performed best on balance, agility, and lower-body strength tests were far less likely to die during the follow-up period than those who performed worst. Even after accounting for existing health conditions, income, body weight, and self-reported exercise habits, the connection held.

Doctors typically size up an older patient’s risk by counting diagnoses: high blood pressure, diabetes, kidney disease. Fitness testing, the researchers argue, measures something a diagnosis list misses, which is how much functional capacity a person’s body still has in reserve. Published in JAMA Network Open, the study is among the largest to test that idea across several fitness domains at once.

What the Physical Fitness Tests Actually Measured

This was a cohort study, meaning researchers measured something about a group of people at one point in time, then followed them to see what happened. Between January 11, 2015, and November 25, 2016, participants completed standardized fitness assessments at 46 testing stations spread across 22 cities and counties in Taiwan. Those results were linked to national health insurance records, which tracked deaths through December 31, 2022.

Of the 13,423 participants in the final analysis, the average age was about 73. Roughly 62.5% were women. Over the follow-up period, 1,631 participants, about 12% of the group, died.

Seven tests covered four areas of fitness. Balance and agility were measured two ways: standing on one leg with eyes open for up to 30 seconds, and an “8-foot up-and-go” test that required rising from a chair, walking 8 feet around a cone, returning, and sitting back down, all timed as one continuous movement. Muscle strength was measured two ways as well: how many times someone could stand up from a chair and sit back down in 30 seconds without using their arms, and how many times they could curl a hand weight in 30 seconds. Heart and lung endurance came from a 2-minute step test, counting how many times a participant could lift each knee to a marked height while marching in place. Flexibility was checked with two reaching tests, one behind the back and one toward the toes while seated.

Participants were then ranked into five equal groups, from lowest to highest performance, for each test. Landing in the top group consistently meant a far lower risk of dying than landing in the bottom one.

Balance and Agility Showed the Steepest Survival Gap

Across several tests, top performers had roughly half, and in some cases less than half, the mortality risk of bottom performers, even after adjusting for age, sex, body weight, income, education, existing conditions, and self-reported physical activity.

On the 8-foot up-and-go, the best performers had a mortality risk about 59% lower than the worst. On the one-leg stance, the gap was about 50%. Lower-body strength and heart-and-lung endurance each landed in the range of 42% to 45%.

Flexibility behaved differently. Extreme stiffness was linked to higher mortality risk, but gains beyond a moderate, functional range of motion produced no further survival benefit. Extreme stiffness appeared to matter far more than exceptional flexibility did.

Combining all seven scores into a single fitness index sharpened the picture. Participants in the top fifth of overall fitness had about 61% lower mortality risk than those in the bottom fifth, a stronger association than any individual test produced on its own. And the pattern was graded: at every step up the index, from worst to best, mortality risk fell.

Most of that difference was concentrated between the very lowest group and the ones just above it. Researchers took that pattern to mean the biggest health gains may come when someone moves out of the worst-performing tier, and argued for prioritizing the least-fit older adults.

Why Balance and Lower-Body Strength Carry So Much Weight

Balance and lower-body strength likely stand out because of their role in preventing falls. Impaired balance, slowed mobility, and weak legs are established risk factors for falls and the fractures that follow, especially broken hips, which rank among the leading causes of hospitalization, disability, and death in older adults. A one-leg stance or a timed up-and-go may catch early declines in muscle control and coordination well before a person ever trips. That remains an interpretation rather than a proven chain of events, since the study tracked deaths from any cause and never measured whether fewer falls or fractures accounted for the gap.

Men and women showed somewhat different patterns. Among men, balance and agility carried the lowest mortality risk, followed by heart and lung fitness. Among women, lower-body strength mattered about as much as balance and agility. Researchers pointed to the higher rates of osteoporosis in older women, along with reports of higher sarcopenia prevalence under certain definitions, as reasons that preserving leg strength and mobility may matter especially for them.

One detail stands out for anyone who assumes a self-report is good enough: the fitness results stayed tied to mortality even after researchers statistically accounted for whether participants said they got regular exercise. Only about a third of the group, 32.8%, reported being regularly active. Measured performance added information that a questionnaire about habits did not capture on its own.

Source : https://studyfinds.com/balance-agility-test-predict-dying-risk-7-years/

Media Skepticism, Not Just COVID News, Predicted Vaccine Conspiracy Beliefs

Most college students used to picture graduation as a finish line. A growing number now seem to see it as a starting gun in a job market they fear AI will reshape. In a new survey of 2,000 American students pursuing higher education, less than half said they feel good about the job market waiting for them after they toss their caps.

Just 45% described themselves as optimistic about the market they will enter post-graduation. That number matters because it comes from the people with the most on the line: students who are paying tuition, taking on debt, and betting years of their lives on the promise that a degree still pays off. Nearly seven in 10, some 69%, said they are worried about landing a job once they graduate, and they pointed to a specific concern. They fear that artificial intelligence is being used to replace human workers in parts of the economy.

That anxiety carries a dramatic nickname in the survey: the “job apocalypse,” a blunt phrase for the worry that whole categories of work could thin out or vanish before today’s undergraduates ever clock in. Commissioned by the AI company Superhuman and conducted by Talker Research, the survey set out to measure how deep that dread runs and what students are doing about it. Both answers turned out to be bigger than a single worried mood.

Bracing for a Job Apocalypse

Fear, it turns out, is changing real decisions, not just gut feelings. Roughly a third of students, 34%, said they are pursuing a higher education degree specifically to avoid the job apocalypse, treating a diploma as a kind of insurance policy against automation. Others reported steering their entire academic path around the threat. About 22% said they changed their major or concentration because of job market concerns, and 12% said they adjusted their career path altogether.

Those shifts add up to a portrait of a generation editing its plans in real time. A student who once leaned toward a field now shadowed by automation may pivot toward something that feels more machine-proof. Another may pile on credentials in hopes that more education equals more security. Whether those bets pay off is an open question, but the survey makes clear the bets are being placed, and placed early.

Underneath the major-swapping sits a quieter hustle. A full 91% of students said they are working to build new skills outside of their regular college courses, unwilling to let a syllabus alone decide their fate. Classroom credits, in other words, no longer feel like enough armor against a labor market many of them expect to be harsh.

Fighting the Job Apocalypse With AI, Not Against It

Then comes the twist. Rather than running from the technology they blame for their nerves, many students are running toward it. Meanwhile, 43% of students said they are using AI itself to learn new skills, turning the perceived threat into a study partner.

That embrace shows up across the survey. Fifty-eight percent of respondents said learning about AI while in college is essential for their career, and almost half, 48%, said learning to use AI properly, including ethically and responsibly, is the single most important skill they expect to gain in college. For a cohort that fears AI could cost them a paycheck, betting on AI fluency as their best safeguard is a pragmatic bet.

Superhuman’s head of education, Jenny Maxwell, framed the pattern as students choosing offense over panic. “AI is having a massive impact on the world, and we know it can be scary for college students who are trying to set themselves up for success in an ever-changing job market,” Maxwell said. “But it’s clear that students understand that learning how to use AI effectively is actually the strongest defense against a potential ‘job apocalypse.’ We believe that it’s not AI that will take most jobs, but someone who uses AI to do their best and most productive work over someone who doesn’t.”

Read that way, the survey describes a generation trying to make itself harder to replace. That logic is simple, if unproven: a worker who commands the tools stands a better chance than one who ignores them. Whether employers actually reward that fluency the way students hope is something no survey can promise.

A Critical-Thinking Cost Students See Coming

For all their willingness to lean on AI, students are not naive about the price of leaning too hard. Sixty-nine percent said it is important to strike a balance between using AI and sharpening their own critical thinking skills, and the survey warns that balance might be slipping. Fully 81% said they believe people are at risk of losing critical thinking skills because of an over-reliance on AI.

Worry about mental atrophy appears to shape the kind of help students actually want from AI. Instead of asking the technology to do their thinking for them, most requested support around the edges of their work. Slightly more than half, 54%, said they would value spelling and grammar help to polish their writing, and 40% wanted reminders about deadlines for projects and assignments.

Beyond the basics, students described a wish list that keeps a human in the driver’s seat. About a third, 33%, said they would appreciate AI that knows their specific class requirements, and the same share wanted a personal assistant to keep them on track through the year. One in four, 25%, said they would want AI guided by input from their own professors, a sign that many still trust a human expert to set the terms.

Source : https://studyfinds.com/fear-of-ai-job-apocalypse-reshaping-how-college-students-plan-their-futures/

Each Heatwave Could Make You Biologically 6 Months ‘Older’, Researchers Say

The Belief That Leadership Isn’t Just for Certain People Helped Some Teens See Themselves as Leaders

Scientists from the University of Pennsylvania have developed a bioengineered chewing gum that can reduce harmful viruses and bacteria linked to head and neck cancer.

Head and neck cancer is one of the most common cancers worldwide, which affects the mouth, throat, voice box, nose, and nearby tissues. A lot of these cases are linked to tobacco and alcohol use. However, there’s also a rise in cancer cases linked to human papillomavirus (HPV) infections. Researchers have been looking for simple, affordable ways to reduce these infections before they lead to serious disease. A new study has found an unusual solution: a specially designed chewing gum.

