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.”

Researchers have uncovered a clue to why immune checkpoint inhibitors—cancer therapies that release the immune “brakes” exploited by tumors to evade attack—show limited efficacy in some brain tumors. A KAIST research team found that B-cell and antibody responses initiated in tumor-draining lymph nodes, rather than T cells alone, are critical to the antitumor effects of anti-CTLA-4 therapy, opening a new avenue for treating intractable brain tumors.

A research team led by Heung Kyu Lee, a professor in the Department of Biological Sciences, identified a previously unrecognized immune mechanism through which anti-CTLA-4, a type of immune checkpoint inhibitor, promotes B-cell responses in tumor-draining lymph nodes, thereby helping the immune system attack brain tumors. The findings were published July 10 in Science Immunology.

Glioblastoma’s stubborn immune barrier

Glioblastoma is one of the most aggressive malignant brain tumors, with frequent recurrence and a poor prognosis even after surgery and radiation therapy. Immune checkpoint inhibitors, which restore the ability of immune cells to attack cancer cells, have produced substantial therapeutic benefits in various cancers. However, their effectiveness in glioblastoma has remained limited because of the highly immunosuppressive environment surrounding the tumor.

Researchers have traditionally regarded T cells—immune cells that can directly attack cancer cells—as the primary target of immune checkpoint inhibitors. B cells, meanwhile, are well known for producing antibodies following infection or vaccination, but their role in brain tumor immunotherapy has remained largely unexplored. The research team therefore investigated whether anti-CTLA-4 could influence B-cell responses as well as T-cell responses.

B cells prove essential

The findings challenged the prevailing T-cell-centered view. In mouse glioma models, anti-CTLA-4 treatment reduced tumor burden and significantly prolonged survival. However, these therapeutic effects were largely lost in mice lacking B cells, demonstrating that B cells are required for the efficacy of anti-CTLA-4 treatment in these models.

The team also identified where B cells played their key role. Rather than being prominent in the brain, where the tumor cells were located, the response increased markedly in the deep cervical lymph nodes, which are located deep in the neck and receive lymphatic drainage from the brain. In particular, germinal center B cells and T follicular helper cells, both of which are important for antibody formation, increased together in these lymph nodes. This was accompanied by an increase in immunoglobulin G, or IgG, responses. IgG is a major class of antibody that can recognize cancer cells as targets and help immune cells eliminate them.

The resulting IgG antibodies bound to the surface of glioma cells, helping macrophages—immune cells that engulf foreign substances and cancer cells—remove the tumor cells more effectively.

Watching tumor clearance unfold

The research team also examined this process directly in vivo. Using a specialized dual-reporter glioma model expressing the red fluorescent protein mCherry and the green fluorescent protein EGFP, the researchers successfully visualized tumor-infiltrating phagocytes actively engulfing glioma cells following anti-CTLA-4 treatment.

The study provides the first functional evidence that B-cell immune responses—previously known mainly for their roles in infection and vaccination—can be a key factor determining the effectiveness of immunotherapy for hard-to-treat brain tumors. It also expands the conventional T-cell-centered framework of cancer immunotherapy by showing that treatment efficacy can be strongly shaped by immune responses originating not only within the tumor but also in tumor-draining lymph nodes outside it.

Yumin Kim, a postdoctoral researcher in the KAIST Department of Biological Sciences, served as the first author of the study, with Lee serving as the corresponding author. Ji Eun Oh, a professor from the KAIST Graduate School of Medical Science and Engineering, also contributed to the research.

Most of us would like to hang around on the planet for as long as possible, and thankfully, lifespans in many countries are increasing. Scientists are also developing a new field known as longevity medicine, which aims to help people stay healthier for longer as they age.

But according to an international group of researchers, interventions should happen much earlier, perhaps even before birth. In a correspondence published in the journal Nature Health, they propose a new global consortium called PROSPER (Pregestational and Pediatric Research for Optimal Healthspan and Early-life Resilience). Instead of treating aging in middle age, their idea is to better understand, measure and eventually help improve the way our bodies age.

The scientists argue that our future health isn’t a blank slate at birth. External factors such as maternal and paternal health, nutrition, sleep and early-life experiences leave lasting impressions on our biology. Instead of looking at early life as just a time of growth, the authors see it as a critical window to build up the body’s baseline resilience, helping us stay healthier later in life.

So what exactly are they suggesting?

