Monthly Archives: June 2025

Research Finds No Link Between Loneliness and Increased Risk of Death

For decades, loneliness has been portrayed as a dire threat to health, with some reports equating its dangers to smoking fifteen cigarettes a day. Influential voices, including the U.S. Surgeon General, have amplified the concern, framing social isolation as a significant public health issue with potentially fatal consequences. These perspectives have fuelled an urgency in both academic circles and policymaking to address loneliness as a contributor to premature death, particularly among older adults. Yet, new research is now challenging this prevailing narrative with surprising findings that suggest the link between loneliness and mortality may not be as clear-cut as once thought.

An international study led by researchers at the University of Waterloo’s School of Public Health Sciences has found no association between loneliness and increased risk of death among older adults receiving home care services. Drawing on data from over 380,000 individuals aged 65 and above in Canada, Finland, and New Zealand, the study employed rigorous statistical methods, including standardised assessments and survival analysis, to examine whether feelings of loneliness predicted mortality within one year. Contrary to widespread assumptions, the results showed that lonely older adults were less likely to die within a year compared to those who did not report feeling lonely, even after adjusting for age, pre-existing health conditions, and other risk factors.

“This research runs counter to much of the existing literature, which is largely based on studies of the general population,” said Dr. Bonaventure Egbujie, the study’s lead author and a professor at Waterloo. “When we isolate loneliness as a variable, independent of other health and social determinants, it does not appear to significantly increase the risk of death in this population.” The findings underscore the importance of distinguishing between correlation and causation. While loneliness may accompany poor health, it does not necessarily drive it—at least not in ways that translate into increased mortality in the short term.

The study also sheds light on the prevalence and complexity of loneliness among older adults. Rates of reported loneliness ranged from 15.9 percent in Canada to 24.4 percent in New Zealand. Interestingly, individuals who were physically healthier and received less informal support from family or friends were more likely to report feeling lonely. This counterintuitive pattern suggests that loneliness is not merely a by-product of physical frailty or intensive care needs. Still, it may instead reflect broader social or emotional dynamics, including unmet expectations for connection and engagement.

Rather than dismissing loneliness as benign, however, the researchers emphasise that its impact on mental health remains profound. “Loneliness is still a serious threat to psychological well-being,” noted Dr John Hirdes, senior author of the study. “Just because it doesn’t raise your risk of dying doesn’t mean it should be ignored. The emotional and cognitive toll of prolonged isolation can be deeply damaging, particularly for older people who may already be vulnerable to depression, anxiety, and cognitive decline.”

From a policy perspective, the study’s authors advocate for a reframing of how loneliness is addressed in the context of elder care. Rather than positioning it primarily as a mortality risk, they urge policymakers and care providers to treat it as a critical issue affecting quality of life. Interventions aimed at reducing loneliness should focus on enhancing meaningful social contact, promoting community engagement, and recognising the emotional needs of older adults, especially those living independently or with limited social networks. Home and community care services, the researchers argue, play a pivotal role in this regard.

Ultimately, the study recommends further longitudinal research to elucidate the long-term effects of loneliness on health and to investigate how cultural norms and variations in healthcare systems influence these outcomes. By moving beyond simplified cause-and-effect models, future studies could better capture the nuanced ways in which loneliness intersects with physical health, emotional well-being, and broader social support structures. In doing so, researchers and practitioners alike can develop more targeted, compassionate, and evidence-based strategies to support the ageing population—not just in surviving but in thriving.

More information: Bonaventure Egbujie et al, Cross-National Evidence on Risk of Death Associated with Loneliness: A Survival Analysis of 1-Year All-Cause Mortality among Older Adult Home Care Recipients in Canada, Finland, and Aotearoa | New Zealand, Journal of the American Medical Directors Association. DOI: 10.1016/j.jamda.2025.105687

Journal information: Journal of the American Medical Directors Association Provided by University of Waterloo

Associations Between Gut Microbiota, Food Insecurity, and Cognitive Decline Risk in Adults

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A recent study, partially led by researchers at Mount Sinai, has unveiled a significant relationship between the composition of the gut microbiome and the risk of cognitive impairment (RCI) in adults. This work highlights the intricate interplay between biological systems and social determinants of health, particularly food insecurity, in shaping brain health outcomes. Importantly, it is the first epidemiologic investigation to examine how food insecurity may alter the connection between gut microbiota composition and cognitive decline.

Published in NPJ Aging, the study examines the role of food insecurity as a modifier of the association between specific microbial groups in the gut and the risk of cognitive impairment. The researchers found that adults with reduced microbial diversity and specific bacterial imbalances were notably more likely to experience cognitive dysfunction. Additionally, food insecurity—defined as limited or uncertain access to nutritionally adequate and safe food—was independently associated with both compromised gut microbiome profiles and diminished cognitive performance, reinforcing its dual role as a social and biological stressor.

Dr Shoshannah Eggers, Assistant Professor of Epidemiology at the University of Iowa College of Public Health and the study’s corresponding author, began this research while serving as a Postdoctoral Fellow at the Icahn School of Medicine at Mount Sinai. “In 2022, over 12 percent of U.S. households—equating to 17 million—experienced food insecurity at some point during the year, an increase from 10.2 percent the previous year,” Dr Eggers noted. “This consistent link between food insecurity and poor health outcomes, including adverse neurological outcomes, demands we examine how physiological systems like the gut microbiome interact with social conditions to influence brain health.”

The research cohort comprised 360 adults from the Survey of the Health of Wisconsin, each providing complete data on food insecurity status, cognitive function assessments, and stool samples for 16S rRNA gene sequencing—an established method for identifying bacterial taxa present in the gut. Using an interpretable machine-learning algorithm, the team was able to detect small networks of co-occurring bacteria, or “microbial cliques,” associated with cognitive impairment. This algorithm not only predicted associations but also provided insight into the underlying structure of those predictions, thereby enhancing interpretability and scientific transparency.