Scientists from the University of Pennsylvania have developed a bioengineered chewing gum that can reduce harmful viruses and bacteria linked to head and neck cancer. While the gum is still being studied and is not available for the public, early findings are promising. Researchers believe it could one day become a simple addition to existing cancer prevention strategies, especially for people at higher risk. However, experts say that it is not a replacement for vaccination, regular screenings, or medical treatment.

What Did The Study Find?

The researchers, led by Henry Daniell of the School of Dental Medicine at the University of Pennsylvania, tested a specially engineered chewing gum made using lablab beans. The gum contains natural antiviral and antibacterial ingredients designed to target harmful microbes found in the mouth.

In laboratory tests using saliva and oral rinse samples from patients with head and neck squamous cell carcinoma (HNSCC), the gum reduced HPV levels by as much as 93% in saliva and about 80% in oral rinse samples. It also almost completely removed two harmful bacteria, Porphyromonas gingivalis and Fusobacterium nucleatum, which have been linked to poorer outcomes in head and neck cancer.

Why Are HPV And Oral Bacteria Important?

HPV is a common virus that spreads through close skin-to-skin contact, including sexual contact. While most HPV infections clear on their own, some high-risk types can remain in the body and increase the risk of cancers, including cancers of the throat.

Researchers have also identified certain bacteria that may create an environment that helps cancer grow or makes treatment less effective. Higher levels of P. gingivalis and F. nucleatum have been linked to worse survival in some patients with head and neck cancer. By lowering both HPV and these harmful bacteria, the chewing gum may help reduce one of the factors linked to cancer development or progression.

How Does The Gum Work?

The gum uses two important components:

• FRIL, a naturally occurring antiviral protein found in lablab beans, helps reduce HPV
• Protegrin, an antimicrobial peptide, targets harmful bacteria in the mouth

As a person chews the gum, these substances are released into saliva, allowing them to act directly where the virus and bacteria are present. This may make the treatment both effective and easy to use without affecting the rest of the body.

Does It Harm Good Bacteria?

One of the most encouraging findings from the study was that the gum appeared to leave beneficial bacteria in the mouth largely untouched. This is important because the mouth contains a healthy microbiome that helps with digestion, protects against infections, and supports overall oral health. Many antibiotics can kill both harmful and beneficial bacteria, but this chewing gum seemed to target the microbes linked to cancer while preserving the healthy ones.

Source : https://www.ndtv.com/health/can-a-chewing-gum-help-reduce-risk-of-head-and-neck-cancer-new-study-says-yes-11870696?pfrom=home-ndtv_lateststories

 

Two-Week Study Pinpoints the True Daily Trigger of Problematic Internet Use

Millions of Americans take antidepressants every day. Millions more reach for diet sodas, sugar-free gum, or low-calorie snacks sweetened with natural and artificial sweeteners. What happens when both of those things meet in the gut at the same time? According to a new study, the answer may be more tangled than previously thought.

Researchers tested 39 commercially available sweeteners, the kind found in everything from soft drinks and candy to cereal and baby formula, against 25 gut bacterial strains and species to see how they interact. Reporting in Molecular Systems Biology, the team found that three-quarters of the sweeteners directly affected the growth of at least one bacterial strain. A bigger surprise came when sweeteners were combined with other commonly ingested compounds, including the widely prescribed antidepressant duloxetine. Those combinations produced more than 100 previously unreported interactions, some of which appeared to harm bacteria closely linked to human health.

Conducted entirely in a laboratory setting, the study does not prove that the same effects occur in a living human body. But the scale of the screening and the depth of the follow-up analysis make it one of the most thorough looks yet at what low-calorie sweeteners might be doing to the microscopic community living in the human digestive system.

How a Sweetener and an Antidepressant Gang Up on Gut Bacteria

Of all the findings in the study, one combination stood out. Isosteviol, a compound derived from the stevia plant and used as a sweetener ingredient, combined with duloxetine, the antidepressant sold under the brand name Cymbalta, to suppress two types of bacteria that scientists associate with a healthy gut, hitting one of them especially hard.

One of those bacteria, Roseburia intestinalis, has been linked to blood sugar regulation and protection against intestinal inflammation. The other, Parabacteroides merdae, is a common gut resident tied to a healthy microbial community. When isosteviol and duloxetine were present together, their combined suppressive effect on these bacteria was greater than what either compound caused on its own.

Duloxetine is no niche medication. In 2022 and 2023, it ranked as the 31st-most-prescribed drug in the United States, with more than 18 million prescriptions filled and more than 4 million patients taking it, according to data cited in the study. Given how widely stevia-derived sweeteners are used in food products, many people may routinely consume both.

How Scientists Tested 39 Sweeteners Against Gut Bacteria

Based at the MRC Toxicology Unit at the University of Cambridge and the European Molecular Biology Laboratory in Heidelberg, Germany, the research team built their experiment around 25 gut bacterial strains and species chosen to represent the broad range of bacteria found in a healthy human gut: friendly probiotic species, common residents, and some opportunistic troublemakers.

Against these bacteria, the team screened all 39 sweeteners they could obtain in pure form, covering both natural options like stevia compounds and monk fruit extract and synthetic ones like saccharin, aspartame, and sucralose. Every sweetener was tested individually against every bacterial strain, producing 975 unique pairings. Interactions counted as real only if they held up across multiple independent experiments and multiple concentrations, a strict standard that filtered out false positives.

For the combination testing, the researchers screened the same 39 sweeteners alongside four compounds commonly consumed with sweeteners: advantame (another sweetener increasingly used in processed foods), caffeine, vanillin (a flavor compound found in everything from cakes to baby formula), and duloxetine. That expanded the analysis to 3,900 three-way interactions between sweeteners, bacteria, and the added compounds.

In total, the combination screen identified 102 significant interactions involving nine gut bacterial species. Most of them, 68 out of 102, were cases where one compound softened the impact of the other. But 34 were cases where the combination hit harder than either compound alone. The strongest of all the compounds involved is isosteviol, followed by duloxetine, acting on Roseburia intestinalis.

Beyond Slowed Growth: Effects on Gut Bacteria and Human Cells

Finding that a sweetener and an antidepressant can together suppress specific gut bacteria would be notable on its own. The researchers went further, building a miniature artificial gut community comprising all 25 bacterial strains and exposing it to the isosteviol-duloxetine combination over several growth cycles to observe how the community changed under pressure.

Combined treatment caused a significant drop in overall species diversity. Of the 25 bacteria, 24 grew less in isolation after exposure to both compounds together.

To understand what was happening at a molecular level, the team analyzed changes in proteins made by Roseburia intestinalis and Parabacteroides merdae after exposure. The compounds appeared to interfere with the bacteria’s ability to manage what moves in and out of the cell, specifically disrupting proteins that carry small molecules across the outer membrane. A separate genetic analysis using a library of bacterial mutants identified the same membrane transport proteins as key determinants of bacterial survival of the isosteviol-duloxetine combination.

One of the more arresting downstream results involved the spent liquid from the bacterial community, essentially the chemical output that bacteria produce and release. Applied to human cells in a dish, fluid from communities treated with the isosteviol-duloxetine combination was significantly more toxic to HeLa cells than fluid from untreated communities. Researchers ruled out the compounds themselves as the direct cause; the altered bacterial output appeared to drive the effect.

When Caco-2 cells, a human cell line modeled on the lining of the colon, were exposed to the same bacterial fluid, secretion of two immune signaling proteins, interleukin-6 and interleukin-8, fell by more than 75% compared with fluid from untreated communities. These proteins are part of the gut’s immune defense. Their suppression could, depending on the context, indicate a weakened ability to fight off pathogens, though the researchers note that the significance would depend on a person’s individual health.

Bacteria exposed to the combination also produced different amounts of butyric acid, a compound tied to anti-inflammatory effects, improved insulin sensitivity, and protection against diet-related obesity, and one that gut cells burn for energy. In Roseburia intestinalis, butyric acid dropped by more than 25% after co-exposure. These are the kinds of bacterial outputs that researchers link to broader human health.

Source : https://studyfinds.com/could-common-antidepressant-and-sweetener-combo-quietly-fight-gut-bacteria/

Each Heatwave Could Make You Biologically 6 Months ‘Older’, Researchers Say

Summer heat is more than a seasonal discomfort. A new study suggests it may be aging people from the inside out, faster than the calendar ever could. Researchers found that exposure to extreme heat events was linked to accelerated biological aging in middle-aged and older adults. Under the study’s strictest heatwave definition, each additional heatwave event was associated with pushing the body’s internal clock forward by roughly half a year, though the size of that effect varied considerably depending on how heatwaves were defined, and was weaker or statistically insignificant under looser definitions. As heatwaves grow more frequent and more intense worldwide, that finding carries serious consequences for public health.

Biological age and calendar age are not always the same thing. A person who is 58 years old on paper might have a body that functions more like a 62-year-old, or a 54-year-old, depending on how their cells, organs, and metabolism are holding up. Scientists can estimate this “biological age” by measuring things like blood pressure, cholesterol, blood sugar, and other indicators of how the body is really doing. When biological age outpaces calendar age, it signals faster physical deterioration and has been linked to higher risks of heart disease, cognitive decline, and earlier death. This study asked a pointed question: could repeated exposure to extreme heat be pushing that biological clock forward?

