Monthly Archives: April 2026

Serious COVID-19 and Flu Infections Could Trigger Lung Cancer Years Later, Researchers Say

Severe COVID-19 and influenza infections may leave lasting damage in the lungs that increases the risk of lung cancer months or even years later. New research from the University of Virginia (UVA) Health suggests that these serious infections can create conditions in the lungs that allow cancer to grow more easily. The study also brings encouraging news: vaccination appears to prevent many of these harmful changes and may reduce the long-term risk.

Researchers led by Jie Sun found that severe viral infections can “reprogramme” immune cells in the lungs. Instead of protecting the body, these altered cells may create an environment that supports tumour growth over time. Because of this, the research team recommends that doctors carefully monitor patients who have recovered from severe COVID-19, influenza, or pneumonia so that lung cancer can be detected early, when treatment is more effective.

Respiratory infections such as COVID-19 and the flu are common causes of lung injury, but their long-term effects have not been fully understood. To explore this, the researchers studied both laboratory mice and human patient data. They found that mice with severe lung infections were more likely to develop lung cancer and had higher death rates from the disease. Similar patterns were observed in people, where those who had been hospitalised for COVID-19 showed a higher incidence of lung cancer.

The study identified a 1.24-fold increase in lung cancer risk among patients who had experienced severe COVID-19. Importantly, this increased risk was seen regardless of smoking status or other health conditions. According to Jeffrey Sturek, these findings suggest that severe respiratory infections may need to be considered alongside traditional risk factors such as smoking. In the future, doctors may recommend regular lung screening for certain high-risk patients who have recovered from serious infections.

The researchers also uncovered possible biological explanations for this increased risk. Severe infections were found to alter key immune cells, including neutrophils and macrophages, which normally help defend the lungs. After infection, some of these cells appeared to promote inflammation and create a “pro-tumour” environment. Changes were also observed in the epithelial cells lining the lungs, which could further contribute to cancer development.

Reassuringly, vaccination seemed to prevent many of these harmful effects by reducing the severity of infection. The increased cancer risk was mainly seen in patients with severe illness, while those with mild COVID-19 did not show the same pattern. In fact, they showed a slight decrease in risk. The researchers emphasise that preventing severe infection through vaccination may also help reduce long-term complications, including those linked to cancer.

Given the large number of people worldwide who have experienced severe respiratory infections, the findings have important implications for healthcare. The researchers suggest that individuals recovering from serious lung infections—especially those with a history of smoking—may benefit from closer monitoring for lung cancer. They hope this work will help doctors identify high-risk patients earlier and lead to better strategies for prevention and treatment in the future.

More information: Wei Qian et al, Respiratory viral infections prime accelerated lung cancer growth, Cell. DOI: 10.1016/j.cell.2026.02.013

Journal information: Cell Provided by University of Virginia Health System

Novel Model Calculates Essential Ageing Metric from Clinical Biopsies

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A new computer-based tool has been developed to study ageing by analysing routine biopsy images. Instead of directly measuring DNA in a lab, this method looks at images of cells and tissues to detect subtle structural changes. These changes can reveal what is happening at the ends of chromosomes, where protective sections of DNA—called telomeres—are located. The findings were published in Cell Reports Methods on March 16, 2026.

The tool, called TLPath, was created by scientists at the Sanford Burnham Prebys Medical Discovery Institute. It is based on the idea that as cells age, their shape and structure change in ways that can be measured. By analysing these patterns in biopsy images, the model can estimate the length of telomeres without needing specialised laboratory tests.

Telomeres are repeating DNA sequences that protect the ends of chromosomes. Each time a cell divides, these telomeres become slightly shorter. This is a natural process, but over time, shorter telomeres are linked to ageing and a higher risk of diseases such as heart disease and cancer. Scientists have long known that telomere length is related to a person’s age, but measuring it directly can be complex, expensive, and difficult to scale for large studies.

To build the model, researchers used data from the Genotype-Tissue Expression Project, a large research programme supported by the National Institutes of Health. This dataset included thousands of high-quality biopsy images from different tissue types, along with laboratory measurements of telomere length. By training the model on this paired data, the system learned to recognise visual patterns linked to telomere length.

The model works by breaking each biopsy image into many small sections and analysing each one in detail. It looks for hundreds of structural features within cells and tissues, then combines this information to produce an overall prediction. After training, TLPath was able to accurately estimate telomere length in new samples it had not seen before. In fact, it performed better than simply using a person’s age to make predictions and could even detect differences between individuals of the same age.

