Monthly Archives: July 2025

Major Cancers More Prevalent in Economically Disadvantaged Japanese Communities, 16-Year Study Finds

A comprehensive analysis of sixteen years of data on Japanese adults has revealed that five common cancers—lung, stomach, colorectal, liver, and breast—occur more frequently in communities characterised by lower employment rates or reduced income levels.

Cancer continues to impose a significant burden due to its high morbidity and mortality, making effective prevention strategies a public health priority. A growing body of evidence indicates that certain cancer types are closely linked to individual socioeconomic status (SES), with disparities in both incidence and mortality reflecting broader social inequalities. For example, individuals with lower SES are disproportionately affected by lung cancer, a trend that may be partially attributed to higher smoking prevalence within these populations. Education level also plays a pivotal role in cancer outcomes, as those with higher levels of education are more likely to avoid health-risk behaviours, such as tobacco use.

While several prevention initiatives targeting individuals with low SES have been implemented—such as screening and treatment programmes for breast and cervical cancer aimed at low-income or uninsured women—participation rates in these efforts remain suboptimal. Studies have consistently shown that individuals with lower income or educational attainment are less likely to engage in cancer screening. These low participation rates are influenced not only by direct financial barriers but also by contextual regional factors, including limited access to healthcare services in socioeconomically disadvantaged areas.

In contrast to approaches focused solely on individual SES, interventions that consider broader community-level circumstances have, in some instances, yielded more successful outcomes. For example, culturally tailored screening initiatives and community-based hepatitis B testing programmes have demonstrated improved participation rates and better health outcomes. These findings suggest that regional SES disparities—pervasive within many countries—must be taken into account when designing public health interventions. Populations with similar socioeconomic conditions tend to cluster geographically, shaping the overall SES of a community. This clustering influences the development of local social systems, which in turn affect health outcomes and access to preventive services.

As such, the SES of a community and the supporting social infrastructure can significantly impact both the onset and progression of disease. Demonstrating the relationship between community-level SES and cancer is therefore essential for informing more effective and equitable prevention strategies. By aligning interventions with the socioeconomic characteristics of specific regions, policymakers and public health professionals can better position themselves to reduce cancer disparities and improve population health outcomes at both the individual and community levels.

More information: Satoru Kanda et al, Association between socioeconomic background and cancer: An ecological study using cancer registry and various community socioeconomic status indicators in Kanagawa, Japan, PLOS One. DOI: 10.1371/journal.pone.0326895

Journal information: PLOS One Provided by PLOS

Adult Survivors of Childhood Cancer Face Heightened Risk of Severe COVID-19 Outcomes

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Individuals who survived cancer during childhood face a significantly heightened risk of developing severe illness from COVID-19, even many years after their initial diagnosis. This conclusion is based on a recent study conducted by researchers at Karolinska Institutet and published in The Lancet Regional Health – Europe. The findings shed light on the long-term health vulnerabilities that persist in this group, long after the apparent resolution of their primary illness. Although treatments for childhood cancer have vastly improved survival rates over the past few decades, they may leave survivors with lasting physiological impacts that compromise their ability to cope with serious infections later in life.

In this comprehensive population-based registry study, scientists investigated the outcomes of adult survivors of childhood cancer during the COVID-19 pandemic in Sweden and Denmark. The researchers examined the health outcomes of more than 13,000 individuals who had been diagnosed with cancer before the age of 20 and who were at least 20 years old by the time the pandemic began. These individuals were compared to both their siblings and a control group of randomly selected individuals from the general population matched for gender and year of birth, thereby ensuring a robust comparative framework.

Interestingly, the study revealed that childhood cancer survivors were somewhat less likely to contract COVID-19 than those in the control groups. However, the most striking finding was that, if they did become infected, they were 58 per cent more likely to develop a severe form of the illness. Severe COVID-19 was defined in the study as a case that resulted in hospital admission, admission to intensive care, or death. This suggests that although survivors may have taken greater precautions to avoid infection, their bodies were less capable of mounting an effective response once the virus had taken hold.

Dr Javier Louro, a postdoctoral researcher at the Institute of Environmental Medicine at Karolinska Institutet and the first author of the study, emphasised the significance of this outcome. “It is important to understand that even though these individuals were not infected more often, the consequences were more serious when they did become ill,” he noted. This observation is particularly critical because it reframes how we assess risk: not only in terms of exposure or likelihood of infection, but in terms of the severity of the health consequences when infection occurs.

Another essential element of the study concerned geographical variation in risk, influenced by national pandemic policies. During periods of high viral transmission, such as the waves driven by the Alpha and Omicron variants, the differences in outcomes were especially stark. In Sweden, which adopted a less restrictive, recommendation-based approach to managing the pandemic, the increased risk to childhood cancer survivors was more pronounced than in Denmark, which implemented stricter, early-stage mitigation measures. This comparison suggests that public health policy can play a significant role in protecting vulnerable groups, especially when their susceptibility is not immediately apparent.

The study’s authors conclude that adult survivors of childhood cancer should be explicitly recognised as a high-risk group in the event of future pandemics or large-scale health emergencies. Their inclusion in vaccination priority lists, along with tailored guidance and protections during periods of high transmission, could be crucial in reducing the disease burden in this population. More broadly, the study underscores the necessity of considering long-term survivorship in the planning of public health responses, recognising that the shadow of childhood illness can extend well into adult life, shaping how individuals experience and survive new health threats.