Researchers analyzed data from more than 2,300 adults across China and found strong evidence of an association, particularly under the stricter definitions of what counts as a heatwave. The clearest links between heat and faster aging appeared under those more demanding definitions, and each extra day of heat exposure added incrementally to the effect. Urban residents, people with higher body weight, and those living in southern or subtropical parts of the country faced the sharpest acceleration.

Gauging Biological Aging From Heatwave Exposure
To measure biological aging, researchers used a validated method that combines eight different blood and health markers into a single estimate of how old a person’s body actually functions. Those markers included cholesterol, blood sugar, blood pressure, kidney function indicators, and an inflammation signal. By comparing this biological age to a person’s actual calendar age, researchers calculated what they called “biological age acceleration,” essentially how far ahead of schedule the body was aging.

Participants were drawn from a large national health survey of Chinese adults. Out of those enrolled, 2,318 adults aged 45 and older met the study’s requirements. Their average age was 58.7 years, just over half were women, and most lived in rural areas. Biological age measurements were taken at two points in time: 2011 and 2015.

Heatwave exposure for each participant was measured using weather data from the 12 months before each biological age assessment. Researchers pulled daily temperature records from 50 cities across China and defined heatwaves in 12 different ways, varying both how hot it had to be and how many consecutive days the heat had to last. Under the strictest definition, at least four consecutive days where temperatures exceeded the hottest 2.5% of days typical for that city, each additional heatwave event was associated with a 0.531-year increase in biological age acceleration. Each additional day of heatwave exposure added another 0.057 years to that biological age gap. Associations were weaker or not statistically significant under looser heatwave definitions, meaning the strength of the finding depended meaningfully on how heatwaves were measured.

People who experienced more intense heatwave exposure were aging biologically at a measurably faster pace than their peers who experienced milder heat conditions, even after researchers accounted for factors like smoking, drinking, weight changes, depression, diabetes, and high blood pressure.

Who Got Hit Hardest by Heatwave-Driven Aging
Not everyone was equally affected. Heatwaves tracked more strongly with faster biological aging in certain groups. People with a body mass index at or above 23 kg/m² showed a more pronounced effect compared to leaner individuals. Urban dwellers experienced stronger aging effects than rural residents. Those living in southern China or subtropical climate zones also showed greater acceleration.

Researchers noted several possible reasons for these patterns. Carrying more body weight can make it harder to stay cool, placing additional strain on the heart and circulatory system. Urban areas tend to trap heat more than rural ones, a phenomenon known as the “urban heat island effect,” where buildings, pavement, and limited green space push temperatures even higher at night. People in southern and subtropical zones already contend with higher baseline temperatures, meaning heatwaves pile additional thermal stress on top of an already demanding climate.

No meaningful differences in the heatwave effect emerged between men and women, or across different age groups.

Metabolic Stress Behind Heatwave-Driven Aging
Beyond tracking who aged faster, the research team also tried to understand why. In the human participants, heatwave exposure was consistently tied to higher levels of total cholesterol and a blood sugar marker called HbA1c, which reflects average blood sugar over roughly three months. Both of these markers are components of the biological age algorithm used in the study, so they are best understood as part of a broader pattern of metabolic stress associated with heat exposure rather than as independently proven disease mechanisms.

To probe a possible biological explanation, researchers reanalyzed existing gene-activity data from aged mice that had been exposed to repeated heat conditions in a separate experiment. Liver tissue from those mice showed 29 genes switched on or off differently compared with unexposed controls. These genes clustered around two biological processes: fat metabolism and the body’s ability to use blood sugar efficiently, a function that declines in a condition known as insulin resistance.

Heat stress, the researchers explained, can trigger a cascade of internal disruptions, including cellular damage from unstable molecules, problems with the energy-producing parts of cells, and strain on the system responsible for building proteins correctly. All of these processes are closely tied to how quickly a body ages at the cellular level.

Animal work involved a small sample and should be considered exploratory. But combined with the human data, the pattern offered a suggestive biological picture: heat may throw off the body’s ability to regulate fat and blood sugar, and that metabolic disruption could contribute to accelerated aging.

Between 2011 and 2015, about 58.8% of the study participants showed accelerated biological aging, meaning their bodies aged faster than their calendar years would predict. On average, biological age across the group increased from 57.3 years in 2011 to 62.3 years in 2015. Findings held up across multiple rounds of sensitivity testing, including analyses that removed participants with extreme or minimal changes in biological age and models that accounted for regional differences in climate and urbanization.

As climate change drives more frequent and severe heatwaves globally, the collision of a warming planet and a rapidly aging population creates a compounding risk that existing public health systems may not be equipped to handle. Extreme heat poses more than a short-term danger. For older adults especially, it may be steadily eroding the body’s biological reserves, one sweltering summer at a time.

Source: https://studyfinds.com/scorching-summers-may-be-speeding-up-how-fast-your-body-ages/

The Protein Network That Cleans Up Workout Damage, and Why It Doesn’t Last

Financial stress is something millions of people know all too well. Most have dealt with the anxiety of an overdue bill or smaller than expected paycheck at some point. Now, a sweeping new study tracking people across seven decades suggests that kind of hardship may be linked to something far more lasting than day-to-day stress: measurable differences in the brain that show up decades later.

Researchers followed a group of British adults from birth through their early 70s. Those who experienced financial hardship at multiple points tended to score lower on memory and mental-speed tests by middle age. Later in life, brain scans showed a pattern consistent with tissue loss in certain regions. For a few smaller groups, including men and people carrying a particular Alzheimer’s-linked gene, the pattern looked even stronger, though those pieces of the puzzle are still tentative.

Published in the journal Innovation in Aging, the study draws on data from the 1946 British birth cohort, a landmark project that has tracked thousands of people born in a single week in March 1946. With decades of financial records and repeated cognitive testing, researchers had a rare chance to see how money troubles that stretch across a lifetime relate to brain health, rather than relying on a single snapshot.

Nearly 3,000 People Were Tracked From Birth Through Their 70s

Researchers drew on two groups within the cohort. The main group, 2,759 people who were still alive at 69, took cognitive tests at ages 53, 63, and 69. A smaller group of about 400 people also came in for brain scans between ages 69 and 74.

Money trouble was tracked two ways: whether household income fell into the bottom fifth of the group at ages 26, 43, and 53, and whether people said they struggled to cover basic needs at ages 36, 43, and 53. Anyone who hit either mark at two or more checkpoints was labeled as having faced it persistently, which didn’t necessarily mean an unbroken decade of poverty, just hardship that kept resurfacing.

To measure mental sharpness, participants took a timed letter-search test for processing speed and a word-recall test for memory. Brain scans measured the physical size of different regions, including the fluid-filled chambers that expand as surrounding tissue shrinks. A smaller subset also had their brains checked for amyloid, a sticky protein tied to Alzheimer’s, though that piece applied only to people carrying a specific gene variant, not everyone in the study.

Financial Hardship Was Linked to Lower Scores by Age 53

People with more exposure to low income or financial strain scored lower on both memory and processing speed by age 53, years before most people start thinking about memory loss at all. The clearest differences showed up among those who’d faced hardship repeatedly rather than just once or twice, though the study wasn’t designed to prove a single rough patch is harmless either.

Years later, at ages 69 to 71, brain scans told a related story: people with a history of persistent low income had noticeably larger fluid-filled spaces in the brain, the kind that grow as nearby tissue shrinks. Interestingly, people who already scored lower on memory tests at 53 didn’t decline much further afterward. Researchers think that’s not a hopeful sign so much as evidence the damage had, in a sense, already been done by midlife, leaving less room left to lose.

Accounting for other possible explanations, like childhood intelligence, mental health history, and education, didn’t change the picture. That doesn’t prove hardship alone caused these differences, since money troubles are often tangled up with other stresses, but it rules out some of the more obvious alternatives.

Source : https://studyfinds.com/financial-hardship-memory-decline/

For many new mothers, breastfeeding is no longer only a matter of medical advice. On Instagram, it has hardened into something closer to a moral obligation, and a new study puts Spanish parenting influencers at the center of that conversation.

Researchers at Universitat Pompeu Fabra in Barcelona analyzed 592 public comments on Instagram posts from five Spanish momfluencer accounts, all run by women who present themselves as authorities on motherhood and breastfeeding. Writing in the journal Media & Jornalismo, they found that exclusive breastfeeding had turned into what the authors call a “symbolic device” and a “marker of maternal success.” In that framing, a mother who couldn’t or didn’t nurse exclusively was seen as doing more than making a personal choice, and some commenters called mothers who used formula lazy or selfish.

Instagram, the study shows, can take a private parenting decision and turn it into a public performance of what it means to be a “good mother.” For many women in those comment sections, falling short of that standard carried a heavy emotional cost.

How Spanish Momfluencers Are Reshaping Breastfeeding Norms
To build their sample, the authors spent two months observing public Instagram accounts run by Spanish women who describe themselves as prescribers of motherhood and breastfeeding, several of them with professional credentials in nursing or midwifery. From five of these accounts, they selected 15 posts that had sparked debate, each with at least 30 comments and 700 likes, then combed through the comments for patterns in how mothers talked about feeding choices, guilt, family support, and social pressure. Beyond what was said outright, they also traced the assumptions and unspoken rules underneath those conversations.

Formula was generally not treated as a legitimate option in these spaces. One post carried a title flatly rejecting the idea that formula feeding is the easy way out, casting it as something mothers turn to only when a health problem forces their hand. Breastfeeding mothers, by contrast, described their own experience in raw terms: exhaustion, pain, and broken sleep, alongside pride and a deep sense of bonding.