This approach could make it much easier to study ageing and related diseases. Because biopsy slides are already commonly created in clinical care, the main requirement is to digitise and share them for research. With wider access to such data, tools like TLPath could help scientists better understand how ageing works and support efforts to improve health outcomes as people grow older.

More information: Anamika Yadav et al, Tissue morphology predicts telomere shortening in human tissues, Cell Reports Methods. DOI: 10.1016/j.crmeth.2026.101336

Journal information: Cell Reports Methods Provided by Sanford Burnham Prebys

How far is too far? Seniors frequently go the extra mile for care

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Older Americans are often willing to travel considerable distances for medical care, sometimes far more than policymakers and experts assume. This insight comes from researchers at the USC Dornsife College of Letters, Arts and Sciences, highlighting how access to care remains a priority even when it requires significant effort. As hospitals close in some areas, healthcare services consolidate, and telehealth continues to expand, older adults may accept longer journeys for care, though not all are equally able or willing to do so. Socioeconomic factors play a key role in shaping these decisions.

A recent study published in JAMA Network Open found that many Americans aged 65 and older would travel more than an hour for both routine and specialised care. Conducted by researchers at the USC Dornsife Center for Economic and Social Research, the study surveyed a nationally representative sample of older adults. Participants were asked about their current travel times for medical visits and how much farther they would be willing to go before deciding to delay or skip care.

On average, respondents indicated they could tolerate about an hour or more of travel time, particularly for specialised services. For primary care visits, they were willing to travel approximately 68 minutes, while diagnostic tests such as MRIs could justify journeys of around 113 minutes. Specialist consultations prompted the greatest tolerance, with an average of 128 minutes. These findings suggest that older adults place a high value on accessing needed care, even when it involves extended travel.

However, these averages conceal important differences. Individuals in poorer health, those living in large metropolitan areas, and those who had previously experienced transportation challenges were less willing to travel long distances. In contrast, respondents with higher incomes, more education, and reliable access to a car reported a greater willingness to spend additional time travelling. These disparities highlight how health status and resources influence access to care and raise important concerns about equity.

The findings also have implications for how healthcare is delivered. As health systems increasingly consolidate services into regional hubs rather than neighbourhood clinics, understanding patient tolerance for travel becomes more important. While telehealth can reduce the need for travel, it cannot fully replace in-person care, particularly for diagnostic procedures or specialist consultations that require equipment or physical examination. This underscores the need for a balanced approach that considers both virtual and in-person care options.

Transportation policy also plays a critical role in shaping access. Programmes that provide ride services, improve public transit, or partner with community organisations could help reduce barriers for more vulnerable populations. Interestingly, older adults living in large cities were less willing to travel long distances, likely due to traffic, parking, and other logistical challenges that make even short trips burdensome. In contrast, rural residents, who are often accustomed to travelling farther for care, appeared more accepting of longer journeys. Overall, while many older Americans are willing to travel surprisingly far for medical care, their ability to do so depends heavily on health, resources, and transportation access, all of which should inform future healthcare planning.

More information: Jeremy Burke et al, Willingness of Older Adults to Travel for Medical Care, JAMA Network Open. DOI: 10.1001/jamanetworkopen.2025.60280

Journal information: JAMA Network Open Provided by University of Southern California

Teen Aggression May Signal Faster Biological Aging Down the Line

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Adolescents who frequently lash out at others may be setting the stage for long-term physical health challenges, according to research published by the American Psychological Association. The study suggests that aggressive behaviour in early adolescence is not merely a social or emotional concern, but may also carry biological consequences that emerge years later. In particular, researchers found that higher levels of aggression during the teenage years were associated with faster biological ageing and a higher body mass index (BMI) by the age of 30, pointing to a potential link between early interpersonal difficulties and later-life health outcomes.

Lead author Joseph Allen, PhD, of the University of Virginia, emphasised the broader implications of these findings. He noted that the study sheds light on how social challenges during formative years may have enduring effects on physical well-being. Accelerated biological ageing, he explained, has been linked in previous research to an increased risk of conditions such as coronary artery disease, diabetes, hypertension, chronic inflammation, and even premature mortality. These connections underscore the importance of understanding how early behavioural patterns may influence long-term health trajectories.