More information: Javier Louro et al, COVID-19 infection and severity among childhood cancer survivors in Denmark and Sweden: a register-based cohort study with matched population and sibling comparisons, The Lancet Regional Health – Europe. DOI: 10.1016/j.lanepe.2025.101363

Journal information: The Lancet Regional Health – Europe Provided by Karolinska Institutet

Theatre Helps Alleviate Emotional Symptoms in Individuals with Parkinson’s Disease

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A recent clinical study led by a research team at the Universitat Oberta de Catalunya (UOC), in collaboration with the Hospital Sant Pau in Barcelona, has revealed promising results regarding the benefits of theatre on the emotional well-being of people with Parkinson’s disease. Published in the journal Arts & Health under the title “Efficacy of a Theatre-Based Intervention in Patients with Parkinson’s Disease” (2025), the study marks the first formal evaluation of the combined effects of both active and passive engagement in theatrical activities on emotional and cognitive health in this population. The initiative was also backed by the Teatre Lliure, one of Barcelona’s leading cultural institutions, highlighting a fruitful union between healthcare research and the performing arts.

The project included 34 participants aged between 50 and 75 who were living with Parkinson’s disease. These individuals were divided into two distinct groups: one participated in a structured three-month theatre programme hosted at Teatre Lliure, which included live performances, interactive workshops, and a guided tour of the venue; the other group remained at home, engaging in cognitive stimulation exercises. Both groups were evaluated before and after their respective interventions using neuropsychological testing and standardised questionnaires that measured mood, perceived quality of life, and self-reported cognitive changes.

From an emotional perspective, the results were compelling. Participants in the theatre group demonstrated a significant improvement in emotional well-being, as measured by the Parkinson’s Disease Questionnaire (PDQ-39), a widely used tool for assessing quality of life. This enhancement was not mirrored in the group that performed at-home cognitive tasks. Notably, both groups did experience reductions in anxiety and depression, which suggests that while cognitive stimulation has its merits, theatre offers unique advantages. The shared emotional and social experience of live performance and participation in creative group work appeared particularly effective in lifting mood and countering feelings of emotional isolation.

A particularly striking finding of the study was the immediate impact of group theatre workshops on participants’ emotional state. Pre- and post-session evaluations indicated a marked decrease in emotional burden following each workshop, suggesting that theatrical engagement may offer a powerful outlet for emotional processing. Researchers attributed this effect to theatre’s inherent demand for expressive communication and emotional openness, which enables participants to externalise their inner experiences in a safe and structured environment. The communal nature of these workshops also played a key role, encouraging empathy and mutual support among participants.

The theatre programme itself was thoughtfully constructed. It combined five live performances—each paired with preparatory sessions designed to enhance audience engagement—with five workshops led by professional actors and theatre facilitators. These workshops used techniques such as physical warm-ups, spatial awareness exercises, improvisation, and collaborative storytelling to target emotional expression and body awareness. According to the researchers, these methods are central to the benefits observed, as they enable participants to explore and articulate their emotions while reinforcing a sense of physical presence and interpersonal connection, both of which are often diminished in individuals with Parkinson’s disease.

While objective measures of cognitive function did not reveal significant changes, participants in the theatre group reported a subjective improvement in their day-to-day cognitive abilities. This enhanced self-perception may lead to greater confidence in managing everyday tasks, thereby indirectly contributing to improved quality of life. Participant feedback was overwhelmingly positive, with the workshops receiving an average satisfaction score of 4.5 out of 5, theatre performances 4.4, and the guided tour 4.8, suggesting that, beyond clinical measures, the programme succeeded in delivering a significant experience to those involved.

This pioneering study adds to a small but growing body of research advocating the integration of artistic practices into therapeutic contexts. Until now, only two other studies had investigated the use of theatre for people with Parkinson’s, both yielding encouraging but unconfirmed outcomes. The rigorous methodology employed in this new research strengthens the case for theatre as a complementary treatment, particularly for symptoms that do not respond well to pharmacological interventions, such as apathy and social withdrawal. The findings align with the World Health Organization’s 2019 recommendation endorsing the arts as a “social prescription” to enhance well-being. As Parkinson’s diagnoses continue to rise—currently affecting between 120,000 and 150,000 individuals in Spain, with 10,000 new cases each year—creative, community-based interventions like these may offer invaluable tools for improving the lives of those living with the disease.

More information: Marco Calabria et al, Efficacy of a theatre-based intervention in patients with Parkinson’s disease, Arts & Health. DOI: 10.1080/17533015.2025.2488361

Journal information: Arts & Health Provided by Universitat Oberta de Catalunya (UOC)

Innovative 3D-Printed Smart Pen Detects Signs of Parkinson’s Through Magnetoelastic Sensing

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Each year, countless individuals displaying early signs of Parkinson’s disease go undiagnosed until the illness has already reached an advanced stage. Parkinson’s is an incurable neurodegenerative disorder characterised by the gradual death of dopamine-producing neurons in the brain, and symptoms such as tremors, muscle rigidity, and bradykinesia often don’t manifest until the damage has become extensive. By the time a patient receives a formal diagnosis, more than half of their dopamine-generating neurons may already be lost, making timely therapeutic intervention more challenging. Although several diagnostic tools are currently available—including imaging techniques to identify cell loss and blood tests to detect inflammatory biomarkers—these methods typically require specialised equipment, access to neurologists, and visits to well-equipped medical centres. For many people, especially those in remote or underserved regions, such tests are simply inaccessible.

In response to this gap in early detection, a team of researchers led by Jun Chen, associate professor of bioengineering at the UCLA Samueli School of Engineering, has developed an ingenious and surprisingly low-cost alternative: a smart, self-powered magnetoelastic pen designed to detect Parkinson ‘s-related motor abnormalities through handwriting analysis. This seemingly ordinary writing instrument disguises an advanced diagnostic tool, capable of capturing nuanced motor signals that may elude both the patient and clinician.