Analyses were stratified by food security status and adjusted for relevant confounders, including age, body mass index (BMI), and smoking status. The researchers identified two microbial cliques whose relationships with cognitive impairment varied depending on participants’ food security levels. For individuals experiencing food insecurity, a microbial group containing Eisenbergiella or Eubacterium exhibited a stronger association with cognitive decline. Conversely, among food-secure individuals, a different clique—comprising Ruminococcus torques, Bacteroides, CAG-352F, and Eubacterium—was more strongly linked to cognitive impairment.

These contrasting microbial signatures between the two groups suggest that the gut-brain axis is modulated not only by microbial composition but also by contextual factors such as nutritional access. According to the study’s senior author, Dr Vishal Midya, Assistant Professor of Environmental Medicine at the Icahn School of Medicine at Mount Sinai, this nuanced interaction implies that future microbiome-based interventions may need to account for food security status. “These findings suggest that food insecurity transcends socioeconomic boundaries and may exert biological effects that influence brain health through the gut microbiome,” Dr Midya stated. “With the prevalence of cognitive impairment rising, especially among older adults, integrating food insecurity into etiological models of cognitive decline is increasingly urgent.”

In light of these findings, the study advocates for more holistic public health strategies that address both dietary accessibility and microbial health. Interventions that pair nutritional support with targeted modulation of the gut microbiome—such as through diet, probiotics, or prebiotics—could potentially mitigate the risk of cognitive decline in populations most vulnerable to both malnutrition and neurological disorders. As our understanding of the gut-brain axis deepens, incorporating social determinants of health into biological research will be vital in developing inclusive and effective public health solutions.

More information: Shoshannah Eggers et al, Food insecurity modifies the association between the gut microbiome and the risk of cognitive impairment in adults, npj Aging. DOI: 10.1038/s41514-025-00241-0

Journal information: npj Aging Provided by The Mount Sinai Hospital / Mount Sinai School of Medicine

Virtual Reality May Aid Stroke Survivors in Restoring Mobility

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A newly updated Cochrane review has concluded that virtual reality (VR) used in conjunction with conventional stroke rehabilitation may support patients in regaining arm movement. The findings suggest that VR can be a valuable adjunct to standard therapy by enhancing the amount of therapeutic activity undertaken. Since greater therapy intensity is associated with better recovery outcomes, VR may offer an accessible and engaging means of supplementing usual care, particularly in settings where clinician time is limited.

This latest review, published today, is the fourth update of a Cochrane analysis released initially in 2011. It now includes results from 190 trials involving 7,188 participants, with 119 new studies added since the last update in 2017. The authors examined a wide array of VR interventions, ranging from basic screen-based games using commercial consoles to fully immersive, head-mounted systems explicitly developed for rehabilitation purposes. The breadth of technologies assessed reflects the increasing interest in digital solutions for neurological recovery.

The international review team, comprising researchers from Australia, Canada, and the United States, found that VR may result in modest improvements in upper limb function and related activities when compared to conventional therapy alone. However, the most notable gains were observed when VR was used in addition to standard care, effectively increasing overall therapy time. These improvements in arm function suggest that VR may serve as a valuable tool to enhance traditional rehabilitation without significantly increasing costs or placing extra demands on clinical staff.

Lead author Professor Kate Laver of Flinders University emphasised the importance of therapy duration in stroke recovery, stating that “spending more time in therapy is known to improve outcomes after stroke.” She explained that virtual reality offers a relatively low-cost, motivating platform through which patients can engage in additional practice, often independently. This added autonomy could be particularly valuable for patients undergoing long-term rehabilitation or those with limited access to one-on-one therapy sessions.

Beyond arm function, the review also found that VR may contribute to improvements in balance and reductions in activity limitations, although the evidence for these outcomes was less robust. Effects on mobility, participation in everyday activities, and quality of life were uncertain due to limited or low-certainty data. Furthermore, many of the included studies were small and used off-the-shelf gaming technologies. Few trials assessed immersive VR systems, and their impact remains largely unexplored. Most VR applications studied focused narrowly on motor function rather than broader, real-life functional skills such as dressing, shopping, or meal preparation.

Professor Laver noted the untapped potential of VR to simulate complex, real-world environments—such as navigating busy streets or shopping in supermarkets—which would allow patients to practise activities that might be unsafe to attempt in reality. Yet, the research to date has primarily relied on basic or generic gaming platforms. The review concludes by calling for more ambitious and rigorously designed trials that focus on immersive and function-specific VR interventions. These future studies could help determine how best to integrate virtual reality into stroke rehabilitation, ensuring it not only supports motor recovery but also enhances overall independence and quality of life for survivors.

More information: Kate Laver et al, Virtual reality for stroke rehabilitation, Cochrane Database of Systematic Reviews. DOI: 10.1002/14651858.CD008349.pub5

Journal information: Cochrane Database of Systematic Reviews Provided by Cochrane

Association Between Excessive Daytime Sleepiness and Mortality Among Middle-Aged Women

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A forthcoming study to be presented at the SLEEP 2025 annual meeting reveals a significant association between excessive daytime sleepiness and elevated all-cause mortality among middle-aged women. The research highlights that this link is not observed in younger or older female cohorts, suggesting a potential age-specific vulnerability.

The analysis demonstrated that women aged between 50 and 65 years who exhibited high levels of daytime sleepiness—measured using the Epworth Sleepiness Scale—faced a 16% higher adjusted risk of all-cause mortality compared to those with normal sleepiness levels. This association was held even after adjusting for potential confounders, including age, race, ethnicity, body mass index (BMI), and existing comorbidities. Interestingly, this elevated risk was not observed in women under 50 or those over 65, suggesting a potentially unique susceptibility during midlife.