The study, published in the journal Health Psychology, followed a cohort of 121 adolescents—46 males and 75 females—from both suburban and urban communities in the southeastern United States. Beginning at age 13, participants were tracked into adulthood through a comprehensive, multi-informant approach. Researchers gathered self-reported measures of aggression, alongside parent-reported levels of family conflict and peer evaluations of relationship behaviours. This longitudinal design allowed for a nuanced examination of how early social dynamics evolve and relate to later biological outcomes.

When participants reached age 30, researchers assessed biological ageing using a set of blood-based biomarkers. These included indicators such as C-reactive protein, blood glucose levels, and white blood cell counts, among others. By applying a sophisticated algorithm that integrates these 12 markers, the researchers generated an estimate of each individual’s biological age. This measure, Allen noted, often provides a more accurate prediction of future health and mortality risk than chronological age alone, offering a deeper insight into the body’s physiological condition.

To ensure robustness, biological ageing was evaluated using two established methods: the Klemera-Doubal approach and PhenoAge. Both methods incorporate a range of physiological indicators—including blood pressure, inflammation, cholesterol, glucose regulation, and immune function—to estimate how “old” a person’s body appears biologically. Across both measures, the findings were consistent: individuals who exhibited higher levels of aggression in early adolescence tended to show more advanced biological ageing by age 30. Importantly, these associations remained significant even after accounting for factors such as gender, socioeconomic status, early illness, and adolescent body composition.

Further analyses revealed that the pathway from early aggression to accelerated ageing was not direct, but instead operated through ongoing relationship difficulties. Males and individuals from lower-income backgrounds were more likely to exhibit faster biological ageing, patterns that appeared linked to higher levels of relational conflict—such as strained parent-child interactions or punitive peer behaviour. Crucially, early aggression alone did not predict later ageing unless it persisted in the form of chronic interpersonal problems. These findings suggest that the lasting health impact may stem less from isolated behaviours and more from enduring patterns of conflict. While the study does not establish causation, it highlights the importance of supporting adolescents in developing healthier relationships, which may have benefits extending well beyond emotional well-being to influence long-term physical health.

More information: Joseph Allen et al, Predictions from early adolescent interpersonal aggression to accelerated aging in adulthood: Relational and biological mechanisms of linkage, Health Psychology. DOI: 10.1037/hea0001576

Journal information: Health Psychology Provided by American Psychological Association

Johns Hopkins Study Finds Smoking Speeds Eye Ageing via Epigenetic Alterations

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Through a series of experiments supported by the National Institutes of Health, researchers at Johns Hopkins Medicine have advanced understanding of how smoking damages the eye and contributes to the development of age-related macular degeneration (AMD), the leading global cause of vision loss and blindness among people aged 50 and older. While it has long been recognised that smokers are about four times more likely to develop AMD than non-smokers, the biological pathways underlying this increased risk have remained unclear, limiting efforts to understand how smoking influences disease onset and progression fully.

In findings published on 16 January 2026 in the Proceedings of the National Academy of Sciences (PNAS), the research team investigated how retinal pigmented epithelial (RPE) cells respond to cigarette smoke exposure. These cells play a critical role in protecting and maintaining photoreceptors necessary for vision. The scientists compared changes in RPE cells from young (3-month-old) and older (12-month-old) mice—roughly corresponding to early adulthood and late middle age in humans—following both acute exposure to cigarette smoke condensate and prolonged daily exposure over four months.

According to James T. Handa, senior investigator and chief of the retina division at the Wilmer Eye Institute, smoking has traditionally been linked to ageing through the release of tissue-damaging free radicals. However, this study demonstrates that smoking also induces epigenetic alterations—changes in gene expression that do not involve modifications to the DNA sequence itself. These epigenetic shifts affect how RPE cells function and respond to environmental stress, potentially undermining the eye’s ability to maintain normal physiological processes over time.

To uncover these mechanisms, the researchers used advanced genomic tools, including single-nucleus ATAC sequencing and RNA sequencing, to analyse RPE cells at multiple time points after smoke exposure. These methods allowed the team to identify dysfunctional cell populations and examine changes in chromatin accessibility—the degree to which genetic material is available for activation. Reduced chromatin accessibility was associated with diminished cellular adaptability, indicating that affected cells may struggle to function properly or survive under stress conditions.

