When French writer Marcel Proust famously recalled his childhood from the taste of a Madeleine cookie, his stomach may have done some of the work. We generally associate our memories almost exclusively with the brain, which we imagine forms and stores them. New research led by Scott Kanoski, professor of biological sciences at the USC Dornsife College of Letters, Arts and Sciences, has found that our gut may also play an important role in helping us remember experiences, especially those involving food.

The study, published in Nature Communications, focused on the vagus nerve, a major communication highway that connects the digestive system to the brain. Scientists have long known that the vagus nerve helps regulate digestion, hunger and feelings of fullness. Now, researchers have uncovered evidence that signals traveling from the gut through the vagus nerve can also help form memories.

Memorable munchies

The researchers found that when rats consumed nutritious foods, neurons communicating to the hippocampus, a part of the brain critical for learning and memory, released higher levels of a chemical called acetylcholine. This neurotransmitter supports memory formation and helps the brain encode new experiences.

The response depends on signals traveling from the gut via the vagus nerve. When the researchers interrupted vagus nerve communication, the increase in acetylcholine disappeared. These rats also performed worse on memory tests that required them to remember where they had recently found food.

The scientists also discovered that the brain’s memory system seems to respond primarily to a food’s nutrients, not just its pleasing taste. Rats that ate sugar or fat showed strong memory-related brain activity. Those given sweet-tasting but low-calorie or noncaloric liquids did not show the same response. This suggests that the brain reacts to the actual nutritional value of food, rather than just its flavor.

“We think the mechanism likely evolved to help animals remember vital information about food sources,” says study first author Logan Lauer, a Ph.D. student in Kanoski’s lab. Recalling where certain plants sprout first in the spring can help hungry animals find important nutrients. Signals from the gut tell the brain, “This meal provided valuable nutrients, so remember where and how you got it.”

Brain-boosting research

Although high-fat and high-sugar foods sparked strong memory responses, the study also found that chronic exposure to these items worsened memory formation over time.

Rats that consumed this type of diet early in life showed weaker communication between the gut and the hippocampus later on. Even after returning to a healthier diet, these animals had reduced memory-related brain responses and poorer performance on food-location memory tasks.

The findings could have important implications for human health. Scientists already know that obesity, poor diet and metabolic disorders such as diabetes are associated with cognitive decline. This new research suggests one reason why: Constant exposure to junk food may disrupt the connection between our gut and our brain.

The work could also shed new light on neurodegenerative diseases.

“The disruption of acetylcholine signaling in the hippocampus is one of the earliest neurochemical changes in Alzheimer’s disease,” says Kanoski. “By revealing that this system is boosted by gut signaling from the vagus nerve, novel therapeutic targets could leverage this information to explore vagus nerve-based approaches, such as vagus nerve stimulation.”

The discovery also raises the possibility of new treatments to strengthen communication between the gut and the brain. Therapies that stimulate the vagus nerve or improve gut health could potentially help protect memory and cognitive function.

While much more research is needed to determine whether the same mechanisms operate in humans, the findings add to a growing body of evidence that the gut and brain are deeply connected.

Every year, untreated tooth decay sends thousands of young U.S. children to emergency departments for dental problems doctors can’t treat. Many eventually undergo surgery under general anesthesia, while others endure pain and infection.

A simple, inexpensive liquid called silver diamine fluoride, or SDF, could spare many of those children. Applied to a cavity with a tiny sponge-tipped applicator in a few seconds per tooth, SDF arrests decay without drilling, shots or sedation.

Dentists have used SDF successfully for decades in many countries and off-label in the United States since 2014, when it was approved as a medical device to treat tooth sensitivity. However, it has lacked the large U.S. population clinical trials on efficacy and safety needed for FDA approval as a drug to treat cavities.

Now, a University of Michigan-led clinical trial has produced that evidence.

Trial data backs a simple treatment

Published in JAMA Pediatrics, the Phase III trial enrolled 830 children younger than 6 who were recruited through dental offices, pediatric medical practices, Head Start and Early Head Start programs in Michigan, New York and Iowa.

Researchers found that 38% SDF arrested tooth decay in more than half of children’s affected baby teeth when treated at 6-month intervals. Unlike conventional treatment, which removes part of the tooth before placing a filling, SDF is simply painted onto the cavity.