Lead author Dr Arash Maghsoudi, a biomedical engineering PhD and instructor at Baylor College of Medicine in Houston, emphasised the clinical importance of this finding. “Identifying middle age as a critical period suggests clinicians should prioritise Epworth Sleepiness Scale assessments and address excessive daytime sleepiness in women approaching their 50s and early 60s,” he noted.

Daytime sleepiness is widely recognised as a key patient-reported outcome that can signal a host of health concerns, including increased vulnerability to adverse health events and a lower quality of life. According to the American Academy of Sleep Medicine, excessive daytime sleepiness is characterised by a persistent inability to remain awake and alert during the main periods of wakefulness, leading to unintentional dozing or falling asleep.

The study involved a retrospective review of the electronic medical records of 40,250 female veterans spanning from 1999 to 2022. The researchers focused on patients who had either been diagnosed with a sleep disorder or had received care for sleep-related issues. The average age of participants was 48 years. To quantify levels of daytime sleepiness, the research team employed a validated natural language processing tool to extract scores from clinical notes related to the Epworth Sleepiness Scale. This standardised questionnaire assesses the likelihood of dozing off during typical daily activities.

What adds nuance to the study’s conclusions is the absence of a significant association between excessive sleepiness and mortality in older women despite their higher burden of chronic health conditions. Dr Maghsoudi observed that this divergence might reflect hormonal, metabolic, or resilience-related mechanisms specific to midlife physiology. “It implies hormonal, metabolic, or resilience factors that warrant mechanistic follow-up for women in middle age,” he stated.

Taken together, these findings underscore the importance of heightened clinical awareness around sleep health in midlife women. As the data suggest, this age group may represent a window of increased vulnerability where daytime sleepiness is not merely a benign symptom but a potential marker of broader health risks. Further investigation into the biological pathways underlying this age-specific relationship could yield valuable insights into preventive strategies and targeted interventions aimed at improving longevity and quality of life in this population.

More information: Arash Maghsoudi et al, Excessive Daytime Sleepiness and All-Cause Mortality in Female Veterans: A Retrospective Cohort Analysis, SLEEP. DOI: 10.1093/sleep/zsaf090.0929

Journal information: SLEEP Provided by American Academy of Sleep Medicine

Exercise shown to protect the brain at the cellular level in Alzheimer’s disease

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In a groundbreaking study combining cutting-edge genetic tools with an established model of Alzheimer’s disease, researchers from Mass General Brigham, in collaboration with colleagues at SUNY Upstate Medical University, have pinpointed specific brain cell types most responsive to physical exercise. Employing advanced single-nuclei RNA sequencing (snRNA-seq), the team examined the molecular effects of exercise on individual brain cells, illuminating the cellular mechanisms that link physical activity to improved brain health. Importantly, these findings were validated using brain tissue from human subjects, reinforcing their clinical relevance. The complete study is published in Nature Neuroscience.

Although the protective effects of exercise on cognitive function have long been recognised, the precise cellular and molecular underpinnings remained elusive. Senior author Dr Christiane D. Wrann, DVM, PhD, a neuroscientist and head of the Program in Neuroprotection in Exercise at the Mass General Brigham Heart and Vascular Institute and the McCance Center for Brain Health at Massachusetts General Hospital, explained the significance of the new findings. “While we’ve long known that exercise helps protect the brain, we didn’t fully understand which cells were responsible or how it worked at a molecular level,” she noted. “Now, we have a detailed map of how exercise impacts each major cell type in the memory centre of the brain in Alzheimer’s disease.”

The research concentrated on the hippocampus, a critical brain region associated with memory and learning that is notably vulnerable to early degeneration in Alzheimer’s disease. Utilising the snRNA-seq technology—an innovation that enables researchers to analyse gene expression at the single-cell level—the team was able to dissect the distinct responses of various brain cell types to physical activity. This granular approach allows for a much more precise understanding of the disease’s pathology and the benefits of exercise.

In the experimental phase, the team used a widely studied mouse model of Alzheimer’s disease, providing the animals access to running wheels. Those who engaged in voluntary running showed marked improvements in memory function compared to their sedentary counterparts. When the researchers analysed the brains of these exercised mice, they discovered exercise-induced changes in gene expression across thousands of individual cells. Particularly notable were alterations in microglia—a type of immune cell in the brain implicated in neurodegenerative disease—and a newly identified subset of astrocytes known as neurovascular-associated astrocytes (NVAs), which interact closely with the brain’s blood vessels.

Among the most intriguing molecular findings was identifying the gene Atpif1, a metabolic regulator that appears to play a key role in neurogenesis—the process by which new neurons are generated. The team found that modulation of this gene influenced the production of new brain cells, suggesting it could be a promising target for therapeutic intervention. Dr Joana Da Rocha, a postdoctoral researcher in Dr Wrann’s laboratory and lead author of the study, highlighted the importance of this discovery. “That we were able to modulate newborn neurons using our new target genes underscores the promise of our study,” she said, pointing to the potential for these findings to guide future drug development.

To confirm that their observations in mice applied to humans, the researchers examined a large dataset of human brain tissue from individuals diagnosed with Alzheimer’s. Their analysis revealed strong parallels between the cellular changes observed in the exercised mice and those found in the human samples, reinforcing the results’ translatability. Co-senior author Dr Nathan Tucker, a biostatistician at SUNY Upstate Medical University, underscored the broader implications of the work: “This study not only sheds light on how exercise benefits the brain but also uncovers potential cell-specific targets for future Alzheimer’s therapies. Our findings provide a valuable resource for the scientific community focused on Alzheimer’s prevention and treatment.”