Across both young and older mice, acute smoke exposure led to the formation of dysfunctional RPE cell clusters characterised by reduced expression of genes essential for normal cell function, decreased chromatin accessibility, and lower activity of genes associated with key “hallmarks of ageing,” such as genomic stability, telomere maintenance, and mitochondrial health. These changes closely resembled patterns observed in human AMD, suggesting that cigarette smoke can rapidly induce disease-like cellular dysfunction. Notably, the researchers observed that in young mice, certain ageing-related genes—linked to mitochondrial function, protein stability, cellular recycling, inflammation, and metabolism—were activated in response to smoke exposure. In contrast, this protective response was absent in older mice.

Further experiments showed that activation of these genes helped protect younger cells from death, while older cells without this response were more vulnerable. Additional analyses of human donor RPE cells identified nearly 1,700 genes with altered expression shared between mouse and human dysfunctional cells, highlighting common pathways that may drive AMD development. The findings suggest that environmental stressors such as smoking can disrupt the eye’s genetic regulatory systems, impairing its ability to remain healthy. Looking ahead, the researchers aim to determine which of these changes are reversible and how ageing and prolonged smoke exposure together contribute to more severe eye damage and complications associated with advanced AMD.

More information: Krishna Kumar Singh et al, Molecular underpinnings of induced degenerative heterogeneity in the retinal pigment epithelium, Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.2505412123

Journal information: Proceedings of the National Academy of Sciences Provided by Johns Hopkins Medicine

Changes in Smoking Habits and Their Links to Parkinson’s Disease and Risk of Death

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A large new study of smokers suggests a complex relationship between smoking behaviour, Parkinson’s disease, and mortality. Researchers found that people who were currently smoking had a lower risk of developing Parkinson’s disease, while those who quit smoking experienced a lower risk of death. The findings were published on 25 February 2026 in Neurology®, the medical journal of the American Academy of Neurology. Importantly, the study does not establish that smoking prevents Parkinson’s disease; rather, it identifies an association that warrants further investigation.

Study author Jun-Hyuk Lee, MD, PhD, of Eulji University School of Medicine in Seoul, South Korea, emphasised that the well-established harms of smoking remain substantial. Smoking continues to be a leading cause of preventable death worldwide and is strongly linked to serious conditions such as heart disease, cancer, and chronic respiratory illness. While the study observed that individuals who quit smoking had a higher risk of Parkinson’s disease compared to those who continued smoking, it also demonstrated that quitting was associated with a meaningful reduction in mortality risk. The overall health benefits of cessation, therefore, remain clear and compelling.

The research followed more than 410,000 adults in South Korea who were all smokers at baseline, with an average age of 52 years. Participants were tracked for approximately nine years. Throughout the study period, they underwent repeated health screenings—initially at baseline, then roughly two years later, and again after another two years. At each point, participants reported their smoking habits, including frequency and quantity, allowing researchers to examine changes in smoking behaviour over time.

Based on these patterns, participants were categorised into four groups: persistent smokers who never quit, relapsed smokers who initially quit but later resumed smoking, recent quitters who stopped after several years, and sustained quitters who quit early and remained smoke-free. Over the course of the study, 1,794 individuals developed Parkinson’s disease. The incidence was lowest among persistent smokers (0.33%) and relapsed smokers (0.41%), and higher among recent quitters (0.67%) and sustained quitters (0.71%).

A total of 31,203 participants died during follow-up. Mortality rates varied modestly across groups: 7.24% among persistent smokers, 8.09% among relapsed smokers, 8.76% among recent quitters, and 7.91% among sustained quitters. After adjusting for factors such as income, alcohol consumption, and physical activity, researchers found that persistent smokers had the lowest risk of Parkinson’s disease. In contrast, both recent and sustained quitters had a 60% to 61% higher risk compared to persistent smokers, while relapsed smokers had a similar risk to those who continued smoking.

When examining mortality outcomes, however, a different pattern emerged. Sustained quitters had a 17% lower risk of death compared to persistent smokers, and recent quitters had a modest 3% reduction. Relapsed smokers showed no difference in mortality risk relative to persistent smokers. The researchers concluded that while current smoking status appears linked to Parkinson’s risk, quitting smoking offers clear survival benefits. They also noted limitations, including reliance on self-reported data and a study population largely composed of Korean men, which may limit broader generalisability.