Their proposal is not about any specific treatments or interventions. Rather, it’s about building the scientific and research infrastructure needed for future discoveries.

First, they want a way to gather and combine existing health data from different countries so researchers can look at long-term trends. They also suggest creating shared biobanks that would store biological samples to help find specific health markers tailored to growing bodies.

Once that foundation is built, the goal is to run international studies to test whether improving everyday variables such as childhood nutrition, sleep, the microbiome and metabolic health can alter long-term health trajectories and biological aging.

Health care shakeup

But to do this, health care needs to change, the scientists say. Currently, it is split into separate areas such as maternity care, pediatrics and adult medicine that rarely talk to each other. What’s more, current tools for measuring biological aging were designed for adults and are not applicable to the rapidly changing biology of a growing child.

“The absence of structured frameworks to monitor and modulate early-life determinants of aging therefore represents a substantial gap in traditional medicine,” the researchers commented in their paper.

To fix this, they propose a lifetime roadmap that joins these areas together, embedding proactive checks right into routine doctor visits.

Ultimately, these checks would focus on different aspects of health at every stage of development. For example, they would encourage healthier parental lifestyles for up to a full year before pregnancy, monitor infant sleep and nutrition, and track fitness and mental health through adolescence.

Many of the world’s leading causes of irreversible blindness, including glaucoma and age-related macular degeneration, share a common problem: the buildup of fluid, waste and inflammatory debris in the back of the eye.

However, for decades, scientists have lacked a clear understanding of how the eye clears this waste away.

New research from the University of British Columbia and the University of Toronto has identified what appears to be a missing piece of the puzzle: a previously unknown waste drainage system at the back of the eye. The hidden circulatory pathway, called the posterior ocular lymphatic outflow, or POLO pathway, provides a route for fluid and waste to exit the eye and enter the body’s lymphatic system.

“The retina is one of the most metabolically active parts of the body, constantly generating byproducts that need to be cleared,” said Dr. Neeru Gupta, professor and head of UBC’s department of ophthalmology and visual sciences. “This discovery helps explain how the eye flushes this waste and promises to transform how we think about and treat a range of eye conditions.”

A foundation for future therapies

Diseases like glaucoma, macular degeneration and retinal disorders are all associated with fluid buildup, accumulation of metabolic waste and tissue stress and inflammation. Age-related macular degeneration alone affects approximately 2.5 million Canadians.

The discovery of the POLO pathway suggests there is a natural system responsible for clearing this material and opens new opportunities to harness this system to treat disease.

“This gives us a whole new framework for understanding these diseases and a potential target for therapeutics,” Gupta said. “The question now is: How can we enhance or exploit this cleanup system to treat or even prevent disease?”

Hiding in plain sight

For more than a century, the eye was thought to lack a lymphatic system, which is present in nearly every other organ and helps to regulate fluid, remove waste and support immune function.

Gupta and Dr. Yeni Yücel, professor and director of ophthalmic pathology at the University of Toronto, began challenging that idea in 2009 with the discovery of a lymphatic-related drainage pathway at the front of the eye, termed the “uveolymphatic” pathway. Yet the back of the eye, where many blinding diseases are rooted, has remained largely unexplored.

“The retina is responsible for vision and it’s also where many of the most serious vision-loss diseases occur,” Yücel said. “Understanding how this part of the eye maintains a balanced environment and flow of materials is critical.”

To uncover the POLO pathway, the team used advanced imaging in mice, combining MRI, near-infrared fluorescence and microscopic analysis. They introduced fluorescent tracer molecules into a thin space at the back of the eye and tracked their movement in real time.

This allowed them to identify small lymphatic vessels in the choroid, a thin layer beneath the retina. Fluid drained from the back of the eye into surrounding orbital tissue and, within minutes, reached nearby lymph nodes that link the eye to the broader lymphatic system.

“Because lymphatic vessels in the choroid were thought not to exist, the team used multiple techniques to demonstrate both their presence and function,” added Yücel, a pathologist-scientist at St. Michael’s Hospital. “We were surprised to see such a direct route for fluid to leave the eye and connect with the lymphatic system. It suggests the back of the eye has an active clearance pathway, which could play an important role in removing fluid, proteins and inflammatory material that build up in disease.”

Further research is needed to understand how the lymphatic pathway operates in humans and how it could be targeted with therapeutics.

But the researchers say it could one day lead to improved drug delivery to the back of the eye, new therapies that enhance fluid clearance and deeper insight into how pressure, inflammation and fluid dynamics contribute to vision loss.