In sum, this research not only maps the beneficial impact of physical activity at the single-cell level but also opens the door to new lines of inquiry into how lifestyle interventions can influence the course of neurodegenerative disease. By bridging the gap between animal models and human pathology, the study offers compelling evidence that physical activity could one day inform precision medicine approaches to combat Alzheimer’s disease, both as a preventive measure and as a foundation for targeted therapeutics.

More information: Joana Da Rocha et al, Protective exercise responses in the dentate gyrus of Alzheimer’s disease mouse model revealed with single-nucleus RNA-sequencing, Nature Neuroscience. DOI: 10.1038/s41593-025-01971-w

Journal information: Nature Neuroscience Provided by Mass General Brigham

Struggling to Lift 5 kg Could Signal Declining Health and Underlying Chronic Conditions, Researchers Warn

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A groundbreaking international study has identified a simple yet powerful predictor of health in older adults: the ability to lift a 5-kilogram object. Led by researchers from the University of Sharjah in the United Arab Emirates and drawing data from over 51,000 individuals aged 50 and above across 15 countries, the study found a strong association between difficulty lifting 5 kg and a range of chronic illnesses and diminished quality of life. This research, published in Scientific Reports, is among the first to propose an everyday activity—lifting a modest weight—as a practical method to assess muscle strength and anticipate future health challenges.

Professor Rizwan Qaisar, the study’s lead author, explained that participants who reported struggling to lift 5 kilograms were significantly more likely to suffer from various health conditions over the following years. These included depression, chronic lung disease, stroke, hip fractures, osteoarthritis, joint disorders, high cholesterol, and even Alzheimer’s disease. Crucially, these risks persisted regardless of the participant’s age or gender, pointing to the test’s broad applicability across older demographics. The researchers argue that the inability to perform this task reflects underlying muscle weakness, a condition that often goes undetected until it contributes to serious illness or disability.

Traditional methods for assessing muscle strength typically involve costly equipment and specialised clinical settings, limiting their accessibility—especially in low-resource environments. This new approach, by contrast, empowers individuals to conduct a basic health check using nothing more than an everyday household object. A 5-kilogram item could be a bag of sugar, a small kitchen appliance, or a medium-sized pet. If such an object feels difficult to lift, it may be an early signal of muscular decline, foreshadowing more serious health deterioration.

The study’s significance extends beyond merely identifying correlations. By analysing data from the Survey of Health, Ageing, and Retirement in Europe (SHARE) between 2013 and 2020, the researchers found that nearly 20% of participants initially struggled to lift 5 kg. Over the following four years, those individuals were more likely to develop a lower quality of life, experience depression, and exhibit weaker grip strength. Osteoarthritis was also notably more common in this group. These findings held even after adjusting for age and gender, reinforcing the robustness of the 5 kg test as a predictive measure.

Notably, men who reported difficulty lifting 5 kilograms were at a higher risk than women for developing many of these conditions, suggesting potential biological or lifestyle-related differences in how muscle weakness manifests and affects overall health. The study emphasises that muscle weakness should not be viewed as a natural or harmless aspect of ageing. Instead, it represents a clear and measurable risk factor for multiple chronic diseases. Early detection through simple tests could facilitate prompt intervention and prevent the progression of debilitating conditions.

The researchers stress the urgency of integrating this test into broader public health strategies. “Lifting 5 kilograms: a simple act, a powerful health predictor,” co-author Dr Fabio Franzese of the SHARE Berlin Institute stated. He highlighted how lifting a modest weight, when viewed through the lens of clinical research, becomes a valuable tool for early intervention. The implications are vast—not only for individual self-assessment but also for enabling healthcare professionals to identify at-risk patients without costly diagnostic technologies.

Professor Azhar Hussain, another co-author from the University of Sharjah, echoed this sentiment, describing the test as a potential game-changer in preventative medicine. He emphasised its practicality: it’s inexpensive, requires no training, and can be used universally. For older adults, particularly those living alone or without immediate access to healthcare, the ability to assess one’s strength with such simplicity could prompt earlier consultations with doctors, encourage lifestyle changes such as increased physical activity, and reduce long-term healthcare costs.

Ultimately, this research reframes muscle weakness not as a minor inconvenience of ageing but as a sentinel marker of broader physiological decline. By advocating a widely accessible self-test based on lifting a 5-kilogram object, the scientists offer a compelling vision of preventative care grounded in simplicity and universal applicability. Their work underscores the need to reconceptualise everyday movements as meaningful indicators of internal health—and, perhaps, as the first line of defence in preserving well-being in later life.

More information: Rizwan Qaisar et al, The simple task of lifting five kilograms serves as a predictor of age-related disorders in old adults, Scientific Reports. DOI: 10.1038/s41598-025-03128-y

Journal information: Scientific Reports Provided by University of Sharjah

Breakthrough in Gene Therapy Offers Hope for Preserving Memory in Alzheimer’s Patients

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Researchers at the University of California San Diego School of Medicine have unveiled a pioneering gene therapy that offers new hope in the fight against Alzheimer’s disease. This innovative treatment could shield the brain from degenerative damage and help preserve cognitive abilities, marking a significant shift in therapeutic strategy. Unlike existing Alzheimer’s medications, which typically target the buildup of toxic protein plaques in the brain, this gene therapy aims to modify the behaviour of brain cells directly—potentially addressing the disease at its biological root rather than merely alleviating its symptoms.

Alzheimer’s disease, a progressive neurological disorder, affects millions globally and is marked by the accumulation of abnormal proteins such as beta-amyloid and tau. These proteins interfere with neuronal communication, eventually causing brain cell death and the decline of cognitive functions like memory, reasoning, and personality. Existing treatments offer only modest symptomatic relief and do not stop the underlying disease process. The newly developed gene therapy diverges from this traditional path by intervening at a cellular level, reprogramming the brain’s cells to function more healthily in the face of disease.