More information: Sung-Ho Ahn et al, Dynamic Smoking Patterns and Risk of Parkinson Disease and All-Cause Mortality A Competing Risk Analysis Approach, Neurology. DOI: 10.1212/WNL.0000000000214651

Journal information: Neurology Provided by American Academy of Neurology

Residential Proximity to Nuclear Plants Associated with Greater Cancer Mortality

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Counties in the United States located nearer to operational nuclear power plants (NPPs) experience higher cancer mortality rates than those farther away, according to a new study led by researchers at the Harvard T.H. Chan School of Public Health. While the findings identify a notable association, the researchers emphasise that they do not establish causality and instead point to the need for further investigation into the potential health impacts of nuclear energy.

This study is the first in the 21st century to examine the relationship between proximity to NPPs and cancer mortality across all U.S. counties and all operating nuclear facilities. It will be published on 23 February 2026 in Nature Communications. Previous research on this topic has produced mixed results globally, and studies within the United States have been relatively limited in scope, often focusing on a single plant and its surrounding population.

To address these gaps, the researchers conducted a nationwide analysis of cancer mortality between 2000 and 2018 using a “continuous proximity” approach. This method captures the combined influence of multiple nearby nuclear power plants rather than assessing exposure based on a single facility. Data on plant locations and operational timelines were obtained from the U.S. Energy Information Administration, including some facilities near the U.S.–Canada border. In contrast, county-level cancer mortality data were sourced from the Centers for Disease Control and Prevention.

The analysis incorporated a wide range of potential confounding factors to strengthen the validity of the findings. These included socioeconomic indicators such as educational attainment and median household income, demographic characteristics including racial composition, and environmental conditions such as average temperature and humidity. Health-related variables, including smoking prevalence, body mass index (BMI), and proximity to healthcare services, were also accounted for in the statistical models.

The results showed a consistent pattern: counties closer to nuclear power plants had higher cancer mortality rates, even after adjusting for these variables. Over the 18-year study period, the researchers estimated that approximately 115,000 cancer deaths in the United States—equivalent to around 6,400 annually—could be associated with proximity to NPPs. The observed relationship was particularly pronounced among older adults, suggesting that age may influence vulnerability to potential risks.

The findings align with earlier research conducted by the same team in Massachusetts, which reported higher cancer incidence among populations living closer to nuclear facilities. However, the researchers acknowledged several limitations, including the absence of direct radiation measurements and the assumption of equal impact across all NPPs. Overall, the study underscores the importance of continued research, particularly as nuclear power is increasingly promoted as a low-carbon energy source in efforts to address climate change.

More information: Yazan Alwadi et al, National analysis of cancer mortality and proximity to nuclear power plants in the United States, Nature Communications. DOI: 10.1038/s41467-026-69285-4

Journal information: Nature Communications Provided by Harvard T.H. Chan School of Public Health

Examining the Effects of Sleep Aids on Insomnia in Obstructive Sleep Apnoea

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Obstructive sleep apnoea is a common condition where a person’s breathing repeatedly stops and starts during sleep because the airway becomes blocked. These pauses in breathing can lower oxygen levels in the body and often wake the person up, even if they do not realise it. As a result, sleep becomes broken and less restful. Over time, this condition can affect overall health and has been linked to issues such as heart problems, metabolic conditions, and a reduced quality of life.

Many people with obstructive sleep apnoea also struggle with insomnia, meaning they have trouble falling asleep, staying asleep, or waking too early. When both conditions happen together, it is known as COMISA. This combination can make treatment more difficult. One common treatment for sleep apnoea is a machine that helps keep the airway open during sleep. Still, people with insomnia may find it harder to use this treatment regularly or comfortably.

Doctors often recommend a type of therapy that helps people change their sleep habits and thoughts about sleep as the first approach for insomnia. However, in everyday practice, many people are prescribed sleeping pills instead. While these medications can help with sleep, there are concerns that some of them might make breathing problems worse during the night, which could be risky for people with sleep apnoea.

To better understand this issue, a group of researchers in Japan carried out a large study. They reviewed many previous studies and compared different types of sleep medications to see how well they worked and how safe they were for people with sleep apnoea. In total, they looked at 32 studies covering 12 different sleep medicines, as well as a comparison with no medication. They examined a wide range of outcomes, including how the medications affected sleep patterns, breathing during sleep, and how well people tolerated the treatments.

The results showed that sleep medications do not all work in the same way. Some may be more helpful for people who have trouble falling asleep, while others may be better for those who wake up during the night or too early in the morning. This suggests that choosing the right medication should depend on the specific sleep problem a person is experiencing, rather than using a one-size-fits-all approach.