Guilt and Sacrifice: Breastfeeding as the “Good Mother” Test
One of the strongest patterns was guilt. Mothers wrote about agonizing over feeding decisions in ways that went well beyond the practical, and several said they pushed through real physical pain and sleep loss mainly out of fear of being judged as bad mothers if they stopped. One commenter recounted breastfeeding her son for two years while waking as many as seven times a night, until the exhaustion tipped into depression and she left her paid job.

Yet many of the same comments recast that suffering as proof of love. Nursing was described as the most rewarding and most sacrificing part of motherhood, even as women admitted how brutal it could be. Pain wasn’t framed as a problem to fix. For a lot of commenters, it read as evidence of devotion.

Criticism of the pressure to breastfeed rarely grew into a broader social or political argument. Most of it stayed personal, framed as one woman’s private struggle rather than a sign of a system that leaves working parents stranded. Spain grants four months of paid maternity leave, while health guidance urges exclusive breastfeeding for six. A handful of commenters flagged that gap, and one argued the government should simply extend paid leave instead of forcing mothers to improvise their way across it. Those structural complaints, though, were the exception.

Fathers on the Sidelines
Another clear finding was how seldom fathers showed up as equal partners. When they did appear, it was usually as helpers rather than people equally on the hook. Some mothers recounted pediatricians framing the father’s job as helping out in other, lesser ways, language that quietly slots him into a secondary role rather than a shared one.

Some comments mentioned fathers getting tired or impatient, but treated it as a scheduling headache rather than a question of shared duty. One mother wrote that her partner blamed breastfeeding for all their relationship troubles, and that the two had slept apart since their baby was two months old. Of the 592 comments studied, only two mentioned any family outside the traditional mother-father setup, and neither drew a single reply.

Source: https://studyfinds.com/breastfeeding-becomes-moral-test-for-mothers-on-instagram-study-finds/

Parkinson’s disease slowly destroys the brain cells that produce dopamine, a chemical messenger essential for controlling movement. For decades, a drug called levodopa, usually paired with carbidopa, has been the go-to treatment for managing symptoms. Over time, though, some patients develop fluctuating responses, involuntary movements and other complications that make the drug harder to manage. Now a new study in mice points to an unlikely helper that might boost how well levodopa works: freeze-dried bee venom.

Researchers at the University of Guadalajara in Mexico gave mice a toxin-induced brain lesion that mimics some features of Parkinson’s disease, then tested whether adding bee venom to standard levodopa treatment could improve how the animals moved and remembered things. The study, published in the journal Neuroprotection, found that mice getting the combination moved better and did significantly better on a short-term memory test than mice getting levodopa alone.

Parkinson’s is best known for tremors and stiff, halting movement, but it quietly wrecks memory too, a side of the disease that gets far less attention. A treatment that could help with both would be worth watching closely.

A Toxin Injection Created One-Sided Brain Damage in Mice
Researchers injected a toxin that wipes out dopamine-producing brain cells into just one side of the brain in adult male mice. That one-sided approach lets researchers compare the damaged side against the healthy side in the same animal, making it easier to spot movement problems.

Four groups of mice were studied: healthy controls given saline, untreated brain-damaged mice, mice given levodopa and carbidopa from day 13 through day 30, and mice given that same combination plus freeze-dried bee venom every 48 hours, an hour after each levodopa dose. Group sizes ranged from six to seven animals, small but typical for this kind of early-stage animal research.

Researchers then put the mice through three tests. One checked whether the mice used both front paws evenly while exploring a clear tube, since brain-damaged mice tend to lean on their good side. Another counted how often mice grabbed food from both sides of a narrow corridor, a task that’s especially sensitive to dopamine loss. The last one checked whether mice noticed a new object placed among familiar ones, something healthy mice do naturally but memory-impaired mice often miss.

Bee Venom Group Matched Healthy Mice on Movement Tests
By day 30, mice on levodopa alone still leaned heavily on their good paw. Mice getting bee venom alongside levodopa used both paws about as evenly as healthy mice did, a real step up from both the untreated group and the levodopa-only group.

A similar pattern showed up in the food-grabbing test. Mice on the combination treatment retrieved food from both sides of the corridor far more evenly than either the levodopa-only group or the untreated mice, suggesting an extra boost for coordinated movement.

Memory results stood out most. Mice that got only the toxin, and even those on levodopa alone, stopped noticing new objects by day 21 and day 30, a sign of memory trouble. Mice getting bee venom kept noticing new objects just as well as healthy mice did, at both time points. (One wrinkle worth flagging: the paper also shows this same group already scoring better on the memory test on day 13, before treatment had even started. That’s a timing inconsistency the study doesn’t explain, and it should be sorted out before the finding is taken at face value.)

A Bee Venom Compound Can Reach the Brain and Affect Neurons
Bee venom is packed with active compounds, one of which, a tiny molecule called apamin, can slip past the barrier that normally keeps most substances out of the brain. Earlier research suggests apamin changes how easily brain cells fire and adapt, though scientists are still figuring out exactly how.

Bee venom has also been used in traditional medicine for inflammation for centuries, and earlier lab studies hint that it might calm brain inflammation and help dopamine-producing cells survive. This study did not test any of that directly. The authors are upfront that these explanations are still guesses, borrowed from earlier research rather than anything measured here.

Researchers Never Directly Measured the Brain Cells
Here’s the biggest gap: researchers never actually looked at the brain cells themselves. They confirmed the injections landed in the right spot, but didn’t count how many dopamine-producing cells survived or measure inflammation. That means there’s no way yet to know why bee venom seems to help, and the results shouldn’t be read as proof that it protected any brain cells.

It’s also worth remembering this was a small, short mouse study, just 17 days of treatment in a handful of male mice, and mouse results often don’t hold up in people. The authors themselves say the next step is digging into the actual brain tissue to see what’s really going on.

Whatever is happening at the cellular level, the mice on bee venom kept moving and remembering better than the ones on levodopa alone. Parkinson’s still has no cure, and levodopa still tends to get harder to manage over the years. If bee venom holds up under more rigorous testing, it may turn out to be a simple add-on that helps a decades-old drug do its job a little longer.

Source: https://studyfinds.com/bee-venom-helps-parkinsons-drug/

One Type of Mouth Bacteria Keeps Turning Up in People With Hand Arthritis

After Watching a TV Drama, the Brain Tracked Rivalries More Clearly Than Friendships

Why Your Waistline May Reveal More Cancer Risk Than the Scale Does

Millions of Americans take antidepressants every day. Millions more reach for diet sodas, sugar-free gum, or low-calorie snacks sweetened with natural and artificial sweeteners. What happens when both of those things meet in the gut at the same time? According to a new study, the answer may be more tangled than previously thought.

Researchers tested 39 commercially available sweeteners, the kind found in everything from soft drinks and candy to cereal and baby formula, against 25 gut bacterial strains and species to see how they interact. Reporting in Molecular Systems Biology, the team found that three-quarters of the sweeteners directly affected the growth of at least one bacterial strain. A bigger surprise came when sweeteners were combined with other commonly ingested compounds, including the widely prescribed antidepressant duloxetine. Those combinations produced more than 100 previously unreported interactions, some of which appeared to harm bacteria closely linked to human health.

Conducted entirely in a laboratory setting, the study does not prove that the same effects occur in a living human body. But the scale of the screening and the depth of the follow-up analysis make it one of the most thorough looks yet at what low-calorie sweeteners might be doing to the microscopic community living in the human digestive system.

How a Sweetener and an Antidepressant Gang Up on Gut Bacteria

Of all the findings in the study, one combination stood out. Isosteviol, a compound derived from the stevia plant and used as a sweetener ingredient, combined with duloxetine, the antidepressant sold under the brand name Cymbalta, to suppress two types of bacteria that scientists associate with a healthy gut, hitting one of them especially hard.

One of those bacteria, Roseburia intestinalis, has been linked to blood sugar regulation and protection against intestinal inflammation. The other, Parabacteroides merdae, is a common gut resident tied to a healthy microbial community. When isosteviol and duloxetine were present together, their combined suppressive effect on these bacteria was greater than what either compound caused on its own.

Duloxetine is no niche medication. In 2022 and 2023, it ranked as the 31st-most-prescribed drug in the United States, with more than 18 million prescriptions filled and more than 4 million patients taking it, according to data cited in the study. Given how widely stevia-derived sweeteners are used in food products, many people may routinely consume both.

How Scientists Tested 39 Sweeteners Against Gut Bacteria

Based at the MRC Toxicology Unit at the University of Cambridge and the European Molecular Biology Laboratory in Heidelberg, Germany, the research team built their experiment around 25 gut bacterial strains and species chosen to represent the broad range of bacteria found in a healthy human gut: friendly probiotic species, common residents, and some opportunistic troublemakers.

Against these bacteria, the team screened all 39 sweeteners they could obtain in pure form, covering both natural options like stevia compounds and monk fruit extract and synthetic ones like saccharin, aspartame, and sucralose. Every sweetener was tested individually against every bacterial strain, producing 975 unique pairings. Interactions counted as real only if they held up across multiple independent experiments and multiple concentrations, a strict standard that filtered out false positives.