In experiments conducted on mice exhibiting symptoms of Alzheimer’s disease, the research team delivered the gene therapy directly during the symptomatic phase. Remarkably, the treatment preserved the animals’ memory that relies on the hippocampus—a key brain region involved in learning and memory and one of the first areas affected by Alzheimer’s. Furthermore, when comparing the treated Alzheimer ’s-afflicted mice to healthy age-matched controls, researchers observed that the treated group displayed similar gene expression patterns. This finding suggests that the therapy protects against cognitive decline and may restore diseased brain cells to a more normal functional state.

What sets this approach apart is its potential to shift the paradigm from damage control to proper intervention. While much Alzheimer’s research has focused on clearing harmful proteins after they’ve accumulated, often with limited clinical impact, the UC San Diego team’s work underscores the power of targeting gene regulation within neurons. By reprogramming how these cells behave—encouraging resilience and normal function even in the presence of disease pathology—the therapy may offer a fundamentally different, perhaps more effective, way of tackling neurodegeneration.

Of course, as promising as these early findings are, the transition from animal models to human applications remains a complex and critical next step. There are considerable challenges in ensuring gene therapies’ safety, precision, and efficacy in the human brain. Regulatory approval, ethical considerations, and the logistics of delivery mechanisms must all be navigated carefully. However, the robust response observed in the treated mice provides strong justification for advancing the research into clinical testing.

This study represents a growing wave of interest in gene therapies as tools to combat chronic and previously untreatable brain disorders. Suppose future trials in humans yield similar success. In that case, this therapy could one day offer individuals with Alzheimer’s a way not just to delay the loss of memory and function but to reclaim aspects of brain health thought to be irreversibly lost. The potential for such a therapy to change the course of the disease is immense—not only in alleviating suffering but in transforming how we understand and manage neurodegenerative conditions altogether.

More information: Dongsheng Wang et al, Neuron-targeted caveolin-1 overexpression attenuates cognitive loss and pathological transcriptome changes in symptomatic Alzheimer’s disease models, Signal Transduction and Targeted Therapy. DOI: 10.1038/s41392-025-02258-z

Journal information: Signal Transduction and Targeted Therapy Provided by University of California – San Diego

Preventing Falls Before They Happen: The Promise of Early Intervention for Seniors

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As people age, their bodies inevitably change, affecting strength, mobility, and sensory function. Tasks that once seemed effortless become more challenging. Muscle mass tends to diminish, visual acuity declines and joints may become less flexible, all of which contribute to a gradual decrease in stability. This decline results in a startling statistic: nearly one in three individuals over 65 suffer a fall each year. The consequences of these falls are far from trivial. They often lead to broken bones, head injuries, or prolonged immobility, and in some cases, they can be fatal. In the United States alone, the financial toll of treating fall-related injuries amounts to billions of dollars annually. While ageing is unavoidable, falling does not have to be an inevitable consequence of getting older.

Recognising the need for early intervention, Jiaen Wu of Stanford University and his colleagues sought to explore whether balance impairments could be detected before they led to dangerous incidents. “One big challenge is that small balance impairments can go unnoticed until someone actually falls,” Wu explains. “So, we wanted to ask: Can we detect these impairments before someone gets hurt?” Together with collaborators Michael Raitor, Guan Tan, Kristan Staudenmayer, Scott Delp, Karen Liu, and Steven Collins, Wu investigated whether tracking the way people walk—long before any signs of frailty appear—could help forecast an individual’s risk of falling later in life. Their research, recently published in the Journal of Experimental Biology, provides compelling evidence that subtle variations in walking patterns may hold the key to fall prevention.

The researchers recruited ten healthy young adults between 24 and 31 to test their hypothesis. Each participant was fitted with a waist harness, attached to ropes and reflective markers positioned at the body’s front, back, and sides. This configuration enabled a sophisticated array of eleven cameras to record precise movements as each person walked on a treadmill at a steady pace of 1.25 metres per second. The team examined numerous aspects of gait, such as the consistency of foot placement and the degree of lateral movement in the person’s centre of mass. These initial measurements served as a baseline for each individual’s natural walking behaviour under normal, unimpaired conditions.

Next, the researchers introduced simulated impairments that mimicked the challenges associated with ageing. Participants walked again while wearing ankle braces to restrict joint mobility, a mask that limited vision, or pneumatic jets that disrupted their balance with bursts of air. These added hindrances caused noticeable disruptions in walking patterns. Step widths became more erratic, the timing between steps grew less regular, and the predictability of movement decreased. These findings mirrored the kinds of instability often seen in elderly individuals, indicating that visual obstructions or reduced joint function could profoundly affect a person’s ability to walk safely and steadily.

The team analysed the data and found that not all walking metrics were equally valuable for predicting fall risk. Of the six variables measured during normal walking, only three reliably signalled a person’s vulnerability to balance disturbances: variability in step width, irregularity in step timing, and the placement of each foot. Each of these indicators proved to be over 86 per cent effective in predicting whether someone would struggle to maintain balance when impaired. Surprisingly, when the researchers added a recovery test—tugging on the ropes attached to each walker’s harness to simulate a sudden loss of balance—the new data did not significantly enhance the accuracy of fall predictions. “We thought that seeing how people recover from a pull would reveal more about their balance ability,” Wu reflected, “but in this study, the normal walking data was just as informative in most cases.”

Perhaps the most striking insight from the study was that comparing an individual’s gait to their baseline proved far more predictive than comparing it to a group average. This finding suggests that the key to assessing fall risk is personalised, longitudinal monitoring rather than one-off clinical evaluations. Current practice typically involves assessing gait only after mobility issues have already emerged. Wu and his colleagues propose a paradigm shift: by measuring walking patterns earlier in adulthood—when movement is still largely unimpaired—clinicians could identify subtle deviations that indicate future risk. Such an approach could provide critical early warnings, enabling timely interventions that prevent falls before they occur. In doing so, it could reduce healthcare costs and preserve countless older adults’ quality of life and independence.