The innovative pen, featured as the cover article in the June edition of Nature Chemical Engineering, contains a flexible, silicone-based magnetoelastic tip and utilises ferrofluid ink—an engineered liquid infused with magnetic nanoparticles. As the pen moves across a surface or even through the air, it harnesses the dynamic changes in magnetic fields that occur due to motion. These changes are registered by a conductive coil of yarn wrapped around the barrel of the pen, allowing it to translate physical gestures into rich streams of data. Remarkably, the device is entirely self-powered, requiring no external batteries or wires. While it’s not designed for legible writing per se, the pen excels in picking up micro-movements that are imperceptible to the human eye, converting them into electrical signals that can then be analysed for signs of neuromotor dysfunction.

To test the pen’s diagnostic capability, the researchers conducted a pilot study involving 16 participants, three of whom had been diagnosed with Parkinson’s disease. Participants were asked to perform simple handwriting tasks, during which the pen recorded their motions in detail. The resulting data was processed using a neural network trained to identify Parkinson ‘s-specific motor patterns. Notably, the system achieved an average classification accuracy of 96.22%, effectively distinguishing between individuals with the disease and healthy participants. This high level of precision demonstrates the pen’s potential as a reliable screening tool that could flag individuals for further assessment long before more conspicuous symptoms emerge.

Professor Chen emphasised the significance of the tool in a broader healthcare context: “Detection of subtle motor symptoms unnoticeable to the naked eye is critical for early intervention in Parkinson’s disease,” he said. The accessibility and affordability of the diagnostic pen make it an attractive option for use in a wide range of settings, including primary care clinics and facilities in low-resource communities. Its portability and ease of use could make it especially valuable in areas where specialist care is sparse and diagnostic delays are common.

Looking forward, the research team envisions their device being deployed as a simple screening instrument during routine medical check-ups. A patient could be asked to complete a brief handwriting task, the results of which would be instantly processed to provide a risk assessment for Parkinson’s or similar neurodegenerative conditions. If early signs are detected, patients could be referred for more comprehensive neurological evaluation and, if necessary, begin early interventions aimed at slowing disease progression. Such a shift towards early and accessible detection could not only improve individual outcomes but also reduce the societal burden associated with long-term Parkinson’s care.

Ultimately, the smart pen represents a marriage of bioengineering ingenuity and practical clinical need. By transforming something as ordinary as handwriting into a diagnostic tool, the UCLA-led team has opened the door to a new paradigm in neurological screening—one where subtle signs are captured before they escalate into life-altering impairments. The implications are far-reaching: earlier diagnosis, greater treatment efficacy, and a more proactive approach to one of the most pervasive neurodegenerative diseases in the world.

More information: Jun Chen et al, Neural network-assisted personalized handwriting analysis for Parkinson’s disease diagnostics, Nature Chemical Engineering. DOI: 10.1038/s44286-025-00219-5

Journal information: Nature Chemical Engineering Provided by University of California – Los Angeles

Heart Health at Risk from Air Pollution Exposure

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A groundbreaking study published today in Radiology, the journal of the Radiological Society of North America (RSNA), has revealed that prolonged exposure to air pollution is linked to early signs of heart damage. Using advanced cardiac magnetic resonance imaging (MRI), researchers were able to detect increased levels of diffuse myocardial fibrosis—a subtle yet profound form of scarring in the heart muscle. This type of tissue damage is an early warning sign. It is associated with an increased risk of heart failure over time, even in individuals who do not yet show symptoms of cardiovascular disease.

Cardiovascular disease continues to be the foremost cause of death worldwide, and while numerous studies have demonstrated a correlation between poor air quality and heart-related illnesses, the exact mechanisms by which pollution affects heart tissue have mainly remained speculative. This new research adds an essential piece to the puzzle by using state-of-the-art imaging technology to visualise and quantify structural changes in the heart that may develop silently over years of exposure to air pollution.

Lead investigator Dr Kate Hanneman, from the Department of Medical Imaging at the Temerty Faculty of Medicine, University of Toronto, and the University Health Network, explained the motivation behind the study: “We know that people exposed to higher levels of air pollution are at greater risk of developing cardiovascular conditions, including myocardial infarction. What we wanted to understand was the biological mechanism behind this increased risk—what exactly is happening inside the heart tissue.” Her team utilised non-invasive MRI to precisely assess myocardial fibrosis and its association with a specific type of air pollutant, known as PM2.5.

PM2.5 refers to delicate particulate matter that measures 2.5 micrometres in diameter or less—roughly 30 times smaller than the width of a human hair. Due to their minuscule size, these particles can bypass the body’s natural defences in the respiratory tract and penetrate deep into the lungs, eventually entering the bloodstream. Familiar sources of PM2.5 include vehicle emissions, industrial output, and wildfire smoke. Long-term exposure to these particles has been associated with systemic inflammation and vascular dysfunction, but their specific role in heart tissue scarring had not been clearly defined until now.

The study population consisted of a total of 694 participants, divided into 201 healthy individuals and 493 patients diagnosed with dilated cardiomyopathy—a condition in which the heart becomes weakened and enlarged, thereby impairing its ability to pump blood effectively. This diverse sample allowed researchers to observe the effects of air pollution in both individuals with existing heart conditions and those without. Notably, the results revealed that prolonged exposure to PM2.5 was associated with higher levels of myocardial fibrosis in both groups. This suggests that fine particulate air pollution may contribute to a standard underlying pathological process regardless of baseline heart health.