For the combination testing, the researchers screened the same 39 sweeteners alongside four compounds commonly consumed with sweeteners: advantame (another sweetener increasingly used in processed foods), caffeine, vanillin (a flavor compound found in everything from cakes to baby formula), and duloxetine. That expanded the analysis to 3,900 three-way interactions between sweeteners, bacteria, and the added compounds.

In total, the combination screen identified 102 significant interactions involving nine gut bacterial species. Most of them, 68 out of 102, were cases where one compound softened the impact of the other. But 34 were cases where the combination hit harder than either compound alone. The strongest of all the compounds involved is isosteviol, followed by duloxetine, acting on Roseburia intestinalis.

Beyond Slowed Growth: Effects on Gut Bacteria and Human Cells

Finding that a sweetener and an antidepressant can together suppress specific gut bacteria would be notable on its own. The researchers went further, building a miniature artificial gut community comprising all 25 bacterial strains and exposing it to the isosteviol-duloxetine combination over several growth cycles to observe how the community changed under pressure.

Combined treatment caused a significant drop in overall species diversity. Of the 25 bacteria, 24 grew less in isolation after exposure to both compounds together.

To understand what was happening at a molecular level, the team analyzed changes in proteins made by Roseburia intestinalis and Parabacteroides merdae after exposure. The compounds appeared to interfere with the bacteria’s ability to manage what moves in and out of the cell, specifically disrupting proteins that carry small molecules across the outer membrane. A separate genetic analysis using a library of bacterial mutants identified the same membrane transport proteins as key determinants of bacterial survival of the isosteviol-duloxetine combination.

One of the more arresting downstream results involved the spent liquid from the bacterial community, essentially the chemical output that bacteria produce and release. Applied to human cells in a dish, fluid from communities treated with the isosteviol-duloxetine combination was significantly more toxic to HeLa cells than fluid from untreated communities. Researchers ruled out the compounds themselves as the direct cause; the altered bacterial output appeared to drive the effect.

When Caco-2 cells, a human cell line modeled on the lining of the colon, were exposed to the same bacterial fluid, secretion of two immune signaling proteins, interleukin-6 and interleukin-8, fell by more than 75% compared with fluid from untreated communities. These proteins are part of the gut’s immune defense. Their suppression could, depending on the context, indicate a weakened ability to fight off pathogens, though the researchers note that the significance would depend on a person’s individual health.

Bacteria exposed to the combination also produced different amounts of butyric acid, a compound tied to anti-inflammatory effects, improved insulin sensitivity, and protection against diet-related obesity, and one that gut cells burn for energy. In Roseburia intestinalis, butyric acid dropped by more than 25% after co-exposure. These are the kinds of bacterial outputs that researchers link to broader human health.

Source : https://studyfinds.com/could-common-antidepressant-and-sweetener-combo-quietly-fight-gut-bacteria/

Skipping breakfast before a gym session is hard enough. A new study points to an odd trick that might make the empty-stomach grind a little easier: a whiff of chocolate. Men who breathed in the scent of chocolate before and during a weight session cranked out more repetitions than they did after smelling plain water, and they managed it without rating the harder workout as any more punishing than usual.

No one ate a single square. Every bit of the boost came from smell alone. When the same men sniffed dark chocolate, they reported feeling less hungry and more full before lifting. When they sniffed milk chocolate, they mostly rated the scent as more pleasant. Both scents beat water on total reps completed.

Published in the journal Frontiers in Physiology, the research is preliminary, so it shows that the two happened together rather than nailing down exactly why. Still, the basic result is hard to ignore: a smell, and nothing more, nudged how much work tired muscles were willing to do.

How the Chocolate Smell Study Worked

Twenty-three healthy men took part at the University of Malaya in Kuala Lumpur, Malaysia. All were seasoned lifters, training at least twice a week for a minimum of two years, with an average age of about 23. Each showed up having fasted overnight for at least 10 hours, copying the state of someone who trains first thing in the morning on an empty stomach.

Each man completed three separate sessions spaced at least four days apart. One session paired the workout with the smell of dark chocolate (90% cocoa), another with milk chocolate, and a third with plain water for comparison. By design, neither the participants nor the staff counting reps were told which scent was which, a standard step to limit bias. Scents were prepared as liquids in small glass jars, and each man inhaled for 30 seconds at a time, both before lifting and between sets.

For the workout itself, participants did repeated sets of leg extensions, a seated machine move that targets the muscles at the front of the thigh, using a weight set to 80% of the most they could lift 10 times. They kept going until they couldn’t finish another set. After each set they rated how hungry they felt, how much they wanted to eat, how pleasant the smell was, and how hard the effort felt.

More Reps From the Chocolate Smell

Dark chocolate produced the biggest jump: 18 more total reps than water, and nine more than milk chocolate. Milk chocolate landed in the middle, beating water by nine reps. Counted in whole sets, dark chocolate added one full set over both the water and milk chocolate conditions.

Curiously, all that extra work didn’t register as extra suffering. Effort ratings climbed as the sets piled up, exactly as expected, but they came out about the same no matter which scent sat in the jar. The chocolate smells helped men grind out more without making any single set feel tougher.

Appetite is where the two scents parted ways. Dark chocolate reliably dialed down hunger and the urge to eat while raising the sense of fullness. Milk chocolate did none of that; it simply smelled better to the participants. Across every condition, the less hungry a man felt going in, the more reps he tended to finish.

What the Science Can’t Explain Yet

Researchers ran the numbers to see whether lower hunger or greater pleasantness could account for the extra reps. Those tests came back inconclusive. The study can show that chocolate scents and stronger performance traveled together; it can’t yet prove the scent caused the gain or trace the biology behind it. Hormones, brain signals, and other bodily measures that might confirm a mechanism simply weren’t recorded.

One leading guess ties back to appetite. Smelling a familiar food can trigger what scientists call a cephalic-phase response, the body’s head start on digestion that begins before any food arrives. A rich, bitter dark chocolate scent may cue that response and quiet hunger for a while, which could free a lifter from the nagging pull of an empty stomach. That fits earlier research linking lower pre-workout hunger to better lifting, though the authors treat it as a plausible story rather than settled fact.

Source : https://studyfinds.com/whiff-of-chocolate-before-workout-may-curb-hunger-lift-reps-new-study-shows/

People who speak more than one language seem to have younger brains, according to research presented Monday at the Federation of European Neuroscience Societies (FENS) Forum 2026 [1].

Our brains are made up of billions of nerve cells which need to communicate with one another. As we age, the connectivity in our brains tends to deteriorate and, as a result, our memory and the speed of our thinking also decline.

The new research found that the more languages people speak, the younger their brains appear. Learning an extra language at a younger age and learning to become highly fluent in another language also seem to slow brain aging.

The research was presented by Dr. Lucia Amoruso from the Basque Center on Cognition, Brain and Language, San Sebastián, Spain, who worked with a team from the Latin American Brain Health Institute at the Universidad Adolfo Ibañez, Chile, the Cognitive Neuroscience Center at the Universidad de San Andres, Argentina, and the Global Brain Health Institute at Trinity College Dublin, Ireland.

The researchers recently published a study [2] showing that in countries where people typically speak more than one language, people seem to age more slowly. In the new study, the researchers carried out detailed analysis on a group of people from the Basque region of Spain who spoke between one and four different languages including combinations of Spanish, Basque, French and English.

They began with a group of 728 people to create a “brain aging clock.” They used a technique called magnetoencephalography which measures brain activity by the faint magnetic fields produced when brain cells are active. The researchers used artificial intelligence to process data on brain activity in people of different ages to show what is a normal level of brain connectivity at any given age.

Then the team used this clock to gauge the ‘brain age’ of a second group of 144 people.

When they compared people’s real age with the age of their brain, they found that those who spoke two languages had brains that appeared around six years younger than those who spoke only one language. For people who spoke three languages, their brains were around seven years younger, and for those who spoke four languages, their brains were around 13 years younger.

Dr. Amoruso said: “In simple terms, people who spoke more languages tended to have brains that looked younger than expected for their chronological age. The effect was not only related to the number of languages spoken. Higher language proficiency and earlier acquisition of a second language were also associated with more delayed brain aging. This suggests that multilingual experience matters as a gradient: it is not simply about being bilingual or not, but about the depth and duration of language experience.”

The researchers took account of factors such as people’s age, sex and education, but caution that they cannot rule out the potential influence of other factors that may have an impact on the brain, such as lifestyle and social engagement.

Dr. Amoruso and the team now hope to carry out similar work in people with neurodegenerative conditions, such as Alzheimer’s disease, where brain aging and resilience are especially important. They also plan to look at whether speaking two or more languages that are very similar could have a bigger effect on the brain, as managing closely related languages may require greater language control.

Source : https://studyfinds.com/speaking-another-language-could-slow-aging-in-the-brain/

Scientists Use Tragic Childhood Syndrome To Argue DNA Tags Help Cause Old Age Decline

Cancer has a dirty trick: it can put itself to sleep. When tumor cells slip into a kind of biological hibernation, they become hard to kill, shrugging off treatment and lying low until conditions improve, then waking up and bringing the disease back. For decades, researchers have struggled to shut down this hiding strategy without causing serious harm elsewhere in the body. A team in Switzerland has now built a molecule that flips on and off with flashes of light, giving scientists a precise new way to probe, and possibly disrupt, the way sleeping cancer cells hide.