Importantly, the study did not find strong evidence that most sleep medications made breathing problems worse overall. For many of the drugs studied, breathing measures were similar to those seen with no treatment. However, one medication was found to lower oxygen levels during sleep, which raises concerns. Because of this, the researchers advise doctors to be careful when prescribing these medicines. Treatment should be tailored to each individual, with close monitoring to ensure both sleep and breathing remain safe and well managed.

More information: Taro Kishi et al, Comparative effects of hypnotic agents on sleep architecture and respiratory outcomes in obstructive sleep apnea: A systematic review and network meta-analysis, Psychiatry and Clinical Neurosciences. DOI: 10.1111/pcn.70036

Journal information: Psychiatry and Clinical Neurosciences Provided by Fujita Health University

Newly developed tool assists Parkinson’s patients in making decisions about deep brain stimulation

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Deciding whether and when to pursue deep brain stimulation (DBS) can feel overwhelming for people living with Parkinson’s disease. Although DBS is widely recognised as one of the most effective treatments for managing movement-related symptoms, it is also a complex and highly individual decision. The therapy involves surgically implanting a battery-powered device that delivers electrical signals to specific regions of the brain responsible for movement control. For many patients, balancing potential benefits against uncertainties can make the decision-making process particularly challenging.

To address this, experts at the University of Colorado Anschutz developed the first evidence-based decision tool specifically designed to support patients considering DBS. The tool aims to improve understanding of the procedure while strengthening patients’ confidence as they weigh their treatment options. Findings published in the Journal of Parkinson’s Disease show that most patients found the tool helpful, were satisfied with its content, and would recommend it to others navigating similar decisions.

The research team, led by Michelle Fullard, emphasised that the goal was not simply to provide information, but to enable meaningful shared decision-making between patients and clinicians. According to Fullard, patients at every stage of the DBS journey reported that the tool added value. By using it independently, patients can arrive at medical consultations better informed, allowing for more productive and balanced discussions with their healthcare providers.

The development of the decision aid followed a rigorous, patient-centred framework. Researchers began by identifying gaps in the information patients felt they needed, then conducted a comprehensive review of existing evidence. An initial version of the tool was created and subsequently refined through multiple rounds of testing in clinical settings. In total, more than 120 patients participated across different phases, including needs assessment, prototype testing, and final evaluation, ensuring the tool was both practical and responsive to real-world concerns.

Early testing revealed that many patients experienced significant decisional conflict, particularly due to uncertainty and limited knowledge about DBS. The tool directly addresses these issues by presenting information in a clear, accessible format. In evaluation studies, 94 per cent of participants said they would recommend it, 91 per cent found the language easy to follow, and 87 per cent expressed satisfaction with its overall quality. A distinctive feature of the tool is its personalised symptom report, which allows patients to input their symptoms and receive tailored feedback on the likelihood of improvement following DBS. This helps to correct common misconceptions and manage expectations about surgical outcomes.

The study also uncovered important gender-related insights. Women in the study were more likely to live alone and expressed a greater need for detailed information about post-operative support, including assistance with meals and daily activities. This aligns with earlier research led by Fullard, which found gender differences in how patients seek information, evaluate risks, and decide on DBS. Despite similar rates of Parkinson’s disease between men and women, women remain underrepresented among DBS recipients. Researchers suggest that differences in lived experience and support needs may contribute to this disparity, underscoring the importance of tailored decision-making resources.

More information: Michelle Fullard et al, Development and acceptability of a deep brain stimulation surgery decision aid for Parkinson’s disease, Journal of Parkinson’s Disease. DOI: 10.1177/1877718X261425106

Journal information: Journal of Parkinson’s Disease Provided by University of Colorado Anschutz

Refined Genetic Risk Score Offers Better Insight into Diabetes, Obesity and Their Consequences

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Type 2 diabetes (T2D) and obesity are complex metabolic conditions shaped by a combination of genetic and environmental factors, with some biological pathways overlapping while others remain distinct. Increasingly, researchers are turning to polygenic risk scores (PRS) to understand these conditions better. A PRS aggregates the effects of many genetic variants across the genome, offering an estimate of an individual’s likelihood of developing a disease as well as potential long-term health outcomes. Drawing on genetic data from several of the world’s largest biobanks, investigators at Mass General Brigham developed advanced metabolic PRSs for both obesity and T2D. These new models not only surpassed existing approaches in predicting disease risk but also demonstrated a strong ability to anticipate future complications and medical interventions. The findings have been reported in Cell Metabolism.