Notably, the most pronounced effects were observed in women, smokers, and individuals with hypertension—groups already known to be at heightened risk of cardiovascular complications. These findings underscore the complex interplay between environmental exposures and individual susceptibility. According to Dr Hanneman, “Even modest increases in air pollution levels appear to have measurable effects on the heart. Our study suggests that environmental air quality may influence heart structure and function more significantly than previously understood.”

In addition to clarifying the biological impact of air pollution on cardiac tissue, the study also raises important implications for clinical practice and public health policy. Incorporating a patient’s history of air pollution exposure into cardiovascular risk assessments could help identify those at greater risk and ensure earlier intervention. For instance, individuals who live or work in areas with poor air quality—such as urban centres or industrial zones—may benefit from more frequent cardiovascular screening or targeted prevention strategies.

Perhaps most concerning is the fact that the levels of air pollution associated with myocardial fibrosis in the study were below many internationally accepted safety thresholds. This finding reinforces the growing consensus that there may be no truly safe level of exposure to air pollution. “Public health measures are urgently needed to further reduce air pollution, even in regions where air quality has improved in recent years,” Dr Hanneman stated. Moreover, the study highlights the expanding role of radiologists in environmental health, showing how advanced imaging can serve as a powerful tool to uncover the hidden impacts of environmental exposures on the human body.

More information: Kate Hanneman et al, Association between Long-term Exposure to Ambient Air Pollution and Myocardial Fibrosis Assessed with Cardiac MRI, Radiology. DOI: 10.1148/radiol.250331

Journal information: Radiology Provided by Radiological Society of North America

Bereavement and Financial Strain May Heighten Alzheimer’s Risk and Affect Brain Structure

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Chronic stress, particularly stemming from major life upheavals, can exert a profound influence on brain health. A new study led by researchers at the Barcelona Institute for Global Health (ISGlobal) and the Barcelonaβeta Brain Research Centre (BBRC), both supported by the ”la Caixa” Foundation, has shed light on the biological consequences of bereavement, unemployment, and financial loss. The findings, published in Neurology, indicate that these stressors are linked to early biomarkers and structural brain changes associated with Alzheimer’s disease, and that their effects vary according to gender and educational background.

The study, spearheaded by ISGlobal researcher Dr Eider Arenaza-Urquijo, examined over 1,200 cognitively unimpaired participants from the ALFA (ALzheimer’s and FAmilies) cohort, the majority of whom had a familial predisposition to Alzheimer’s disease. Through the use of magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) analysis, the researchers explored associations between life stressors and both grey matter volume and key Alzheimer’s biomarkers. As explained by Eleni Palpatzis, a predoctoral researcher and lead author of the study, these markers included beta-amyloid proteins, phosphorylated tau, and neurogranin—each closely tied to the early neurobiological underpinnings of Alzheimer’s.

In individuals who had experienced the death of a partner, the researchers observed significant alterations in Alzheimer ‘s-related biomarkers. Notably, there was a reduction in the beta-amyloid 42/40 ratio, a shift that signals increased amyloid aggregation in brain tissue. This was accompanied by elevated levels of phosphorylated tau, a protein implicated in neuronal degradation, and higher concentrations of neurogranin, which rises when synaptic connections begin to deteriorate. Gender appeared to play a moderating role in these associations: men exhibited a greater decline in the beta-amyloid ratio, whereas women showed more substantial increases in tau and neurogranin levels. Furthermore, these effects were exacerbated in participants with lower levels of education, suggesting that social determinants may amplify the neurobiological consequences of bereavement.

In contrast, economic adversity—specifically unemployment and financial loss—was linked not to changes in CSF biomarkers but rather to reductions in grey matter volume within brain regions integral to emotional and cognitive regulation. Again, the impact of these stressors appeared to diverge by gender. Unemployment disproportionately affected grey matter in men, whereas financial strain had a more significant impact on women’s brain structure. These findings underscore how stress-related neuropathology may manifest differently across demographic groups, shaped by longstanding societal and economic inequalities.

This study builds upon prior research by the same group, which demonstrated that exposure to significant stressors in midlife can increase vulnerability to Alzheimer’s disease. The new findings add a nuanced layer, revealing how such experiences do not exert uniform effects. Instead, the extent and nature of their impact are modulated by intersecting social variables such as gender and educational attainment. Women and individuals with fewer educational opportunities are not only more likely to encounter life stressors but also to bear a disproportionate biological burden from them—an intersection that may help explain higher rates of Alzheimer’s within these populations.

Commenting on the gendered dimensions of these results, Dr Arenaza-Urquijo noted that men may be especially vulnerable to the loss of a partner, given their tendency to maintain fewer emotionally supportive relationships outside their romantic ones. The isolation that follows bereavement may be particularly acute for them, potentially accounting for the observed changes in amyloid processing. Furthermore, unemployment—often more socially stigmatised among men—may also carry heightened emotional consequences that translate into structural brain changes. Women, on the other hand, may be more affected by financial instability, a finding the researchers attribute to historical disparities in financial security and the greater emotional toll economic anxiety takes on women’s mental health.

Taken together, these findings provide compelling evidence that adverse life events, particularly those that intersect with social vulnerabilities, may have measurable and lasting effects on the brain. They underscore the importance of addressing social and psychological risk factors early in life as part of a broader strategy for Alzheimer’s prevention. Beyond the molecular markers and neuroimaging data, the study invites reflection on the deeply human experiences of loss, insecurity, and inequality—and their biological echoes in the brain’s architecture and chemistry.