Behind this cellular sleep state, at least in certain cancers, sits a protein called the glucocorticoid receptor, a sensor inside cells that reacts to stress hormones. When it switches on, it can push cancer cells, especially in some solid tumors such as lung cancer, into a drug-resistant, dormant state. The obvious fix would be to destroy the receptor outright, but there is a catch: the same receptor does important jobs all over the body, including calming inflammation. Removing it everywhere would cause real damage. What was needed was a way to hit the receptor inside a tumor and leave the rest of the body alone.

That is what the team set out to build. Their solution, described in the journal Proceedings of the National Academy of Sciences, is a class of molecules called photoPROTACs: drug-like compounds engineered to destroy the stress hormone receptor, but only when a specific color of light switches them on. Shine the right light on them, and they go to work. Keep them in the dark, and they stay idle.

A Kill Switch for a Stress Hormone Receptor

It helps to know what a PROTAC is. A PROTAC is a molecule that grabs onto a specific protein inside a cell and tags it for destruction by the cell’s own waste-disposal system. It works like slapping a “delete me” sticky note on an unwanted protein. PROTACs have stirred huge excitement in medicine because they can eliminate proteins that ordinary drugs cannot touch.

Conventional PROTACs have a problem: they are always on. Once taken, they work throughout the entire body, destroying their target in cancer cells and healthy cells alike. For a receptor this important to normal health, that is a dealbreaker.

To get around it, the team embedded a light-sensitive part directly into the PROTAC molecule. By adding a chemical structure that physically changes shape depending on the wavelength of light hitting it, they created a molecular switch. In one shape, called the E-form, the molecule has the right geometry to do its job and destroy the receptor. In the other, the Z-form, it bends into a configuration that leaves it far less active. The switch runs both ways: one wavelength turns the molecule on, another turns it off.

Building the Light-Activated Cancer Switch

Researchers built and tested several versions of these light-switchable molecules, hunting for the best balance of stability and responsiveness. Two lead compounds, KH-5-306 and KH-5-309, stood out. Both flipped almost completely between their active and inactive shapes under different wavelengths of light and showed no signs of wearing out after repeated exposure.

Inside cells, both compounds destroyed the stress hormone receptor in their active E-form at very low doses. Switched to the inactive Z-form, the effect dropped sharply, though the inactive form still held on to some activity. Because the Z-form naturally drifts back toward the active E-form at body temperature, researchers kept it locked in place during experiments by hitting the cells with brief bursts of ultraviolet light every 30 minutes, a lab-only workaround they confirmed did not harm the cells or disturb the biology under study, and not a method meant for patients.

Additional tests confirmed the receptor destruction ran through the cell’s normal disposal machinery: when a separate inhibitor blocked that machinery, the photoPROTACs stopped working. The compounds also left a closely related receptor alone, even at higher doses, a sign the molecules were hitting their intended target and not damaging look-alikes. And the effect proved temporary. When the active compound was washed away after 12 hours, receptor levels started climbing back within 24.

Waking Up Sleeping Lung Cancer Cells

With the chemistry checked, researchers moved to a test closer to real medicine. They took human lung cancer cells and treated them with dexamethasone, a common steroid that switches on the glucocorticoid receptor and nudges these cells into a dormancy-like state. That setup mirrors a real problem: dexamethasone is routinely given to cancer patients to manage inflammation and treatment side effects, yet it may quietly push tumor cells toward this drug-resistant sleep.

After confirming that dexamethasone triggered the expected dormancy response, the team tested whether the lead photoPROTAC, KH-5-309, could reverse it. Cells treated with the active E-form saw the dormancy-linked gene activity roll back toward normal, and a sweep across thousands of genes confirmed the shift toward a more active state. By contrast, the inactive Z-form left those genes essentially untouched, behaving in this experiment as a neutral control on par with no treatment at all.

Source : https://studyfinds.com/scientists-built-cancer-kill-switch-that-turns-on-with-flash-of-light-study-shows/

Slathering on lotion after a morning shower feels like a task checked off for the whole day. A new study suggests that confidence may be misplaced. Researchers tested four popular moisturizers and found that, under the conditions tested, the measurable hydration boost they give skin generally fell back toward untreated skin within roughly three to five hours, long before bedtime rolled around.

Dry skin is more than a cosmetic nuisance. When the outer layer loses too much water, it grows more open to infection, sun damage, and conditions such as eczema, the chronic itchy rash that leaves skin red and flaking. Doctors often recommend moisturizers to help support that protective outer layer, and most of these products work by pulling water into the skin and trying to hold it in place. Yet advice on how often to reapply has mostly run on habit, not hard numbers.

Published in the journal SKIN, this research set out to put a clock on the question. By measuring how long four common moisturizers kept skin more hydrated than bare, untreated skin, the team produced something the drugstore aisle rarely offers: an evidence-based estimate of how long that extra hydration may last after a single application.

How the Moisturizer Study Was Done

Thirty healthy adult volunteers signed up, and researchers dabbed four store-bought moisturizers onto separate spots along their forearms. The lineup covered a ceramide and hyaluronic acid cream (CeraVe Moisturizing Cream), a glycerin and petrolatum cream (Cetaphil Moisturizing Cream), a urea and shea butter repair cream (Eucerin Advanced Repair Crème), and a multi-hyaluronic acid botanical serum (SkinMedica HA5). One spot on each arm got nothing at all, serving as a plain-skin benchmark.

To track hydration, the team relied on an FDA-cleared device that reads how much water sits in the skin without ever breaking the surface, essentially a moisture meter pressed against the arm. Readings came at the start, then at one hour, four hours, and 24 hours after application. Spots were assigned at random across participants so that no single product always landed on the same patch of arm, a small step that keeps one lucky location from skewing the numbers. Between checks, volunteers went about ordinary life and simply avoided washing or scrubbing the test patches. Lab readings happened under steady temperature and humidity, while the hours in between unfolded wherever daily life took each person.

What the Moisturizer Study Found

Over the full day, only the botanical serum kept skin measurably more hydrated than untreated skin in the researchers’ 24-hour statistical analysis. Averaged across the entire day, the three creams showed no meaningful difference from untreated skin, a result that sounds damning until you look at the timing instead of the daily average.

That timing told a different story. Using a statistical model, researchers estimated the point when each product’s hydration benefit fell back to the level of untreated skin. The glycerin and petrolatum cream held its lead for about three hours, the urea and shea butter cream for roughly three and a half, and the serum stretched to nearly five hours. Short-lived gains like these wash out when smoothed over a full day, which is why the creams looked flat in the 24-hour average while still appearing to provide measurable hydration in the early hours after application.

One product behaved differently. Rather than producing a noticeable rise and decline in hydration, the ceramide cream closely tracked untreated skin throughout the study. Researchers offered a cautious possibility: it may help stabilize the skin barrier instead of producing a measurable spike in water content, a quieter effect their measurements were not designed to capture directly. They stressed that this explanation remains speculative. It does raise an interesting question, though, about whether an effective moisturizer always has to produce a dramatic hydration spike or whether maintaining steadier conditions could also be beneficial.

What the Findings Mean for Reapplying

For someone managing a condition that demands steady moisture, a once-in-the-morning, once-at-night routine could leave stretches of the afternoon when skin hydration has fallen back toward untreated levels, at least under the single-application conditions this study tested. Eczema and similar conditions flare when the skin barrier becomes compromised, so maintaining hydration is often an important part of care. Whether topping up more often would improve outcomes is a question the researchers did not test directly, so the practical advice stops short of recommending a specific reapplication schedule. Anyone considering changing their skincare routine, particularly for a medical skin condition, should discuss it with a healthcare professional.

Cost muddies the picture too. The serum lasted longest in this study but also carries the highest price, while the cheaper, easier-to-find creams showed shorter hydration intervals. Spending more bought more hours here, yet the study never examined whether reapplying a lower-cost moisturizer more frequently could produce similar results.

Source : https://studyfinds.com/your-morning-moisturizers-hydration-boost-may-fade-by-lunch-study-finds/

 

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Some national pride goes beyond flying a flag or cheering at the Olympics. It runs on a quieter, more brittle conviction that one’s country is exceptional, perhaps even the greatest, and that the rest of the world stubbornly refuses to admit it. Psychologists have a name for that mindset: national narcissism.

While national narcissism appears to be a comfort for many of its adherents, according to a new study that tracked hundreds of young adults over time, holding it was linked to higher stress down the road.

Researchers long assumed the relationship ran in one direction. People who feel bad about themselves, the thinking went, grab onto an inflated sense of national pride like an emotional life raft, with stress, depression, and a bruised sense of self-worth pushing them toward grand beliefs about their nation. Research published in the Journal of Research in Personality complicates that story.

Rather than emotional pain feeding national narcissism, the data points the predictive arrow the other way, and the relief people might hope to get from the mindset does not seem to arrive, at least within the window the study covered.

That twist matters because so much public commentary treats wounded pride as the cause and grievance as the symptom. These findings flip the order, at least for young adults: the belief appears to come first, and the stress follows.

Inside the National Narcissism Study

A team based in the Czech Republic and Poland followed 688 Czech young adults between the ages of 18 and 30 across two survey rounds set roughly a year apart. Most participants were women, and the group ran the gamut from full-time students to working adults and people outside the workforce. Participants answered questions about their national pride, stress levels, depressive feelings, and personality, including a measure of how emotionally reactive they tend to be in general.