More information: Jiaen Wu et al, Detecting artificially impaired balance in human locomotion: metrics, perturbation effects and detection thresholds, Journal of Experimental Biology. DOI: 10.1242/jeb.249339

Journal information: Journal of Experimental Biology Provided by The Company of Biologists

Study Finds Connection Between Brain Health and Socioeconomic Standing

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In a landmark international study, researchers have drawn on genetic data from nearly one million individuals to examine the links between socioeconomic status (SES) and brain health. The team analysed how four key indicators — occupation, income, education, and social deprivation — correlate with genetic variation, revealing that a substantial portion of the genetic influences on these traits are shared. Specifically, around 75 per cent of the genetic effects associated with each of the four SES measures overlapped, suggesting the presence of a common genetic factor influencing social and economic positioning. This unified SES signal allowed researchers to assess shared social influences across the individual, household, and broader community.

This genetic factor of SES was studied in a cohort of 947,466 people using a genome-wide association study (GWAS) method. GWAS allows scientists to identify regions statistically associated with particular traits in the human genome. The team identified 554 specific genomic regions tied to SES through this technique. However, it is essential to note that these findings do not suggest that SES is genetically determined in a deterministic sense. Instead, the data reflect patterns in how specific genetic variants may correlate with social outcomes when embedded within broader environmental and societal contexts.

To better understand whether and how SES impacts brain health, the researchers then turned to a separate group of approximately 40,000 individuals who had undergone brain imaging. Their focus was on white matter hyperintensities — small lesions in the brain that increase with age and are linked to poorer thinking skills heightened dementia risk, and general declines in brain function. They found that people with higher SES tended to have fewer white matter hyperintensities, suggesting that socioeconomic advantage may offer some protection against age-related brain changes. This indicates a likely causal relationship in which SES influences neurobiological outcomes, not merely correlates with them.

Despite the genetic associations identified, the study was careful to underscore genetics’s modest role in explaining SES differences. Common genetic variation accounted for only about nine per cent of the variation in socioeconomic status among the study population. The vast majority of social standing, income, and education differences are shaped by environmental factors — including social policies, access to education, systemic inequalities, and even chance events. In this context, genes may set the stage, but the play is directed by the conditions in which people live, learn, and work.

Dr David Hill, lead author and MRC Research Fellow at the University of Edinburgh’s School of Philosophy, Psychology and Language Sciences, emphasised the significance of identifying a shared genetic factor for SES. According to Hill, this composite measure enabled a more comprehensive understanding of the socioeconomic forces that influence brain structure. “By using this common socioeconomic status factor,” he said, “we were able to capture aspects of socioeconomic status shared between the individual, the household, and the area in which one lives. This enabled us to better identify the causal effects of socioeconomic status on brain structure.”

Co-author Dr Charley Xia offered a vital clarification: the findings should not be misconstrued as evidence that brain health is genetically predetermined. “Studies examining traits such as socioeconomic status using genetic data can be easily conflated,” Xia warned. “We have not shown that brain health is genetically determined – rather that through genetic data we were able to identify socioeconomic status as a modifiable environmental influence on brain health in older age.” Overall, the research illustrates the potential of combining genetic and environmental data to understand better how societal inequalities might translate into long-term differences in brain health and cognitive ageing.

More information: David Hill et al, Deciphering the influence of socioeconomic status on brain structure: insights from Mendelian randomization, Molecular Psychiatry. DOI: 10.1038/s41380-025-03047-4

Journal information: Molecular Psychiatry Provided by University of Edinburgh

A Novel Blood Epigenetic Biomarker of Ageing Emphasises Intrinsic Capacity

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An international team of scientists has unveiled a new biological age estimator—a blood-based “epigenetic clock” that measures how well an individual is ageing rather than merely indicating their chronological age. This innovative metric, known as the Intrinsic Capacity Clock (or IC Clock), shifts the focus from chronological age to functional age, assessing a constellation of six vital domains that together constitute what the World Health Organization (WHO) refers to as intrinsic capacity (IC): mobility, cognition, mental health, sensory function (vision and hearing), and vitality, particularly about nutrition.

As outlined in a recent publication in Nature Aging, the IC Clock represents a significant advance in geroscience and healthy longevity. Rather than concentrating on age as a linear trajectory toward decline, this tool emphasises the preservation of function—something older adults consistently rank as more important than survival or disease avoidance. “Maintaining function during the ageing process matters to older adults,” notes Dr David Furman, PhD, the study’s senior author and Associate Professor at the Buck Institute, where he directs the Bioinformatics and Data Science Core. “Function should inform medical care instead of focusing on getting patients to some disease-free state.” Initially proposed by WHO, the concept of intrinsic capacity was formally recognised in 2022 in the International Classification of Diseases (ICD-11), marking a conceptual shift in how ageing-related decline is clinically identified and potentially treated.

The IC Clock is the result of a transatlantic collaboration between researchers at the Buck Institute for Research on Aging in California and the Hospital-University Institute HealthAge in Toulouse, France, in conjunction with the French research organisation INSERM and the Université de Montpellier. This partnership reflects a growing convergence of North American and European efforts to develop tools for enhancing a healthy lifespan. The foundation of the IC Clock lies in data from the INSPIRE-T cohort—a ten-year longitudinal study involving 1,000 participants aged between 20 and 102 years from the region around Toulouse. Over the first four years of data collection, researchers captured extensive information on each individual’s physical and cognitive function, lifestyle, and biological samples, including blood, saliva, urine, and dental plaque, which were collected annually.