“This is a very effective and safe treatment—even in children as young as 1,” said Margherita Fontana, professor of dentistry at the University of Michigan School of Dentistry and the study’s lead investigator.

Tooth decay is the most common chronic disease of childhood, affecting more than 40% of U.S. children. Left untreated, cavities can cause severe pain, infection, difficulty eating and sleeping, missed school and repeated medical visits.

SDF may be especially valuable for very young children, older adults, people with developmental or physical disabilities, patients with severe dental anxiety and others who cannot easily tolerate or access conventional dental treatment, Fontana said.

A cosmetic trade-off, but wider reach

Its primary drawback is cosmetic, she said. The silver permanently darkens the decayed portion of the tooth.

“If we want more children and families to benefit from this treatment, we need rigorous evidence showing both that it works and that it’s safe. From a public health perspective, if we want broader implementation across the United States, including in medical settings, we need carefully collected data in U.S. populations, and we now have that,” Fontana said.

The study began in 2018 and progressed despite the challenges of the COVID-19 pandemic.

“In medicine, clinicians want high-quality evidence before changing practice,” Fontana said. “It is important to have data they can refer to because young children often see pediatricians years before they ever visit a dentist. Broader acceptance could allow many more cavities to be treated while a referral to a dental home is successful and before they become painful, infected or require surgery.”

Fontana and co-researchers from New York University, the University of Iowa and Indiana University, together with the NIH’s National Institute of Dental and Craniofacial Research, completed a study that provides clinical trial data needed by the manufacturer to submit a dental caries drug application to the FDA. The product used in this trial, Advantage Arrest 38% SDF, was provided by Elevate Oral Care.

Path toward broader approval

Amr Moursi, professor of pediatric dentistry at New York University College of Dentistry, said the study provides important data for broadening use of SDF.

“Our results support FDA approval of SDF for managing tooth decay in young children. Removing SDF from off-label status would be an important innovation that could lead to increased use by providers, enhanced payments by insurers and more consistent product quality,” said Moursi, a co-principal investigator on the study.

For some children, reapplying SDF every few months may be all that’s needed until the baby tooth naturally falls out. For adults, it may serve as a long-term treatment or as a bridge until a restorative procedure is affordable or practical.

“For almost anyone, this can arrest the decay and stop the infection and the pain it causes,” Fontana said. “This could benefit many people.”

When humans tackle many everyday tasks, ranging from driving to completing household chores and work assignments, they rely heavily on working memory. This is the brain’s ability to temporarily store and manipulate important information that can help complete a task in the immediate future.

This temporarily stored information can be used to make decisions and plan subsequent actions, such as which supermarket aisle to visit next or where to turn while driving. While many studies have investigated working memory processes, the impact of distractions or unexpected events on these processes remains poorly understood.

Researchers at the University of Texas at Austin recently conducted a study aimed at better understanding how people respond to distractions while completing tasks. Their findings, published in Communications Psychology, suggest that working memory is highly flexible and can rapidly reprioritize the information it is temporarily holding after an interruption.

“A key factor influencing the dynamic allocation and updating of cognitive resources is an individual’s state relative to their goals,” Ziyao Zhang and Jarrod A. Lewis-Peacock wrote in their paper. “For instance, when following a mental shopping list, decisions about which item to prioritize depend largely on the person’s location. In real-world scenarios, agent states are dynamic and often disrupted by urgent distractions or important interruptions. How people adapt to such perturbations remains unclear because studies of distraction resilience in working memory typically fix agent states.”

Assessing responses to distraction with the ‘Snake’ game

To investigate the effects of distractions on working memory processes, Zhang, Lewis-Peacock and their colleagues conducted a series of experiments involving 50 adult participants. The participants were asked to play a version of the arcade game Snake, which became widely popular after it was introduced on early Nokia cellphones.

The game requires players to use keyboard arrows to control a snake on a screen, moving it onto specific targets (i.e., apples) that it will swallow. Eating the apples increases the snake’s length, making it more challenging to navigate the delineated environment on the screen.