To gauge national narcissism, participants rated how strongly they agreed with statements capturing the idea that their nation deserves far more recognition than it gets, scored on a scale from one to four. Stress was measured by asking how often, over the past month, someone felt unable to control important things in life. Depression was screened with two questions about feeling down or losing interest in activities. Researchers then leaned on a statistical method that tracks how one trait at an earlier point predicts another later on, which let them untangle the direction of the links.

With nearly 700 participants, the sample was large enough to catch even modest relationships between the variables. Researchers also controlled for each person’s general tendency toward negative moods, so the results would not simply reflect the fact that some people are gloomier by nature.

National Narcissism Came First, Stress Followed

Only one predictive link surfaced in the analysis: national narcissism in the first round predicted higher stress by the second. Neither stress nor depressive symptoms predicted stronger national narcissism later on. That pattern held whether participants were in their late teens or their late twenties, and it did not shift across the status measures the researchers tested, including education, employment, and financial strain.

Going in, the team expected that people in lower-status spots, younger participants or those with thinner financial cushions, might show a tighter link between emotional distress and national narcissism, since they arguably have more to gain by hitching their self-worth to national identity. That expectation did not pan out. Results looked much the same across the board.

There was one more wrinkle. Stress and depressive symptoms both tracked closely with a person’s baseline tendency toward negative moods, as expected. National narcissism behaved differently: it was not tied to that emotional baseline in the same way, which hints that the belief is not just another expression of a gloomy disposition.

An Endless Chase for Recognition

Why would believing a nation is secretly great breed stress rather than ease it? Drawing on a psychological framework about how people react when their self-worth feels threatened, the authors describe national narcissism as a chase with no finish line. Someone who draws importance from a nation’s supposed greatness stays exposed to a steady drip of threats: foreign criticism, unflattering news coverage, political setbacks, or simply the sense that the world is shortchanging their country. Living in that state of constant vigilance, the authors argue, wears a person down.

They also flag that national narcissism predicted stress but not depressive symptoms over the year studied. One reading is that the puffed-up self-image these beliefs carry may shield people from low mood in the short run, even as the endless hunger for outside validation keeps stress simmering. Another possibility the authors raise is that the heavier emotional toll may need longer than a year to show itself.

Source : https://studyfinds.com/national-narcissism-linked-rising-stress-young-adults/

Quitting the day job to work for yourself carries a certain mythology: the bold young founder, the garage startup, the freedom of answering to no one. A new study that followed thousands of Americans for more than three decades muddies that picture in a blunt way. For a large share of those who struck out on their own, particularly people who did it later in life and never registered a formal company, the move was linked to lower well-being and no extra money to show for it.

That finding lands against a long-running argument about who entrepreneurs really are. Some research has cast self-employment as a young person’s pursuit, fueled by risk appetite that fades with age. Other work puts the peak in midlife, when savings and connections pile up. Researchers Seok-Woo Kwon and Xiaoying Wang of the University of Calgary’s Haskayne School of Business argue both camps may be partly right, and partly fooled by their own math. When everyone gets averaged into a single curve, very different lives get blended into a number that describes almost no one.

Kwon and Wang pulled those lives back apart. Drawing on a federal survey that has tracked the same nationally representative group of 12,686 Americans since 1979, when participants were teenagers, they traced who became self-employed, when, for how long, and how those paths related to their finances and well-being by around age 50. As the study notes, “The key theoretical insight is that there is no single relationship between age and entrepreneurship.” Instead, several different relationships run side by side, each with its own logic.

Four Entrepreneurial Careers Hiding Inside One Average

Analyzed the usual way, with everyone treated as variations on a single trend, self-employment looks like it climbs steadily with age, rising from about 2 percent of people at 18 to roughly 17 percent by 50. That curve is tidy but misleading, because one line averaged across the whole group can hide people moving in opposite directions. A second method sorted participants by their actual year-by-year patterns instead of forcing them onto one trend, and four distinct paths fell out.

Most people, about 69 percent, never really went into business for themselves at all. A small core of career-persistent entrepreneurs, around 6 percent, jumped in young and stayed in, with roughly 80 percent of the group self-employed by their mid-30s and holding there. The remaining two groups dabbled and moved on. Early-adulthood entrepreneurs, about 12 percent, spiked in their twenties and early thirties, then drifted back to conventional jobs. Middle-aged entrepreneurs, about 13 percent, did the reverse, staying employed through their twenties before ramping up after their mid-30s.

Those opposite shapes matter because they cancel each other out in an average. A sample heavy with midlife starters looks like a midlife peak; a sample heavy with young, persistent founders looks like a young person’s trend. Same country, same decades, different conclusions, depending on who happens to be in the room.

Incorporation, Not Timing, Tracked the Payoff

Here is the split that should make anyone weighing self-employment pause: whether the venture was incorporated mattered more for life outcomes than when it started. Incorporating means registering a formal company rather than operating as a freelancer or informal sole proprietor, and the two roads led to opposite destinations.

People who built incorporated businesses tended to come out ahead on both money and mood. Career-persistent incorporated founders showed the largest lifetime-earnings premium, with midlife incorporated starters close behind, and several of these groups reported higher life satisfaction than people who never went into business. Unincorporated self-employment told a darker story. It was tied to lower well-being and produced no measurable earnings advantage at all.

The grimmest combination was starting an unincorporated venture in middle age. That group reported the steepest drop in well-being of anyone studied, with no financial gain to offset it. Some of those midlife starters were chasing opportunity, but others may have been pushed toward it by weaker job-market options or career pressure, a difference the authors say programs aimed at would-be founders ought to screen for before cheering anyone on.

Family Business at the Dinner Table

Where do these paths come from? Long before anyone files paperwork, family shapes the odds. Kwon and Wang tested three kinds of early advantage measured at or before age 18: cultural (magazines, newspapers, and a library card in the home), social (a parent or other family member in the household who owned a business), and economic (family income).

Growing up around a family business was the strongest and most consistent predictor of going into business later, across every path. A childhood steeped in reading material had a narrower role, linked mainly to keeping a formal company running over the long haul rather than to starting one. Family income, the factor many people would bet on first, barely moved the needle on which path someone followed. Money in the household, in other words, mattered less than a working example of someone who ran their own shop.

Source : https://studyfinds.com/self-employment-often-doesnt-pay-off-decades-long-study-of-entrepreneurs-shows/

Ancient DNA Hidden in Pacific Islanders Reveals Three Separate Encounters With a Mystery Ancestor

The United States government’s recent release of hundreds of previously classified Unidentified Anomalous Phenomena (UAPs) cases spanning the 1940s to the present, along with the new Steven Spielberg movie, Disclosure Day, about extraterrestrial life, has fuelled the idea that aliens are visiting Earth.

In fact, polls in Australia, the U.S. and elsewhere indicate around a third of the public believes aliens are here.

However, while what we know about the universe suggests aliens may exist, there are three compelling reasons why they probably aren’t visiting us.

Space is Big – Very Big

To begin with, space is vast – beyond our imagination.

Proxima Centauri, the nearest star to our Sun, is about 40 trillion kilometers away, 268,000 times farther than the Sun is from Earth. That’s 4.3 light years as astronomers measure it. A light year is the distance light travels in one year at 300,000km per second.

We can only travel across space at a fraction of the speed of light with current technology. Even our fastest spacecraft, the Parker Solar Probe, travels at a top speed of roughly 191 kilometers per second – 0.064% the speed of light.

At that speed, it would take about 6,650 years to reach Proxima Centauri, and that’s just in our local stellar neighborhood. So interstellar travel within human lifespans would require much higher velocities.

Let’s assume we did have the means to travel close to the speed of light. That introduces the first problem with traveling at that velocity. Albert Einstein demonstrated that time is relative; the rate of time flow is not the same everywhere in the universe. The faster a spaceship travels from Earth, the slower time will pass for its passengers. This is called time dilation.

For example, when NASA astronaut Scott Kelly arrived back on Earth from a year on the International Space Station, he was milliseconds younger than his identical twin because time moves more slowly for objects in motion, and the International Space Station travels at roughly 28,150 kilometers per hour.

This difference was negligible for the Kelly twins. But for any aliens cartwheeling through our skies, it would be significantly more because of the journey to Earth and back from a distant star system at a necessarily higher speed. They would go home to a planet much older than the one they left – perhaps by a century or more. They would be time exiles.

Unimaginably high energy requirements

Then there’s the unimaginably high energy requirement for interstellar travel.

The mass of the spaceship increases with velocity, so an increasing amount of energy is required to accelerate it.

At the speed of light, the ship becomes infinitely massive, requiring an infinite amount of energy. This is clearly impossible.

Another significant issue is that space is a vacuum – but not completely. There are just enough particles to worry about. They can potentially cause fatal radiation for passengers and the instruments of a high-velocity spacecraft, or destroy it. Sparsely spread hydrogen atoms turn into intense radiation at near light speed, and the heat that is generated would ablate and eventually destroy the hull.

Faster-than-light travel, according to physicist Miguel Alcubierre, is possible, but it comes with its own set of issues and a currently impossible energy requirement.

That raises the question of why spend all this energy to travel to Earth? Anything we have, an advanced civilisation (as they would have to be to get here) would be able to make on their planet.

A Unique Biosphere

Yet another issue is our biosphere, unique to Earth as far as scientists know.