What sets the IC Clock apart from earlier models is its basis in DNA methylation—chemical modifications that serve as molecular indicators of gene expression patterns associated with ageing. The research team demonstrated its superior predictive ability by training the IC Clock model on the INSPIRE-T dataset and validating it using data from the long-standing Framingham Heart Study in Massachusetts. Specifically, the IC Clock outperformed first- and second-generation epigenetic clocks in forecasting overall mortality. According to Furman, it is the only ageing clock that currently integrates all known hallmarks of ageing. Moreover, individuals with higher IC Clock scores exhibited better immune performance, lower markers of inflammation, and healthier behaviours, suggesting that this new measure captures core aspects of biological resilience and systemic integrity.

Crucially, the IC Clock is designed to be practical and scalable. Work is underway to develop a dried-blood spot version of the tool, which would allow for assessments without the need for invasive clinical procedures—particularly advantageous in low- and middle-income countries where healthcare infrastructure is often limited. “If we can offer a scalable, affordable molecular-level tool to assess functional decline,” Furman explained, “the IC Clock could help clinicians, researchers, and policymakers better identify at-risk individuals and tailor interventions that promote a longer, healthier life.” By moving beyond organ-specific diagnostics and toward a unified index of bodily function, the IC Clock could transform preventative care and the global discourse on ageing.

Despite the WHO’s recognition of declining intrinsic capacity as a clinical condition, regulatory frameworks in the United States—most notably the Food and Drug Administration (FDA)—have yet to catch up. The classification of ageing as a disease remains controversial, posing a significant barrier to the approval of interventions targeting ageing-related decline. Furman believes that the IC Clock may help resolve this impasse. “We hope the IC Clock will ultimately enable the FDA to approve treatments that would improve health and function in older adults,” he said, suggesting the clock could become a regulatory anchor for future geroprotective therapies.

Looking ahead, the IC Clock will be deployed in the high-profile XPRIZE Healthspan competition—a global challenge backed by $101 million in funding over seven years, aimed at revolutionising how ageing is managed and mitigated. The Buck-Toulouse consortium has already been named a semifinalist in this ambitious effort, which seeks to identify interventions capable of reversing 10 to 20 years of biological ageing in core domains, such as muscle strength, cognitive capacity, and immune function, within a single year, among adults aged 50 to 80. Their proposed hybrid intervention combines daily supplementation with a ketone ester and a personalised, non-pharmacological protocol called ICOPE-INTENSE. This latter regimen integrates tailored components of exercise, cognitive stimulation, dietary optimisation, and social support—all designed to enhance the pillars of intrinsic capacity. The IC Clock will be the primary biomarker throughout the study to monitor and quantify participants’ functional response to the intervention.

The IC Clock’s development marks a compelling shift in how we approach ageing—not as an inevitable march toward frailty and disease, but as a modifiable state that can be measured, monitored, and potentially improved. In highlighting the biological substrates of functional health and offering a scientifically validated tool to assess them, the IC Clock has the potential to inform clinical decisions, guide public health initiatives, and shape regulatory policies on a global scale. Whether it will ultimately usher in a new era of longevity-focused medicine depends on further validation and scalability and on societal willingness to redefine what it means to age well.

More information: David Furman et al, A blood-based epigenetic clock for intrinsic capacity predicts mortality and is associated with clinical, immunological and lifestyle factors, Nature Aging. DOI: 10.1038/s43587-025-00883-5

Journal information: Nature Aging Provided by Buck Institute for Research on Aging

Healthy Eating Linked to Cardiometabolic Gains, Even Without Weight Reduction

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A new study led by researchers at the Harvard T.H. Chan School of Public Health and Ben-Gurion University in Israel has shed light on a striking finding: many people who adopt a healthy diet can gain significant health benefits without losing weight. Published on 5 June in the European Journal of Preventive Cardiology, the research demonstrates that diet quality alone—independent of weight reduction—can bring about meaningful improvements in cardiometabolic markers. Nearly one-third of study participants who improved their diets experienced no measurable weight loss yet showed notable enhancements in various health indicators.

The study confronts a long-held assumption in public health and clinical practice: that weight loss is the central, if not sole, pathway to improved metabolic health. However, the researchers observed that individuals who did not lose weight nonetheless reaped benefits, including increased levels of HDL cholesterol (commonly known as the “good” cholesterol), reduced levels of leptin (a hormone that regulates hunger), and a decrease in visceral fat, which surrounds internal organs and has been linked to heightened disease risk. These changes are considered strong predictors of long-term cardiovascular and metabolic resilience.

“We have been conditioned to equate weight loss with health, and weight loss-resistant individuals are often labelled as failures,” noted lead author Dr Anat Yaskolka Meir, a postdoctoral research fellow in the Department of Epidemiology at Harvard Chan School. “Our findings reframe how we define clinical success. People who do not lose weight can still improve their metabolism and reduce their long-term risk for disease. That’s a message of hope, not failure.” The study promotes a more inclusive and nuanced understanding of what constitutes progress in dietary and health interventions.

The study analysed data from 761 adults in Israel who had abdominal obesity and participated in three major workplace-based dietary intervention trials: DIRECT, CENTRAL, and DIRECT-PLUS. These trials spanned 18 to 24 months and involved structured random assignments to different healthy eating plans, including low-fat, low-carbohydrate, Mediterranean, and green Mediterranean diets. With ongoing support, participants were encouraged to adhere to these regimens, and adherence rates were consistently high. Comprehensive metabolic assessments were conducted at various points to track physiological responses over time.

Among all participants, 36% achieved clinically significant weight loss, defined as losing more than 5% of their initial body weight. Another 36% experienced moderate weight loss, losing up to 5% of their starting weight. The remaining 28% of participants were classified as weight loss-resistant, either losing no weight or gaining some during the study. While weight loss was associated with clear metabolic advantages—each kilogram of weight lost corresponded to measurable improvements in cholesterol, triglycerides, insulin, liver fat, and other biomarkers—the most surprising outcome was that similar benefits emerged among those who did not lose weight.