In the version of the game used by the researchers, players had to memorize the locations of apples, which appeared on the screen only briefly. Moreover, during some experimental trials, an unexpected target would suddenly appear on the screen. This was another edible fruit (i.e., a grape), which participants had to direct the snake to before reaching the next apple.

“Participants controlled a snake in a rectangular field to locate memorized apples and earn points,” the authors wrote. “Each trial required encoding one, two or four apple locations, followed by memory-guided navigation to capture all apples. In half of the trials, distractions (the sudden appearance of additional target grapes) required participants to deviate from their initial plans and collect grapes before resuming the search for hidden apples.”

Zhang, Lewis-Peacock and their colleagues looked at how participants performed on the Snake game with and without distractions. They also tried to determine what happened to memories related to the locations of nearby apples after unexpected stimuli (i.e., grapes) appeared on the screen.

“Without distractions, participants prioritized nearby targets, using proximity as a cue for memory allocation,” Zhang and Lewis-Peacock wrote. “When distractions perturbed the agent’s position, participants flexibly redistributed resources to prioritize targets nearer the updated position. This flexibility declined with higher memory loads, and critically, reliance on working memory following distraction was limited to a single item regardless of load.”

Interestingly, the team observed that after a distraction, participants typically shifted their focus to a single prioritized memory item, even when they had originally memorized multiple apple locations. After collecting the grapes that had unexpectedly appeared on the screen, they reorganized their working memory to prioritize the remembered apple closest to the snake’s new position on the screen.

Possible implications for memory models

The results of this study suggest that when people are completing a task and a distracting event occurs, they dynamically shift their priorities toward the most immediately relevant information. This allows them to address the distraction without losing sight of their goals.

“These findings reveal dynamic working memory redistribution as a mechanism that enables flexible but constrained resilience to distraction in dynamic environments,” the authors wrote.

Future studies could build on the team’s observations and try to uncover the specific neural processes underpinning the reorganization of temporarily stored information after distractions. Eventually, this could help improve existing working memory models, which may also inform the development of artificial intelligence (AI) systems or other brain-inspired computational systems.

Results from a small clinical trial suggest it may be possible to reduce the risk of dementia by eating during fewer hours of the day. The pilot study, which involved a weight-loss program for older women with overweight or obesity, showed modest cognitive improvements among those who limited their daily eating window instead of just reducing their calorie intake.

“Losing weight alone will ward off some of the aging-related cognitive decline, and these data suggest that there may be additional benefits if you stop eating four hours before going to sleep and reduce food intake to 8–9 hours per day, compared with the usual eating window of 12 hours per day,” said Sue Shapses, Ph.D., RD, DFASN, professor at Rutgers University and Rutgers-RWJ Medical Center and the study’s principal investigator.

Shapses’ group will present the findings at NUTRITION 2026, the flagship annual meeting of the American Society for Nutrition, held July 25–28 in National Harbor, Maryland, just outside Washington, D.C.

Who was in the trial

Alzheimer’s disease and other forms of dementia have become more prevalent as populations age, and women and people who are overweight or obese tend to face a higher likelihood of developing these conditions. Diet and other lifestyle factors have been linked to dementia risk, but few studies have examined whether modifying these factors can reduce that risk.

The trial enrolled 47 women ages 50–79 who were overweight or obese. All participants were counseled to reduce their calorie intake by 500 calories per day. Twenty-six participants were asked to restrict their eating to a window of less than nine hours per day, while the rest maintained a typical eating window of about 12 hours per day.

In the time-restricted eating group, participants generally ate only between 10 a.m. and 6 p.m., with an average daily eating window of 8.2 hours, compared with an average of 12.3 hours per day among those asked to maintain the standard eating window.

Cognitive gains despite similar weight loss

After six months, participants had lost about 15 pounds (6.8 kilograms), on average, about the same in both groups. Compared with participants who maintained a 12-hour eating window, those who consumed food for only 8–9 hours per day showed significant improvements in spatial planning and problem-solving at the end of the weight-loss program. They also showed a trend toward fewer errors on memory and learning tests, but there was no significant difference in performance on multitasking or reaction-time tests.

“There was a modest effect of time-restricted eating on improving spatial planning and problem-solving and reducing errors related to memory and learning,” said Shapses. “These outcomes suggest a better ability to remember information during everyday tasks and fewer mistakes related to memory, attention and problem-solving. Reductions in the eating window predicted greater improvements.”