More information: Eleni Palpatzis et al, Grief and Economic Stressors by Sex, Gender, and Education, Neurology. DOI: 10.1212/WNL.0000000000213377

Journal information: Neurology Provided by Barcelona Institute for Global Health (ISGlobal)

Can Early Academic Grading Contribute to Mental Health Issues in Adolescents?

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Research in Health Economics has shown that introducing academic grading systems—using letters such as A for excellence and F for failure—at an earlier stage in a child’s education may have detrimental effects on mental health.

In Sweden, pupils have historically received individual letter grades since Year 8 (approximately 14 years of age). However, a policy reform implemented in autumn 2012 shifted the onset of grading to Year 6 (around age 12). This change provided researchers with a unique opportunity to evaluate the potential psychological consequences of early grading.

By analysing sociodemographic and clinical data from a substantial cohort of 524,093 Swedish children enrolled in Years 5 through 9, both before and after the reform, researchers uncovered a notable trend: girls exposed to grading from a younger age demonstrated a higher likelihood of developing internalising disorders, including anxiety and depression, by the time they completed compulsory schooling. This effect was particularly pronounced among female students with low to average academic performance.

Further findings indicated that the earlier introduction of grades may also correlate with a heightened risk of alcohol-related disorders among both boys and girls. Although the mechanisms remain complex, the data suggest that early academic evaluation can contribute to significant emotional strain during formative years.

“Sweden, like many other nations, has increasingly embraced standardised testing and more stringent grading practices, frequently overhauling its assessment framework,” said Dr Anna Linder, lead author of the study and researcher at Lund University. “Our findings suggest that such educational reforms can adversely affect children’s mental well-being. Grades themselves are not inherently harmful, but their structure and timing must be thoughtfully designed to accommodate the varying developmental trajectories of children. Feedback should foster growth rather than provoke distress.”

These insights contribute to a growing body of literature that cautions against the implementation of high-stakes evaluation systems during early adolescence. While academic assessment remains a cornerstone of education, this research highlights the importance of striking a balance between accountability and psychological development.

More information: Anna Linder et al, Adolescent Mental Health: Impact of Introducing Earlier Compulsory School Grades, Health Economics. DOI: 10.1002/hec.4982

Journal information: Health Economics Provided by Wiley

Promising New Target in the Brain Unveils Potential Breakthrough for Parkinson’s Therapy

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Groundbreaking research from the University of Sydney has revealed a newly identified brain protein involved in the progression of Parkinson’s disease, along with a promising strategy to modify its harmful effects. This discovery could pave the way for a new class of treatments aimed at slowing, or potentially halting, the course of this debilitating neurological condition. Parkinson’s disease is the second most prevalent neurodegenerative disorder after dementia, affecting over 150,000 Australians and millions more worldwide.

The research, led by Professor Kay Double at the University’s Brain and Mind Centre, is the culmination of over a decade of dedicated investigation into the biological mechanisms behind Parkinson’s. In a 2017 study published in Acta Neuropathologica, her team was the first to identify an abnormal form of a protein called SOD1 in the brains of individuals with Parkinson’s disease. While SOD1 typically plays a protective role in brain cells, the researchers found that it can malfunction in Parkinson’s patients, clumping together and damaging neurons.

In their latest study, published in Acta Neuropathologica Communications, the team extended their earlier work by testing a novel treatment targeting the faulty SOD1 protein. Mice genetically engineered to exhibit Parkinson-like symptoms were given a copper-based supplement over three months. Remarkably, the treated mice showed a significant improvement in motor function, while those given a placebo experienced the expected decline associated with the disease. These results provide strong evidence that intervening in SOD1 dysfunction can reduce or prevent movement-related impairments associated with Parkinson’s disease.

Professor Double expressed cautious optimism about the findings, noting that all treated mice showed significant improvements in mobility. “We hoped that targeting this malfunctioning protein might alleviate symptoms in the mice, but even we were surprised by how effective the treatment was,” she said. “This is an encouraging sign that a similar approach might prove beneficial for people living with Parkinson’s disease.” However, she also emphasised the need for further studies before the method can be safely and effectively applied to human patients.

Parkinson’s disease is marked by the gradual death of dopamine-producing cells in the brain, leading to symptoms such as tremors, rigidity, slow movement, and poor balance. Although current therapies may temporarily ease symptoms, there is no known cure, and existing treatments do little to alter the long-term progression of the disease. Professor Double’s work contributes to a growing body of research aimed at understanding the underlying causes of Parkinson’s, with the ultimate goal of developing treatments that do more than manage symptoms.

The team now plans to explore how best to translate their findings into clinical trials, a crucial step in determining whether targeting SOD1 can become a viable therapy for humans. Professor Double compared the future of Parkinson’s treatment to the multi-faceted strategies used for HIV, suggesting that while a single intervention might not offer a cure, combining approaches could produce meaningful outcomes. With continued research, this protein-targeting breakthrough could mark the beginning of a new chapter in the fight against Parkinson’s disease, offering patients not only symptom relief but also renewed hope for the future.

More information: Kay Double et al, Copper supplementation mitigates Parkinson-like wild-type SOD1 pathology and nigrostriatal degeneration in a novel mouse model, Acta Neuropathologica Communications. DOI: 10.1186/s40478-025-02048-2

Journal information: Acta Neuropathologica Communications Provided by University of Sydney

Rethinking BMI as a Measure of Future Health Risk

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A newly released study by the University of Florida Health has cast serious doubt on the effectiveness of Body Mass Index (BMI) as a predictor of long-term health, particularly in assessing the risk of death. Long used as a standard tool to classify individuals as underweight, healthy, overweight, or obese, BMI has been widely adopted in clinical and public health settings. However, the study, published on June 24 in the Annals of Family Medicine, finds that this standard metric fails to provide an accurate picture of an individual’s future health prospects, particularly in terms of mortality risk. The researchers argue that the measure is fundamentally flawed and should no longer be relied upon as the default method for assessing obesity and its associated health risks.