“This is a foundational discovery that shows the eye is not as closed a system as we previously thought,” Gupta said. “It gives us a new map, a new mechanism and a new set of questions to explore.”

The study was published today in Translational Vision Science & Technology.

Social connections are known to contribute greatly to people’s psychological and emotional well-being. In fact, difficulties socializing and bonding with others have been linked to various psychiatric conditions, including depression, social anxiety disorder (SAD), schizophrenia and post-traumatic stress disorder (PTSD).

Oxytocin, sometimes referred to as the “love hormone,” is known to play a key role in empathy, affection, trust and other aspects of social bonding. Past studies found that delivering oxytocin into a patient’s body through the nose has little to moderate effect on people’s social-bonding experiences.

Researchers at the University of Tsukuba have been assessing the potential clinical benefits of alternative, nonpharmacological interventions that prompt the body to naturally produce more oxytocin. In a recent paper, published in Translational Psychiatry, the team showed that attending live sports with others increased levels of endogenous oxytocin (i.e., oxytocin naturally produced inside the body) and boosted other physiological signals associated with social bonding.

“Our paper grew from a simple question: How much direct interaction do people need to feel connected?” Takashi Matsui, first author of the paper, told Medical Xpress. “As a judoka, I was inspired by the principles of ‘Seiryoku-Zenyo’—the best use of one’s physical and mental energy—and ‘Jita-Kyoei’—mutual welfare and benefit. Together, these principles frame sport as a means not only of personal development but also of fostering unity, empathy and mutual benefit.”

Monitoring heart rate and oxytocin during a live basketball game

Past psychological studies suggest that repeatedly being in close physical contact with others can promote the release of oxytocin inside the body. However, not all psychiatric patients are comfortable with body contact, and some may not have many opportunities to come into close contact with others.

Matsui and their colleagues previously observed that in-person esports that did not require physical contact could still increase some biological signatures of social bonding. Building on their earlier research, they set out to measure physiological signals linked with social bonding while people attended live basketball games.

“One of our earlier studies provided an important clue: During face-to-face competitive and cooperative esports without physical contact, we observed both endogenous oxytocin release and heart rate synchrony—the alignment of bodily responses between people,” said Matsui. “This led us to use TSUKUBA LIVE! to ask whether spectators could become connected hormonally, physiologically and socially simply by sharing attention and emotion, even without playing or directly interacting with one another.”

The researchers selected 60 spectators attending two collegiate basketball games at the University of Tsukuba. Before, during and after each game, they collected three different physiological measurements from the spectators.

First, they collected saliva samples to measure levels of oxytocin and cortisol inside the body. While oxytocin is associated with social bonding and human connection, high levels of cortisol are linked to stress, anxiety and physiological arousal.

The team also recorded the selected spectators’ heart rates using wearable sensors. Finally, they asked them to answer a few questions about their experience of the game, such as how much they were enjoying it, whether they planned to attend again and whether they felt a sense of unity with other spectators.

“This real-world design allowed us to examine how hormonal, cardiovascular and psychological responses unfolded together during a shared sporting experience,” explained Matsui. “We found that live sports spectatorship was accompanied by an oxytocin-linked pattern of heart rate synchrony associated with social connection.”

The researchers observed that oxytocin levels increased in spectators who had lower levels of the hormone before the game and remained elevated in those who had higher levels to begin with. In contrast, the participants’ cortisol levels decreased during the game, suggesting that attendees were less stressed.

“We also found that the spectators’ heart rate patterns became more synchronized,” said Matsui. “Higher oxytocin showed a modest positive association with stronger synchrony, and both were linked to greater enjoyment, unity, immersion and intention to attend a live game again.”

Live sports as social bonding events

The results of this study suggest that attending live sports events can foster social connection and bonding. While these events alone might not be enough to treat complex psychiatric conditions, they could potentially be accessible opportunities to improve patients’ overall well-being and relationships with others.

“We now want to move beyond asking whether sports spectatorship promotes bonding and determine for whom, under what circumstances and in what physiological state it is most likely to foster connection,” added Matsui.

“We are now examining the effects of match outcome, spectators’ previous experience playing the sport and the development of ‘social brain’ mechanisms across the lifespan. Our longer-term goal is to design viewing environments and social contexts that can more reliably bring out the bonding effects of shared sports experiences.”