Clues the team wants to test

The researchers said further studies would be needed to confirm the findings in a larger group of participants. They also plan to investigate mechanisms that might explain the possible benefits of time-restricted eating, such as interactions among circadian rhythms, nutrient-sensing pathways, inflammation and metabolic health.

Implanted medical devices are instruments placed surgically in the body. Many are battery-powered or can be wirelessly recharged. While they can be lifesavers, they are not without problems. They can run out of battery power, and wireless methods for transferring power and data have technical limitations.

One possible solution would be a physical plug that connects an implanted device to external equipment. But that would introduce more issues. The wound would have to remain open, increasing the risk of infection, while rigid materials could also damage surrounding tissue.

To address the challenge, scientists at the University of California, Irvine, have developed a soft, tissue-like port called the Implantable Bioelectronic Outlet, or IBO. It is essentially a hidden electrical socket beneath the skin. If doctors need to download high-speed data, recharge an implanted battery or deliver electrical stimulation, they can insert a tiny needle directly through the skin into the soft port.

Details of the technology are published in the journal Science Advances.

Building a tissue-like plug

The IBO is made primarily from a soft, sponge-like porous polymer with holes about 150 micrometers wide, roughly the diameter of a stylet (a thin needle-like probe). The researchers dipped the foam into a conductive polymer to coat the inner walls of the tiny holes, allowing electricity to flow smoothly through the entire structure while keeping it flexible.

Next, they coated it with a thin, water-resistant silicone layer to keep moisture out and electrically insulate it. Finally, they stacked several of these silicone-coated sponge layers together and bonded them using flexible silicone.

Testing safety and performance

After initial mechanical and electrical tests, they implanted the devices in rodents. The ports allowed the research team to stream high-speed digital brain signals from an internal chip at 16 megabits per second, recharge an implanted battery and deliver nerve stimulation currents.

These IBOs remained functional after more than a year inside the body, and the surrounding tissue showed no major scarring or inflammation. “Chronically implanted IBOs were functional and biologically well tolerated after one year of implantation,” the study authors wrote.

In an experiment with pigs, the outlet was used during surgery to deliver electrical stimulation to the optic nerve and performed just as well as a conventional wired connection. “The IBO addresses key challenges of signal and power transfer for implantable bioelectronics.”

While there is much more work ahead, the team believes its socket could provide a safe and reliable way for external hardware to connect directly to devices inside the body.

Sleep is known to be essential for survival, as it allows both humans and other animals to rest, while the brain consolidates memories and clears out metabolic waste products. For many people worldwide, however, falling asleep at a reasonable time every evening and sleeping enough hours is challenging, due to various conditions such as insomnia, circadian rhythm disorders, depression and anxiety.

While there are now various treatment options for those who are struggling to fall asleep, many existing medications can cause dependence or undesirable side effects, such as next-day drowsiness and rebound insomnia. Better understanding the neurological processes associated with sleep could potentially help to devise more effective and non-addictive medications that induce sleep.

Researchers at the Chinese Academy of Sciences and other institutes in China recently showed that a naturally occurring molecule called tryptamine (TrpA) could contribute to a gradual increase in the brain’s drive to sleep.

Their paper, published in Nature Neuroscience, reports that activating the receptor that detects this molecule could increase the duration and boost the quality of sleep in both mice and pigs.

“Wakefulness produces sleep-promoting substances and the cerebrospinal fluid contains substances that reflect homeostatic sleep pressure,” wrote Huateng Cao, Kui Wang and their colleagues in their paper.

“However, the identities of such molecules, and the neural mechanisms for producing and sensing them, remain mysterious. We show that cerebrospinal fluid levels of TrpA track homeostatic sleep pressure in nocturnal mice and diurnal pigs, reflecting physical activity history independently of light–dark cycles.”

How tryptamine signals the brain’s need for sleep

The familiar feeling of becoming increasingly sleepy after spending several hours awake is scientifically known as “sleep pressure.” This drive to sleep is a key component of sleep homeostasis, or in other words, the biological process that balances the time animals spend awake and asleep.