The study compared BMI with a more direct and biologically relevant technique: bioelectrical impedance analysis (BIA). Unlike BMI, which is based on a simple calculation of weight divided by height squared, BIA measures the body’s resistance to a low electrical current to estimate body fat levels. This method provides a more specific insight into body composition, distinguishing between fat and lean tissue. Over a 15-year tracking period, individuals with high body fat as measured by BIA were shown to have a 78% increased risk of death from any cause compared to those with normal fat levels. More strikingly, they were approximately 3.5 times more likely to die from cardiovascular disease. These findings suggest that BIA offers a much more reliable indication of health outcomes than BMI.

In sharp contrast, BMI proved ineffective in predicting mortality. The data revealed no statistically significant association between BMI and the risk of death from any cause, including heart disease. This lack of correlation persisted even after researchers adjusted for potential confounding factors, including age, race, and income. The study’s authors concluded that BMI’s inability to account for the distribution and composition of body weight — particularly the distinction between muscle and fat — renders it obsolete as a tool for predicting health risks. Its use as a surrogate for body fat, they argue, has led to the widespread misclassification of individuals, sometimes with significant consequences for patient care and policy.

The research was spearheaded by a team in the Department of Community Health and Family Medicine at the University of Florida’s College of Medicine. Lead author Professor Arch Mainous described the findings as a definitive comparison between two competing methods for assessing body fat. Drawing a parallel with product testing, he said, “This is the ultimate Coke versus Pepsi test. And BMI failed.” This memorable analogy underscores the dramatic underperformance of BMI in a head-to-head comparison. The study’s findings suggest that continued reliance on BMI may not only be unhelpful but could actively obscure underlying health issues, delaying more accurate diagnosis and intervention.

The data underpinning the study were drawn from the National Health and Nutrition Examination Survey (NHANES). This long-standing and nationally representative dataset links health information with mortality outcomes from the National Death Index. The researchers analysed the health data of 4,252 individuals, a cohort selected to reflect the demographic makeup of the United States population. This breadth of data lends considerable weight to the findings and increases their relevance to both clinicians and public health policymakers. By using a dataset that spans more than a decade and includes diverse participants, the study offers strong evidence that its conclusions are both valid and generalisable.

One of the study’s senior authors, Dr Frank Orlando, who serves as medical director of UF Health Family Medicine – Springhill, offered a clinical perspective on the implications of the findings. As a family physician, he noted the routine use of BMI as a kind of surrogate vital sign. This quick, easily calculated figure is supposedly a reliable indicator of a patient’s health. However, Dr Orlando criticised this approach, noting that BMI lacks the specificity and accuracy of actual vital signs. “We use BMI to sort of screen for a person having an issue with their body composition, but it’s not accurate for everyone like vital signs are,” he explained. For many patients, especially those with atypical body types or varying muscle mass, BMI may mislead rather than inform.

Ultimately, the study’s conclusions call for a critical reassessment of how health professionals and institutions evaluate body composition and obesity-related risk. BMI, despite its simplicity and ubiquity, appears no longer fit for purpose in a modern healthcare environment that increasingly values precision, equity, and individualised care. By contrast, bioelectrical impedance analysis offers a more nuanced and biologically valid assessment method, and one that is becoming increasingly accessible in clinical settings. As our understanding of obesity and its consequences evolves, so too must the tools we use to assess and manage it. This study adds to the growing consensus that a shift away from BMI is not only necessary but long overdue.

More information: Arch Mainous et al, Body Mass Index vs Body Fat Percentage as a Predictor of Mortality in Adults Aged 20-49 Years, The Annals of Family Medicine. DOI: 10.1370/afm.240330

Journal information: The Annals of Family Medicine Provided by University of Florida

Heart-Healthy Benefits of Leafy Green Vegetables

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Incorporating just a cup and a half of leafy green vegetables into your daily meals could significantly reduce the risk of atherosclerotic vascular diseases (ASVDs), according to compelling new research from Edith Cowan University (ECU), in collaboration with the University of Western Australia and the Danish Cancer Institute.

ASVDs, a subgroup of cardiovascular diseases, are among the leading causes of death worldwide, primarily responsible for heart attacks and strokes. In Australia alone, cardiovascular diseases claim the life of one person every twelve minutes, highlighting the urgent need for preventive strategies. ECU PhD student Montana Dupuy, who led this new research, emphasises the stark toll of these conditions and the promising role that diet may play in addressing them.

The study focuses on Vitamin K1, a nutrient abundant in leafy greens and cruciferous vegetables such as spinach, kale, and broccoli. Ms Dupuy’s findings suggest that higher dietary intake of Vitamin K1 may play a vital role in reducing the risk of ASVD by preventing vascular calcification, an underlying process in the development of cardiovascular disease. “The great news is that these vegetables are easy to include in everyday meals,” she said, noting the accessibility of such dietary changes.

In addition to its potential cardiovascular benefits, Vitamin K1 may also support musculoskeletal health, particularly by contributing to bone strength and overall skeletal resilience. This adds another layer of importance to ensuring adequate intake of this essential vitamin, especially in populations at risk for both heart and bone-related illnesses.

Senior Research Fellow Dr Marc Sim of ECU explained that consuming just a cup and a half of Vitamin K1-rich vegetables daily offers a practical way to enhance one’s nutrient intake. He noted that the study found women who consumed around 30% more Vitamin K1 than currently recommended by the Australian Dietary Guidelines had a lower long-term risk of developing ASVD. “We also observed that participants with higher intakes had less thickening in the carotid arteries—blood vessels in the neck—which is a known marker of atherosclerosis,” he added.