Indeed, those who maintained their weight still showed elevated HDL cholesterol, lower leptin levels, and reduced visceral fat. These effects were particularly evident among older adults and women, who were likelier to fall into the weight loss-resistant category. Such findings upend conventional narratives that link health improvements solely to body mass reduction. Instead, they suggest that the body can adapt positively to better nutrition even without a corresponding weight change, likely through mechanisms involving hormonal regulation, inflammation reduction, and improved fat distribution.

The research team further delved into the biological underpinnings of these differing responses by utilising advanced omics technologies. Specifically, they identified 12 distinct DNA methylation sites—epigenetic markers influencing gene expression—which strongly predicted long-term weight loss success. This discovery lends credence to the notion that weight loss is not simply a matter of willpower or discipline but may also be governed by biological predispositions. “This isn’t just about motivation—it’s about molecular biology,” said Professor Iris Shai, the study’s senior author and principal investigator of the nutrition trials. “We’re starting to uncover why some people respond better than others, and that knowledge could help personalise future dietary strategies.”

Despite its strengths, the study has a few limitations, most notably the underrepresentation of women, who comprised a smaller portion of the participant pool. As women tended to be more weight loss-resistant, further research on gender-specific responses could provide even more refined insights. The authors recommended that subsequent trials ensure balanced representation to understand better how factors like age, sex, and hormonal status may influence dietary outcomes. The results remain compelling and broadly relevant to clinical and public health audiences.

In conclusion, this study delivers a critical message that may reshape how clinicians and the general public perceive dietary success. It underscores that choosing and adhering to a nutritious diet can bring powerful metabolic benefits—regardless of whether or not weight is lost. Such a perspective offers reassurance to individuals who struggle with weight change despite their best efforts, affirming that their health can improve meaningfully. Most importantly, it invites a shift in focus from the scale to the more profound and often unseen inner workings of the human body in response to quality nutrition.

More information: Anat Yaskolka Meir et al, Individual response to lifestyle interventions: a pooled analysis of three long-term weight loss trials, European Journal of Preventive Cardiology. DOI: 10.1093/eurjpc/zwaf308

Journal information: European Journal of Preventive Cardiology Provided by Harvard T.H. Chan School of Public Health

New Research Links Daily Mango Consumption to Improved Heart and Metabolic Health in Postmenopausal Women

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Each year, around 1.3 million women in the United States transition into menopause—a natural life stage accompanied by significant hormonal shifts that can adversely affect cardiovascular health. This transition is linked to a marked increase in the risk of heart disease, which already affects nearly half of American women. Maintaining heart health during this period is essential because women often live one-third to almost half of their lives in a postmenopausal state. In this context, a recent study published in the Journal of the American Nutrition Association offers encouraging evidence: consuming fresh mangos daily may support key cardiovascular markers in postmenopausal women.

The study, conducted by researchers at the University of California, Davis, involved generally healthy women aged between 50 and 70 years who were classified as having overweight or obesity. Participants were instructed to avoid mangos before the study’s second phase, after which they began consuming 330 grams of fresh mango daily—roughly equivalent to 1.5 cups—divided into morning and evening servings. Over two weeks, participants made three laboratory visits, spaced at least 48 hours apart, during which researchers collected data on body metrics, blood pressure, and cholesterol levels. Baseline measurements were recorded at the first visit, with follow-up testing after mango consumption began in the second and third visits.

Findings from the study revealed striking short-term improvements in cardiovascular health. Just two hours after consuming mangos, participants’ supine systolic blood pressure dropped by an average of 6.3 mmHg, while mean arterial pressure declined by 2.3 mmHg. Over two weeks, mango consumption was associated with a notable decrease in fasting cholesterol levels: total cholesterol dropped by nearly 13 mg/dL, and LDL cholesterol—commonly known as “bad” cholesterol—fell by approximately the same amount. These changes are clinically meaningful, especially given the relatively short intervention window and no other lifestyle modifications were required.

Dr Roberta Holt, Associate Researcher at UC Davis and co-author of the study emphasised the implications of these findings for women facing menopause-related health risks. “Post-menopausal women face distinct metabolic changes that can impact their risk of developing cardiovascular disease,” she stated. “These findings help to identify targeted dietary strategies, like eating fresh mangos daily, to aid this at-risk population and support cardiovascular wellness and potential reductions in chronic disease risk.” Holt’s comments highlight the potential for dietary interventions to offer practical, non-pharmaceutical solutions to long-standing public health challenges.

In a follow-up study involving six participants from the original cohort, researchers explored how mangos might affect glucose metabolism—an equally important aspect of cardiometabolic health. Participants underwent three rounds of glucose testing: the first established baseline values, the second followed mango consumption, and the third involved ingesting 83 grams of white bread. The mango outperformed the white bread by a clear margin. Blood glucose levels rose significantly less after eating mango, and insulin levels spiked and declined rapidly, suggesting a more favourable metabolic response. This evidence supports the idea that mangos, beyond their cardiovascular benefits, may help stabilise blood sugar and reduce insulin strain.

While further research is warranted to confirm long-term effects and to broaden the sample size, the study points to mangos as a simple yet effective dietary tool for promoting health in postmenopausal women. With their rich content of antioxidants, fibre, and naturally occurring bioactive compounds, mangos offer a nutrient-dense option that may complement existing dietary strategies aimed at reducing chronic disease risk. Whether used to support blood pressure, cholesterol, or glucose control, fresh mangos present a delicious and health-promoting addition to the diets of those navigating the physiological changes of menopause.

More information: Roberta Holt et al, Short-Term Cardiometabolic Response to Mango Intake in Postmenopausal Women, Journal of the American Nutrition Association. DOI: 10.1080/27697061.2025.2478937

Journal information: Journal of the American Nutrition Association Provided by Wild Hive