To identify chemicals that contribute to the gradual increase in sleep pressure during waking hours, the researchers examined nocturnal mice and diurnal pigs. More specifically, they used a molecular tool they developed to measure levels of TrpA in the animals’ cerebrospinal fluid across different stages of the sleep-wake cycle.

“We developed a ratiometric fluorescent sensor for TrpA and showed that TrpA is produced by wake-active monoaminergic nuclei in the diencephalon and brainstem and is secreted in an activity-dependent manner,” wrote the authors.

“We showed that released TrpA binds to G-protein-coupled receptor 139 (GPR139) and enhances neuronal excitability in the hypothalamic preoptic area to promote sleep. TrpA–GPR139 signaling was necessary for homeostatic sleep rebound and small-molecule GPR139 agonists promoted sleep duration and quality.”

Essentially, Cao, Wang and their colleagues found that TrpA levels in the cerebrospinal fluid of mice and pigs increased as they spent more hours awake, reflecting a growing sleep pressure. Notably, TrpA levels reflected the animals’ history of being awake and active, independently of what time it was.

The team observed that some neurons that are only active while mammals are awake naturally produced and released TrpA. The molecule then appeared to activate a receptor called GPR139, which in turn increased the activity of neurons in the hypothalamic preoptic area, a brain region known to promote sleep.

A possible target for treating sleep disorders

Inspired by their initial findings, the researchers carried out further experiments aimed at testing the effects of compounds that activated the GPR139 receptor. Remarkably, they found that these experimental compounds increased the duration of sleep and boosted the quality of sleep in both mice and pigs.

“Together, our study reveals TrpA as a signal related to sleep homeostasis and GPR139 as a druggable target against its disruption,” wrote Cao, Wang and their colleagues.

The fact that the team could replicate their findings in both mice and pigs suggests that the mechanism they identified may be conserved across various mammalian species. Future studies confirming that the same mechanism is also present in humans could potentially lead to new treatments for insomnia or for other conditions associated with difficulties sleeping and poor sleep quality.

Many people assume that some memory decline is an inevitable consequence of getting older. But a select group of older adults, known as “SuperAgers,” reach their 80s and 90s while retaining memory performance as good as or better than that of people in their 50s and 60s.

Nearly two decades of research has identified unique biological, brain and psychosocial characteristics associated with SuperAgers, but an important question has remained: could SuperAgers simply be people who inherited very little genetic risk for Alzheimer’s disease?

“If that were true, identifying SuperAgers might be as simple as performing genetic testing rather than the comprehensive cognitive evaluations we currently use,” said Emily Rogalski, Ph.D., director of the Healthy Aging & Alzheimer’s Research Care (HAARC) Center at the University of Chicago, who established the definition of SuperAging in 2008 and has been studying this remarkable population ever since.

A new study aimed to directly test that hypothesis using the largest prospectively enrolled SuperAging cohorts and the most up-to-date Alzheimer’s genetic risk measures available.

Testing the genetic explanation

The findings, published in Alzheimer’s Research & Therapy, show that exceptional memory aging cannot be explained simply by low inherited Alzheimer’s disease risk, reinforcing the importance of studying protective pathways directly.

A team led by researchers at the HAARC Center and the Translational Genomics Research Institute (TGen), part of City of Hope, studied a diverse cohort of 142 SuperAgers and 89 cognitively average peers from five regional sites in the U.S. and Canada.

Using DNA extracted from blood samples, the researchers examined the APOE gene, the strongest genetic risk factor for Alzheimer’s disease, and calculated three polygenic risk scores, which tally thousands of genetic variants associated with inherited Alzheimer’s disease risk.

The results provided a clear answer to the central question: SuperAgers could not be distinguished from cognitively average older adults based on either APOE or Alzheimer’s polygenic risk scores. In other words, having exceptional memory in one’s 80s is not simply explained by having exceptionally low inherited Alzheimer’s disease risk.

“The findings reinforce that preserving cognitive health involves more than reducing Alzheimer’s disease risk alone,” said co-first author Ana Capuano, Ph.D., director of the biostatistics core at the HAARC Center.

“Understanding the biological, behavioral and social factors that promote exceptional cognitive aging may ultimately complement traditional disease-focused approaches and help inform more personalized strategies for supporting brain health across the lifespan.”