This growing body of research on Vitamin K1’s role in vascular and bone health is now influencing further studies at ECU’s Future Foods and Digital Gastronomy Lab. There, researchers are developing innovative foods rich in leafy greens, explicitly designed for use in clinical trials. The aim is to improve health outcomes, particularly in populations with specialised nutritional needs, such as residents in aged care facilities.

Dr Liezhou Zhong, an ECU Postdoctoral Research Fellow, explained that the team is working to convert epidemiological findings into tangible, real-world applications. “We are consolidating the data and turning it into food solutions that can be readily adopted by the community,” he said. These specially formulated meals are expected to offer both nutritional and therapeutic value, providing a model for food-based interventions in preventive healthcare.

This research reinforces the notion that small, consistent dietary changes can yield substantial health benefits. By simply increasing one’s intake of dark, leafy greens, individuals can significantly reduce their risk of severe vascular conditions. As the evidence continues to mount, the humble spinach leaf and its cruciferous cousins may prove to be powerful allies in the fight against cardiovascular disease.

More information: Montana Dupuy et al, Higher vitamin K1 intakes are associated with lower subclinical atherosclerosis and lower risk for atherosclerotic vascular disease-related outcomes in older women, European Journal of Nutrition. DOI: 10.1007/s00394-025-03686-x

Journal information: European Journal of Nutrition Provided by Edith Cowan University

Major Study Reveals Elevated Urinary Metal Levels May Heighten Heart Failure Risk

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A groundbreaking multi-cohort study conducted by researchers at Columbia University’s Mailman School of Public Health has revealed compelling evidence that exposure to certain metals, detected through urinary biomarkers, is significantly associated with an increased risk of heart failure (HF). Published in the Journal of the American College of Cardiology, the study is the most extensive investigation of its kind to date, bolstering the case for more substantial public health efforts aimed at mitigating environmental metal exposure. Although metals such as arsenic, cadmium, and molybdenum have previously been implicated in cardiovascular pathology, their specific role in heart failure—a condition with high mortality and rising prevalence—has remained insufficiently explored until now.

The study’s methodological innovation lies in its approach to examining metals not in isolation, as has been common in prior research, but as a composite mixture, thereby capturing a more accurate representation of real-world exposure. “Most previous studies have assessed individual metals in isolation. By examining metals as a mixture, our analysis more closely reflects real-world exposure patterns,” explained Dr Irene Martinez-Morata, the study’s lead author and a postdoctoral research scientist in Environmental Health Sciences at Columbia Mailman. The analysis involved a robust sample of over 10,000 adults from multiple countries, encompassing diverse racial, geographic, and ethnic backgrounds. After rigorous adjustment for traditional heart failure risk factors such as diabetes, hypertension, and obesity, a consistent association was found between elevated levels of urinary metals and increased incidence of heart failure.

The researchers aggregated data from three large-scale longitudinal cohorts with over two decades of follow-up: the Multi-Ethnic Study of Atherosclerosis (MESA), encompassing adults aged 18 to 85 from six urban-suburban regions in the United States; the Strong Heart Study (SHS), which focuses on American Indian adults from various rural communities across Oklahoma, Arizona, and the Dakotas; and the Hortega Study, a general population cohort from Spain. In total, 10,861 participants were included: 6,644 from MESA, 2,917 from SHS, and 1,300 from Hortega. Across the pooled dataset, over a thousand individuals developed heart failure during the follow-up period, and left ventricular function was assessed in a subset to understand cardiac performance dynamics better.

Urinary levels of five specific metals—arsenic, cadmium, molybdenum, selenium, and zinc—were analysed using advanced machine learning techniques to evaluate their combined effect as a mixture. The results were striking. The metal mixture was linked with a 55% increased risk of heart failure among SHS participants, a 38% increased risk in the MESA cohort, and an 8% increased risk in the Hortega cohort. When the metals were analysed individually, a doubling of urinary cadmium levels—commonly found in tobacco, industrial waste, and certain contaminated foods—was associated with a 15% higher risk of heart failure. Likewise, a doubling of molybdenum and zinc levels was linked to 13% and 22% increases in risk, respectively, even though these metals are considered essential for physiological functions in trace amounts.

The disproportionately high risk observed in the SHS cohort, composed of rural American Indian communities, suggests environmental injustice rooted in longstanding exposure to contaminant metals. “The strongest association between the 5-metal mixture and HF risk was seen in the SHS cohort,” Dr Martinez-Morata noted. “This population faces a historically high burden of contaminant metal exposure and cardiovascular disease and public health action is urgently needed.” Such disparities point to systemic environmental inequalities, often stemming from proximity to mining operations, industrial pollution, and underregulated infrastructure that leads to contaminated drinking water and soil.

The sources of toxic metal exposure are multifaceted, ranging from ambient air pollution and industrial emissions to dietary intake through crops grown in contaminated soils. Even seemingly benign consumer goods or nutritional supplements may contain elevated levels of essential metals, such as zinc and selenium, which, in excessive quantities, can become toxic. Smoking devices and vaping tools are also significant contributors to metal exposure. The researchers emphasise that while certain metals are essential for human health in small amounts, chronic exposure to high concentrations—especially from multiple sources simultaneously—poses a significant health risk.