The researchers emphasised that their goal extended beyond predicting whether someone might be diagnosed with obesity or diabetes. Instead, they sought to create a more comprehensive tool that captures broader aspects of metabolic health across an individual’s life course. By integrating diverse genetic signals linked to metabolic function, the team aimed to improve predictions of downstream health consequences. This approach, they suggest, could eventually complement traditional clinical risk factors, supporting more informed decision-making in both prevention and patient care.

To achieve this, the team designed two related but distinct PRSs—one optimised for obesity and the other for T2D. Unlike conventional models that rely heavily on measures such as body mass index (BMI), these scores incorporate genetic variants associated with approximately 20 metabolic traits. These include factors such as fat distribution, insulin sensitivity, and glucose regulation. The models were built using genome-wide association studies (GWAS) drawn from exceptionally large datasets, collectively including more than 8.5 million individuals worldwide. This extensive data foundation allowed for a more nuanced and biologically grounded assessment of metabolic risk.

Importantly, the study demonstrated that individuals identified as high risk by these genetic scores were more likely to experience serious clinical outcomes, including cardiovascular disease and stroke. Among participants who were initially healthy, those with elevated PRS values were roughly twice as likely to require interventions such as GLP-1 receptor agonist therapies or bariatric surgery over a median follow-up period of 5.5 years. These findings highlight the potential of genetic risk profiling to identify individuals who may benefit from earlier or more targeted intervention strategies.

A notable strength of the study lies in its inclusion of multi-ancestry genetic data. By placing particular emphasis on non-European populations, the researchers were able to develop PRSs that performed more effectively across diverse groups, including individuals of African, East Asian, and South Asian ancestry. This represents an important step forward, as many earlier genetic models have been limited by a lack of diversity, reducing their applicability in global populations.

Looking ahead, the research team plans to further refine these tools by exploring genetic subtypes within T2D and obesity. A deeper understanding of these subgroups could improve how patients are classified and selected for clinical trials, ultimately enabling more personalised treatment approaches. The broader vision is to shift clinical thinking beyond simple measures like BMI towards a more sophisticated understanding of genetic susceptibility. By identifying individuals at risk of poor metabolic health trajectories before disease onset, clinicians may be better equipped to intervene early, improving prevention efforts and long-term outcomes.

More information: Min Seo Kim et al, Metabolic polygenic risk scores for prediction of obesity, type 2 diabetes, and related morbidities, Cell Metabolism. DOI: 10.1016/j.cmet.2026.02.009

Journal information: Cell Metabolism Provided by Mass General Brigham

New Study Reveals How to Detect Alzheimer’s Alongside a Difficult-to-Diagnose Dementia

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People living with Alzheimer’s disease frequently have additional neurodegenerative conditions, one of which is the less well-understood frontotemporal lobar degeneration (FTLD). Traditionally, FTLD could only be definitively identified through post-mortem examination. However, emerging research suggests that clinicians may be able to recognise individuals affected by both Alzheimer’s disease and FTLD during life by carefully assessing patterns of neuropsychiatric symptoms.

A study published in Neurology found that individuals with both conditions are more likely to exhibit a broader and more pronounced range of neuropsychiatric symptoms compared with those who have either Alzheimer’s disease or FTLD alone. In other words, the coexistence of these disorders appears to shape a distinct clinical profile that reflects features of both conditions.

These findings carry important implications for patients and their care partners. Individuals affected by both Alzheimer’s disease and FTLD may experience a more complex progression of illness, potentially including a faster decline or different responses to available treatments. Recognising this overlap earlier could therefore support more tailored care planning and better preparation for the challenges ahead.

Lead author Daliah Ross, a postdoctoral fellow in clinical neuropsychology at Brown University Warren Alpert Medical School, noted that the presence of both pathologies is associated with distinct neuropsychiatric patterns. These differences may help guide both diagnosis and treatment strategies. She emphasised that such symptoms can significantly affect the quality of life for patients and their families, as well as the level of support and resources required.

Ross has long focused on improving how neurodegenerative conditions are understood and diagnosed. Through her review of research on neuropathology and clinical presentation, she observed that many individuals with neurodegenerative disease have more than one underlying condition. Despite this, research and clinical approaches have often treated disorders like Alzheimer’s disease in isolation, which does not reflect the reality of many patients’ experiences.