Beyond inherited risk alone

Even when examining rare genetic protective variants previously associated with resilience against Alzheimer’s disease, the researchers found no increased prevalence among SuperAgers.

“This study establishes an important boundary for Alzheimer’s disease genetics,” said Matt Huentelman, Ph.D., professor and director in TGen’s Early Detection and Prevention Division and co-senior author with Rogalski.

“Common genetic risk factors captured by APOE and current polygenic risk scores do not explain the SuperAging phenotype. Future work should move beyond disease-risk models and investigate the broader biological, environmental and experiential pathways that contribute to exceptional cognitive aging.”

This future work will entail a multidisciplinary approach that combines detailed cognitive assessments with brain imaging, blood biomarkers, genetics, neuropathology, immune profiling, sleep and activity monitoring, social and environmental measures, and other indicators of whole-person health.

“For many years, aging research has focused on identifying factors that increase the risk of disease,” added co-first author Ignazio S. Piras, Ph.D., associate professor in TGen’s Early Detection and Prevention Division.

“Those studies are critically important, but the absence of risk factors does not necessarily mean someone possesses the protective factors that support exceptional brain health. This study helps demonstrate that distinction.”

A hopeful signal for aging

Ultimately, the results reinforce a hopeful message: memory decline is not inevitable, and some people can—and do—maintain remarkably youthful memory well into their 80s and beyond.

The search for how and why continues with the help of SuperAger research participants: extraordinary partners in discovery who have generously contributed their time over many years to help scientists understand what successful cognitive aging looks like and point toward new pathways to resilience.

Exercise finds improvements in pain and function may fall short of what patients would notice in daily life, but more studies are needed to make firm conclusions, a new publication in Cochrane Database of Systematic Reviews finds.

Hip osteoarthritis is a condition affecting millions of people worldwide and a leading cause of chronic pain and disability. Exercise is widely recommended as a first-line treatment for managing hip arthritis pain.

Led by researchers from the University of Sydney and the University of Melbourne, the findings show exercise produces small improvements in pain and physical function for people with hip osteoarthritis, but those improvements may not be large enough to make a meaningful difference to patients.

The review included 18 clinical trials involving 1,368 people. Participants were mostly women (63%) and were ages 53–74, meaning the findings may not apply to younger people. Exercise programs in the included studies varied widely, lasting between two and 52 weeks and covering a range of types, including strengthening, aerobic and mind-body approaches.

Compared with no treatment or usual care, exercise probably reduces pain by around 7 points on a 100-point scale. However, experts generally consider an improvement of at least 12 points necessary for patients to notice a meaningful difference in daily life. Physical function showed a similar pattern.

The authors note, however, that these thresholds were derived largely from knee and mixed osteoarthritis populations and may not entirely reflect the hip osteoarthritis experience.

Quality of life, arguably the outcome patients care about most, showed little to no improvement with exercise regardless of the comparison used.

“Exercise is recommended as a primary treatment for hip osteoarthritis, and this review doesn’t overturn that,” said Michelle Hall, co-lead author from the University of Sydney. “But it does suggest we should be honest with patients that the average benefit may be modest and that we need better-designed trials to understand who benefits most and from which type of exercise.”

Not a recommendation against exercise

The review stops short of saying exercise is ineffective or should be abandoned as a recommendation. Exercise carries broad health benefits beyond arthritis, is low-cost and is unlikely to cause harm.

Most studies included in this review were small and unblinded, which may have influenced outcomes. Because pain and function were largely self-reported and participants knew whether they were exercising, exercise may appear more effective than it truly is.

The authors call for larger, better-designed trials to give patients and clinicians a clearer picture of what exercise can realistically achieve for hip osteoarthritis specifically.

“There just isn’t a huge body of evidence out there,” said Belinda Lawford, co-lead author from the University of Melbourne. “For some people struggling with hip pain, exercise can really be their only hope, but I also don’t want to give patients false hope. It’s important future research is done with larger, better-quality trials, examining what types of exercise work specifically for different people.”

People around the world are living longer than ever before but spending more of those additional years in poor health, according to a new Global Burden of Disease (GBD) study published in The Lancet Public Health.