Dr Ana Navas-Acien, chair of the Department of Environmental Health Sciences and senior author of the study, reinforced the central conclusion: “We consistently found higher urinary levels of cadmium, molybdenum and zinc linked to increased heart failure risk. Even after adjusting for diabetes—a known HF risk factor—the zinc association remained significant.” These findings place metal exposure alongside traditional cardiovascular risk factors, highlighting the urgent need for integrating environmental health assessments into cardiovascular disease prevention strategies.

In conclusion, this study represents a significant step forward in environmental cardiology, providing robust evidence that exposure to a mixture of urinary metals substantially increases the risk of heart failure. With its large, diverse sample size, high-quality longitudinal data, and advanced analytical framework, the study presents a compelling case for more rigorous monitoring of environmental metal exposures and targeted public health interventions, especially in vulnerable communities with a history of industrial contamination. As ongoing research continues to illuminate the underlying biological mechanisms, the implications for public policy, clinical guidelines, and community-level health initiatives are profound. The findings confirm that protecting cardiovascular health requires a concerted effort to reduce environmental metal exposure across all populations.

More information: Irene Martinez-Morata et al, Associations Between Urinary Metal Levels and Incident Heart Failure: A Multi-Cohort Analysis, Journal of the American College of Cardiology. DOI: 10.1016/j.jchf.2025.03.046

Journal information: Journal of the American College of Cardiology Provided by Columbia University’s Mailman School of Public Health

Cumulative Exposure to Wildfire Smoke May Gradually Elevate Heart Failure Risk

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Long-term exposure to wildfire smoke may significantly increase the risk of heart failure, particularly among older adults, women, and socioeconomically vulnerable populations, according to a major study published today in JACC, the flagship journal of the American College of Cardiology. This national, population-based investigation is the first of its kind to compare the health impacts of prolonged exposure to wildfire smoke with those of other familiar sources of air pollution. The findings reveal that as the concentration of wildfire-related air pollution increased over two years, the incidence of heart failure rose accordingly, marking an urgent public health concern amid escalating environmental changes.

At the heart of the study is PM2.5, a category of airborne particulate matter measuring 2.5 micrometres or smaller in diameter. These microscopic particles can bypass the body’s natural defences, travelling deep into the lungs and, in some cases, entering the bloodstream. Various sources, including motor vehicles, industrial processes, and the combustion of fossil fuels, emit PM2.5. However, wildfires are increasingly contributing to PM2.5 levels worldwide, a trend that is accelerating due to rising global temperatures and longer dry seasons. The uniquely hazardous composition of wildfire smoke, including organic chemicals and heavy metals, raises additional concern over its effects on human health.

The researchers, led by Dr Hua Hao of the Rollins School of Public Health at Emory University, analysed data from all Medicare Fee-For-Service beneficiaries in the United States between 2007 and 2018. They found that for each one microgram per cubic metre increase in wildfire-related PM2.5 over two years, the risk of heart failure rose by 1.4%. While this may appear minimal on an individual level, the implications are vast: the researchers estimate such exposure could contribute to over 20,000 additional heart failure cases annually among older adults alone. The study also assessed how frequently individuals were exposed to elevated smoke levels, measuring the number of days per year when PM2.5 from wildfires exceeded thresholds of 1 or 2.5 micrograms per cubic metre.

Notably, the increased risk was not uniformly distributed across the population. The data showed that women, Medicaid-eligible individuals, and those residing in lower-income areas were disproportionately affected. These findings underscore the compounded vulnerabilities faced by specific groups due to systemic inequities in healthcare access, environmental safety, and social determinants of health. Dr Hao noted that “even a small increase in smoke exposure can carry serious implications for heart health,” especially among those who are already at heightened risk. Such insights point to the need for targeted protective measures and public health strategies that prioritise at-risk communities.

A notable aspect of the study was its comparison of the health impact of wildfire PM2.5 with that of PM2.5 from other non-smoke sources. The researchers found that for the same increase in particulate concentration, non-smoke PM2.5 was associated with only a 0.5% rise in heart failure risk, compared to the 1.4% increase linked to wildfire smoke. This suggests that smoke from wildfires may be more toxic per unit of exposure than other forms of air pollution. The precise reasons for this disparity are still being investigated, but may include differences in chemical composition, particle size distribution, or the presence of volatile organic compounds in wildfire smoke.

In an accompanying editorial, Dr Joan A. Casey of the University of Washington highlighted the broader environmental context: “By century’s end, under a high-emission climate scenario, 74% of the globe is expected to experience significant increases in the duration and frequency of wildfire events.” Already in the United States, wildfire smoke days — once rare — now occur multiple times a year. This new everyday demands a re-evaluation of how environmental threats are managed, both in terms of mitigation and adaptation. As smoke exposure becomes more frequent, the cumulative cardiovascular burden may grow, particularly for those in smoke-prone regions.

Dr Harlan M. Krumholz, Editor-in-Chief of JACC and Professor at Yale School of Medicine, described the study as a crucial contribution to cardiovascular research. “This study highlights a growing and underappreciated threat to heart health,” he said. “As wildfire smoke becomes more common and more intense, even small long-term exposures are enough to elevate heart failure risk — especially among our most vulnerable populations.” He emphasised the importance of integrating these findings into public health policy, emergency preparedness, and clinical practice. While the study faced some limitations — including possible measurement errors in pollution estimates and unmeasured individual health variables — it offers a sobering look at how environmental stressors are shaping the future of cardiovascular health.

More information: Hua Hao et al, Long-Term Wildfire Smoke Exposure and Increased Risk of Heart Failure in Older Adults, Journal of the American College of Cardiology. DOI: 10.1016/j.jacc.2025.04.058

Journal information: Journal of the American College of Cardiology Provided by American College of Cardiology