Life and the planet co-evolved. Complex life would not exist on Earth if cyanobacteria, a type of single-celled microbe, had not pumped oxygen into our mostly nitrogen atmosphere 2.4 billion years ago.

It’s therefore not toxic for us, but oxygen is reactive and could be highly corrosive for aliens. And while they could wear protective suits like humans do when going to inhospitable environments, reports of visiting aliens do not include any descriptions of spacesuits.

So, Are Aliens Out There?

If aliens are not here, are they out there? It’s an interesting question, scientifically and philosophically. Scientists do not have enough information yet, but they are working on the question.

About 6,200 exoplanets have been found in more than 4,700 solar systems, though none are like Earth or our Solar System.

Most stars could have at least one planet, and there are more than 100 billion stars in our galaxy alone. The number of planets is therefore astronomical, and some may be habitable.

Closer to home, there are worlds with potential for microbial life either past or present – Mars, Europa (a moon of Jupiter), and Enceladus and Titan (moons of Saturn). If we discover life began twice in our Solar System, that will increase the odds of life elsewhere.

Source : https://studyfinds.com/aliens-might-exist-reasons-why-theyre-not-visiting-us/

Your Parents’ DNA May Shape Your Traits in Ways You Didn’t Directly Inherit

Aging Ankles Trade Efficiency for Stability, and New Research Shows Exactly When the Switch Happens

Standing on a bus that lurches forward. Catching a stumble on an icy sidewalk. For younger people, these moments of lost balance are handled almost automatically. Fast, lower-level brainstem circuits fire off corrective signals before anyone even realizes what happened. But as people age, the brain has to recruit backup. A new study finds that older adults and those with Parkinson’s disease rely more on the brain’s higher-level regions just to stay upright, and that this shift can be detected without ever scanning the brain itself.

Researchers at Georgia Institute of Technology, Emory University, Ohio University, and the University of Padova built a computer model that breaks down the muscle responses people produce when knocked off balance into separate parts, each linked to a different level of the nervous system. By analyzing how quickly and intensely leg muscles fire after a person is physically pushed off balance, the team could infer which pathways were likely contributing, whether fast, automatic circuits deep in the brain or slower circuits linked to higher-level brain regions.

Falls are among the leading causes of injury and death in older adults, and balance problems are a hallmark of Parkinson’s disease. Yet doctors have had limited tools to understand why a particular person’s balance is faltering at a brain level. This study, published in eNeuro, offers a potential new way to peer inside the nervous system’s balance-control chain of command using nothing more than muscle recordings and a moving platform.

How Researchers Tested Balance in Older Adults and Parkinson’s Patients

Nineteen older adults without Parkinson’s disease and 17 individuals with Parkinson’s were recruited for the study. Participants with Parkinson’s were asked to stop taking their medications for at least 12 hours before testing so the researchers could observe the disease’s effects without the masking influence of drugs. Each person’s neurologist approved this temporary medication pause.

Participants stood barefoot on a motorized platform that could slide forward or backward without warning. Each person received 48 pushes across six conditions that varied by direction and intensity. Medium and large pushes were adjusted based on each person’s height so the physical challenge was comparable across participants. Everyone was told to cross their arms, stare at a fixed point about 15 feet away, and try to recover their balance without taking a step.

While participants wobbled and corrected, sensors tracked their body motion and electrodes on their lower legs recorded electrical activity in two muscles: one along the shin and one in the calf. These two muscles work in opposition. When one contracts to pull the body forward, the other resists. Together, they offer a window into how the nervous system orchestrates a balance correction.

A Math Model That Separates Fast Brain Circuits From Slow Ones

At the centerpiece of the study was a mathematical model the researchers call a “neuromechanical model.” It reconstructs recorded muscle activity by combining information about how the body moved with time delays that correspond to known speeds of different brain pathways. Faster signals, arriving roughly 120 milliseconds after the push, are consistent with processing in lower, more automatic brain regions. Slower signals, arriving around 200 milliseconds, match the timing expected when information has to travel up to the brain’s outer layer, the cortex, and back down again.

Splitting each balance-correcting muscle response into two components, the model found the first kicked in around 119 milliseconds in older adults without Parkinson’s and 116 milliseconds in those with the disease. The second arrived around 200 milliseconds in older adults and 215 milliseconds in Parkinson’s participants. Both components grew stronger as the pushes got bigger, which makes intuitive sense: a harder shove demands a bigger correction. And the two-loop model was far more accurate than a simpler, single-loop version, with reconstruction accuracy improving by roughly 10 percent when the second, slower loop was included.

Why Muscles Sometimes Fight Against Their Own Balance

Beyond the main muscle that corrects balance, the researchers also examined what happens in the opposing muscle, the one that sometimes fires at exactly the wrong time. This kind of opposing muscle activity is commonly observed in older adults and people with Parkinson’s, creating a tug-of-war in the legs.

Carved into two pieces by the model, opposing muscle activity breaks down into a “destabilizing component” that actually works against balance recovery and a “stabilizing component” that helps the body adjust as the platform slows down. That destabilizing burst arrived at about 181 milliseconds in older adults and 173 milliseconds in those with Parkinson’s, a timing window consistent with circuits running through a cluster of brain structures heavily damaged in Parkinson’s disease.

Among older adults without Parkinson’s, higher levels of this destabilizing muscle activity were linked to worse scores on a clinical balance test that evaluates things like sensory awareness, dynamic walking, and the ability to recover from a push. Put simply, the people whose muscles fought hardest against their own balance corrections tended to be the ones who struggled most on standardized assessments.

That correlation did not hold in the Parkinson’s group. Researchers suggest this disconnect may reflect the broader neurological changes that accumulate as Parkinson’s progresses, making the relationship between any single muscle-activity pattern and overall balance ability harder to pin down.

One difference did emerge between groups: people with Parkinson’s showed a larger acceleration-driven component of the destabilizing opposing muscle activity during forward pushes compared to older adults without the disease. This fits with a well-known feature of Parkinson’s in which muscles contract inappropriately when they should be relaxing.

How Aging Shifts the Balance Burden to Higher Brain Regions

When comparing their findings to previously published data from younger adults, a notable pattern emerged. Older adults, with or without Parkinson’s, appeared to engage the slower, thinking-brain response at smaller push intensities than younger adults did. In younger people, the faster automatic circuits seemed to handle mild disturbances on their own, only calling in reinforcements from higher brain regions when the challenge ramped up. Older adults, by contrast, seemed to need that backup even for gentler pushes.

This observation lines up with a well-established idea in brain science: as people age, the brain compensates for declining automatic processes by calling on additional resources from its outer layers. It is the neural equivalent of needing reading glasses. The hardware still works, but it needs more help to do the same job.

Worth noting is that direct statistical comparisons between the older adult data and the previously published younger adult data were not possible because the experimental setups differed. Still, the pattern is consistent with evidence suggesting that this kind of brain over-recruitment is a signature of aging balance control.

Source : https://studyfinds.com/older-brains-work-harder-falling-muscle-test/

A diagonal earlobe crease called Frank’s sign may signal hidden heart disease risk, especially alongside diabetes, hypertension, smoking, or obesity.

When people think about warning signs of heart disease, symptoms like chest pain, breathlessness, fatigue, or irregular heartbeat usually come to mind. But doctors say there may be another subtle clue hiding in plain sight – right on your ears.

A small wrinkle or diagonal crease on the earlobe, known as Frank’s sign, has increasingly been linked to cardiovascular disease in several medical studies. While it may look harmless, experts believe this tiny mark could signal underlying problems with blood vessels and heart health.

Guava Juice May Boost Hemoglobin in Women

Scientists Destroyed a Few Dozen Neurons in a Fish and Watched Its Social Life Fall Apart

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.

Source : https://apnews.com/article/ai-unemployment-remote-work-hiring-1942a6b0c8dc6f17a30878735a0256ae

Women Over 50 With Low Protein Intake Face Dramatically Higher Odds of Losing Basic Physical Independence

Board-Certified Physicians Put Popular LLMs Through Their Paces, and Found Real Problems

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%).

Source : https://studyfinds.com/half-americans-say-no-fun-in-life/

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.

Source : https://studyfinds.com/rich-salty-cheese-good-gut-health/

Ice Age Icebergs Left 3,000 Scratch Marks in the Great Lakes, and They Recorded Winds Blowing the Wrong Way

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.

 

Source:https://www.channelnewsasia.com/asia/southeast-asia-largest-dinosaur-thailand-dig-up-nagatitan-chaiyaphumensis-6121511

Caring for a Loved One May Slow or Speed Mental Decline, Depending on the Burden

People With Stronger Focus May Pay Less Attention to Social Media Posts, Study Finds

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.”

Source : https://www.indianewsnetwork.com/en/walking-8-500-steps-daily-may-help-prevent-weight-regain-20260511

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.

Source : https://studyfinds.com/exercise-quit-smoking/

Study Links UPFs To Rising Dementia Risk Scores

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.

Source : https://studyfinds.com/chewing-gum-fights-mouth-cancer-hpv/

 

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.”

Source: https://apnews.com/article/kraken-cretaceous-octopus-fossil-ab911a3fcae1f32443770308348cfbe6

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.

Source : https://studyfinds.com/chewing-gum-fights-mouth-cancer-hpv/

 

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.

Source: https://studyfinds.com/why-crabs-walk-sideways/