In the case of FTLD, symptoms such as disinhibition and marked personality changes are not typically associated with Alzheimer’s disease, making the overlap between the two conditions particularly complex. To explore this further, researchers analysed data from 29 Alzheimer’s Disease Research Centres funded by the National Institutes of Health, examining 919 individuals whose diagnoses were confirmed at autopsy and who had intermediate to high levels of Alzheimer’s disease and/or FTLD pathology.

The analysis revealed clear differences in symptom patterns. Compared with individuals who had FTLD alone, those with both Alzheimer’s disease and FTLD were more likely to have experienced anxiety, delusions, and irritability before death. Conversely, compared with those who had only Alzheimer’s disease, the combined group showed higher rates of personality change and disinhibition. Co-author Edward Huey noted that while treatments exist for Alzheimer’s disease, none currently modify FTLD, underscoring the importance of improved diagnosis and the need for further research into mixed forms of dementia.

More information: Daliah Ross et al, Neuropsychiatric Symptoms in Patients With Pathologically Confirmed Comorbid Alzheimer Disease and Frontotemporal Lobar Degeneration, Neurology. DOI: 10.1212/WNL.0000000000214750

Journal information: Neurology Provided by Brown University

UMass Amherst Study Reveals Long-Term Cognitive Risks of Early Adult Alcohol Use

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It is widely recognised that people often turn to alcohol as a way to cope with stress. However, new research led by the University of Massachusetts Amherst suggests something more concerning. When this pattern of “self-medicating” begins in early adulthood, it may lead to lasting changes in the brain that only become noticeable later in life. Even after someone stops drinking for a long time, the effects may still appear in middle age.

The study found that early alcohol use combined with stress can affect how the brain functions years later. People may find it harder to adapt to new or changing situations, be more likely to rely on alcohol again during stressful periods, and be more vulnerable to cognitive decline. Some of these changes resemble early signs of conditions such as Alzheimer’s disease and other forms of dementia. The findings, published in Alcohol Clinical and Experimental Research, offer new insights into how alcohol reshapes the brain over time.

Scientists have long understood that stress and alcohol are closely linked. Alcohol may provide temporary relief from stress, but it can also weaken the brain’s natural ability to cope. Over time, this can lead to increased drinking as the brain becomes less capable of managing stress on its own. At the same time, heavier drinking can create additional stress through poor decisions and negative consequences, forming a cycle that becomes increasingly difficult to break.

To better understand these long-term effects, researcher Elena Vazey and her team studied how alcohol and stress influence the brain’s decision-making systems. Their work, supported by the National Institute on Alcohol Abuse and Alcoholism, used mice because their brain structures are similar to those of humans. The researchers found that the combination of alcohol and stress had a stronger impact than either factor alone, suggesting that together they create unique and lasting damage.

One key finding was that individuals who used alcohol to cope with stress when they were young were more likely to return to drinking later in life, even after long periods without alcohol. This suggests that early exposure may “rewire” the brain in a lasting way. Interestingly, the study showed that while learning ability in middle age was not significantly affected, cognitive flexibility—the ability to adapt quickly to new situations—was clearly reduced.

The researchers focused on a part of the brain called the locus coeruleus, which plays an important role in decision-making and responding to stress. In a healthy brain, this system activates during stress and then settles down once the stress has passed. However, in brains affected by early alcohol use and stress, this system does not switch off properly. As a result, the brain becomes less efficient at guiding behaviour and making decisions.

They also discovered signs of oxidative stress in this area of the brain. This type of cellular damage is commonly seen in people with neurodegenerative diseases. Even after long periods without alcohol, the brains of those exposed to early heavy drinking showed limited ability to repair themselves. This may explain why some people struggle to stay away from alcohol or to make healthier choices later in life.

Overall, the research highlights that early habits can have long-lasting effects on brain health. It suggests that the impact of alcohol is not simply a matter of short-term behaviour but involves bigger biological changes. These findings point to the need for new approaches to prevention and treatment—ones that take into account how the brain is altered over time, rather than focusing only on willpower or immediate behaviour change.

More information: O. Revka et al, Impact of chronic alcohol and stress on midlife cognition and locus coeruleus integrity in mice, Alcohol Clinical and Experimental Research. DOI: 10.1111/acer.70273

Journal information: Alcohol Clinical and Experimental Research Provided by University of Massachusetts Amherst