Researchers found that the global morbidity gap widened in almost all countries and territories analyzed between 1990 and 2023. Globally, while the share of life spent in poor health increased, trends varied by country, and a smaller number of countries saw this share decline.

Within a generation, the global morbidity gap widened by nearly two years, increasing from 8.8 years in 1990 to 10.7 years in 2023. Globally, people spent an average of 14.5% of their lives in poor health in 2023, up from 13.6% in 1990. Instead of occurring only in the final years of life, the widening morbidity gap was observed across the adult lifespan, suggesting that people are spending more years living with disease and disability throughout adulthood.

The analysis, based on GBD 2023 estimates, examined trends in healthy aging from 1990 to 2023 and assessed changes in life expectancy, healthy life expectancy and the morbidity gap across countries, regions, sex and levels of socio-demographic development, while also identifying the leading conditions and risk factors contributing to years lived in poor health.

Longer lives are not translating into healthier lives

Between 1990 and 2023, global life expectancy at birth increased from 64.6 years to 73.8 years, while healthy life expectancy rose from 55.9 years to 63.1 years. Because gains in survival consistently outpaced gains in healthy years of life, people are spending more years living with chronic disease and disability.

While the COVID-19 pandemic temporarily disrupted life expectancy and healthy life expectancy, it did not reverse the broader trend toward a widening morbidity gap.

“Our findings suggest that future gains in population health will come not only from helping people live longer, but from helping them live healthier,” said Dr. Christopher Murray, director of the Institute for Health Metrics and Evaluation (IHME) at the University of Washington School of Medicine and senior author of the study.

“Progress in healthy aging should be measured not only by lifespan, but by healthspan, with greater investment in prevention, long-term disease management and chronic care to reduce years lived in poor health.”

High-income countries face the widest morbidity gaps

The burden of poor health varied substantially across countries and regions, with the longest periods of life spent in poor health generally occurring in places where people live the longest.

In 2023, the United States had the largest national morbidity gap at 14 years, followed by Australia at 13.9 years and Canada at 13.7 years. Countries with higher Socio-demographic Index (SDI) levels generally experienced both longer life expectancy and more years lived in poor health, reflecting gains in lifespan that have not been matched by equivalent gains in healthspan.

The pattern was consistent worldwide. All seven GBD super-regions experienced increases between 1990 and 2023 in both the number of years and the proportion of life spent in poor health. The high-income super-region had the largest morbidity gap in 2023 at 12.7 years, while sub-Saharan Africa had the smallest at 9.0 years.

Women are living longer but spending more years in poor health

Across every region and level of development, women consistently lived longer than men but also spent more years living in poor health. This pattern shows that longer life expectancy among women has not translated into the same gains in healthy years.

In 2023, women experienced an average morbidity gap of 12.1 years, compared with 9.3 years for men. Women also had a larger morbidity gap than men across all SDI quintiles, indicating that women consistently live longer but also spend more years living with disease and disability across different levels of social and economic development.

“Women are living longer than men almost everywhere in the world, but they are also spending more of those additional years in poor health,” said Catherine Bisignano, senior scientific writer at IHME and co-author of the study.

“Improving healthy aging will require greater focus on the conditions and risk factors that drive years lived with disability. Addressing these earlier through prevention and better long-term care could have meaningful social, health system and economic impacts.”

Healthy aging will require a greater focus on prevention and chronic care

More than half of all years lived in poor health worldwide were driven by a relatively small group of largely nonfatal chronic conditions, accounting for 57.4% of unhealthy years in 2023.

Musculoskeletal disorders, particularly low back pain, were the largest contributor to the morbidity gap, followed by mental disorders such as depression and anxiety, sense organ diseases including age-related hearing loss, falls and other unintentional injuries, and other chronic noncommunicable diseases.

Many years spent in poor health were linked to preventable or manageable risk factors. Globally, high fasting plasma glucose, high body mass index, child and maternal malnutrition, and tobacco use were the leading risk factors contributing to the morbidity gap. These patterns varied substantially by region and level of development.

In sub-Saharan Africa and other low-SDI settings, child and maternal malnutrition was the leading risk factor, and air pollution also ranked among the top five.

As populations age, greater emphasis is needed on preventing chronic disease, delaying disability and ensuring access to rehabilitation, mental health services and long-term chronic care.

Tackling key risk factors, investing in prevention and strengthening services that reduce years lived in poor health will be essential to improving healthy aging and lessening the growing toll of disability on people, families and health systems worldwide.

Consuming common foods such as corn chips and popcorn may put pregnant women at risk of exposure to mycotoxins—harmful substances produced by mold—according to Rutgers researchers.

Their study, published in the Journal of Exposure Science & Environmental Epidemiology, found hormone-mimicking mycotoxins in 100% of participants and linked exposure levels to the amount of corn and grain products consumed.

One such mycotoxin is zearalenone, a compound produced by Fusarium fungi that contaminate staple crops such as corn, wheat and oats. Zearalenone can indirectly enter human food supplies through meat and dairy from animals that eat contaminated feed. It is also heat-stable, so it can survive cooking and food processing.

Because zearalenone can mimic estrogen, a hormone critical to pregnancy and fetal development, it is more specifically classified as a mycoestrogen. Other studies suggest that exposure to mycoestrogens may contribute to greater gestational weight gain and lower infant birth weight.

“Mycoestrogens are among the most common food contaminants worldwide, yet evidence on their dietary sources in the United States has been limited,” said Zorimar Rivera-Núñez, an assistant professor at Rutgers School of Public Health and the lead author of the study. “They have potent estrogenic properties, but we know very little about how these exposures may affect pregnant women and their developing babies.”

Tracking exposure during pregnancy

The researchers said the pilot study, known as the Jersey Babies pilot study, is among the first in the U.S. to pair pregnant women’s dietary intake with mycoestrogen biomarkers collected at the same time. This approach can help researchers pinpoint specific dietary sources of mycoestrogen exposure.

The study followed 33 pregnant women recruited from obstetric clinics at Saint Peter’s University Hospital and Rutgers Robert Wood Johnson University Hospital in New Brunswick, N.J. Participants provided urine samples and completed detailed 24-hour dietary recalls at three points in pregnancy, allowing the researchers to closely match what participants ate with what showed up in their urine.

Researchers analyzed the urine samples for several mycoestrogens, including zearalenone. Findings showed at least one mycoestrogen was detected in every urine sample collected.

Zearalenone itself was detected in most participant samples at all three visits. Its levels remained relatively stable across pregnancy for several participants, suggesting that exposure was persistent rather than a one-time event.

Corn products stood out

“Our findings confirm that grain-based foods are important contributors to mycoestrogen exposure among pregnant women in the U.S.,” Rivera-Núñez said. Rivera-Núñez also is a member of the Rutgers Environmental and Occupational Health Sciences Institute.

Researchers found that consumption of corn and other grain products in the 24 hours before a urine sample was collected was strongly associated with higher mycoestrogen levels.

Corn-based foods, including corn, corn chips and corn tortillas, showed the strongest associations, followed by more modest links to cereal grains and oils. By contrast, consumption of chicken and pork showed weaker, inverse associations, suggesting corn and grain products, rather than meat, were the primary dietary contributors to exposure in this study group.

Higher levels among Hispanic participants

The study’s findings also suggest differences by ethnicity.

Participants who identified as Hispanic had mycoestrogen levels higher than those of non-Hispanic participants across the three study visits. Hispanic participants also reported eating more corn and corn-based products, as well as more dairy, than non-Hispanic participants.

“Identifying groups with higher exposures is a critical first step for our mycoestrogen research program,” Rivera-Núñez said. “It helps us understand the factors driving those exposures and provides the information needed to develop strategies that protect maternal and child health.”

Regulators are still catching up

According to the researchers, the U.S. Food and Drug Administration added zearalenone to its Mycotoxin Compliance Program in 2024 but hasn’t yet established maximum allowable limits in food. On a global scale, the European Commission has set limits for zearalenone in cereals, baked goods and infant food.

The researchers said the findings establish mycoestrogens as an emerging and understudied exposure among U.S. pregnant women, setting a foundation for future research into potential reproductive, developmental and child health outcomes.

“Pregnancy represents a unique opportunity for prevention,” Rivera-Núñez said. “By understanding how everyday dietary choices contribute to environmental chemical exposures, we can provide families with information that supports both maternal and child health.”