Monthly Archives: July 2026

Financial Instability Associated with Faster Brain Ageing

Persistent financial hardship is associated with faster cognitive decline and poorer brain health in later life, according to a new study led by researchers at University College London (UCL). Published in Innovation in Aging, the study analysed data from 2,759 participants in the MRC National Survey of Health and Development (the 1946 British birth cohort), following individuals from early adulthood into older age. Unlike previous research that measured financial hardship at a single point in time, this study examined financial experiences over several decades, providing a clearer picture of the long-term effects of chronic financial adversity.

Researchers found that individuals who experienced persistent financial hardship or consistently low income during early and middle adulthood performed worse on cognitive tests by age 53. Among participants who later underwent magnetic resonance imaging (MRI), those with persistent low income also showed poorer brain health between the ages of 69 and 71, including greater brain shrinkage. These findings remained significant even after accounting for childhood cognitive ability, educational attainment, and early-life socioeconomic disadvantage.

According to lead author Dr Jacques Wels, the accumulation of financial hardship over many years, rather than isolated episodes of financial difficulty, appears to have the greatest impact on cognitive health. Senior author Professor Praveetha Patalay suggested that reducing chronic poverty and providing greater support for people experiencing financial hardship may help lower the future burden of cognitive decline and dementia.

The association between financial adversity and poorer brain health was particularly strong among men, individuals who experienced childhood disadvantage, and those carrying the APOE-ε4 genetic variant, which increases the risk of Alzheimer’s disease. Men with persistent financial hardship also performed more poorly on midlife cognitive tests than women in similar circumstances. Researchers suggest this may reflect differences in health behaviours, such as smoking and alcohol use, as well as greater financial stress among men in this generation, many of whom were the primary household earners.

Several mechanisms may explain the relationship between long-term financial hardship and cognitive ageing. Chronic financial stress can increase inflammation, a biological process known to accelerate brain ageing. Constant concerns about money may also increase cognitive load, leaving fewer mental resources available for memory, attention, and other cognitive functions. Although participants experiencing persistent financial hardship showed slower memory decline between ages 53 and 69, researchers believe this likely reflects earlier cognitive losses rather than protection against further decline.

Household income was measured at ages 26, 43, and 53, with participants classified as having persistent low income if they fell within the lowest 20% on at least two occasions. Financial hardship was assessed between ages 36 and 53 using questions about managing household finances and paying bills. Cognitive performance was evaluated through verbal memory and processing speed tests, while MRI scans measured indicators of brain health, including brain atrophy and ventricular enlargement. The findings highlight the importance of addressing long-term financial insecurity as part of strategies to promote healthy brain ageing and reduce dementia risk.

More information: Yiwen Liu et al, Persistent financial adversity and cognitive aging: a life course investigation, Innovation in Aging. DOI: 10.1093/geroni/igag054

Journal information: Innovation in Aging Provided by University College London

Researchers find connection between social media use and mental health risks in young adults

Leave a Reply

Researchers at UTHealth Houston have found that teenagers who spent six or more hours a day on social media were twice as likely to experience symptoms of anxiety and three times as likely to report suicidal ideation as those who spent less than one hour a day on social media. The findings, published in Pediatrics Open Science, were led by Jeff Temple, PhD, professor and associate dean for clinical research at the UTHealth Houston School of Behavioral Health Sciences.

Temple said excessive social media use may affect mental health because young people often compare themselves with the carefully curated lives they see online. Since users typically share only positive moments, adolescents may develop unrealistic expectations and negative self-perceptions. He also suggested that spending so much time online may reduce opportunities for in-person social interactions and other activities that support emotional well-being and help reduce anxiety.

At the same time, Temple noted that the relationship may work in both directions. Young people who are already experiencing anxiety or depression may turn to social media as a way to escape or cope with their emotions. This highlights the complexity of the relationship between social media use and mental health, making it difficult to determine whether one directly causes the other.

Unlike many earlier studies that focused on high school or college students before the rise of newer platforms such as TikTok, this research followed a group of emerging adults over several years. The study analysed annual survey data collected between 2018 and 2025 from 1,066 participants who were, on average, 12 years old when the research began. Participants self-reported the amount of time they spent on social media each day.

Among the participants, 8.5% reported spending less than one hour per day on social media, while more than one-third used it for one to three hours daily. Slightly more than 17% reported using social media for six or more hours each day, with girls reporting higher levels of use than boys. The association between social media use and anxiety symptoms was also stronger among girls. Researchers measured symptoms of depression and anxiety using validated assessment tools that asked participants to report how often they experienced symptoms such as poor appetite, trouble sleeping, feeling on edge, or difficulty relaxing during the previous week.

Temple said the findings support concerns expressed by many families about the effects of social media on young people’s mental health. He emphasised that evidence-based research is essential to understand the issue better and guide effective solutions. By identifying who is most affected, when the risks are greatest, and why social media may contribute to poorer mental health, researchers hope to develop strategies that encourage healthier online habits and improve the quality of social media experiences for young people.

More information: Jeff Temple et al, Associations Between Social Media Use and Mental Health in Emerging Adulthood, Pediatrics Open Science. DOI: 10.1542/pedsos.2026-001552

Journal information: Pediatrics Open Science Provided by University of Texas Health Science Center at Houston

Alzheimer’s Risk Factor May Behave Differently in Hispanic Older Adults, USC Study Finds

Leave a Reply

Researchers at the USC Mark and Mary Stevens Neuroimaging and Informatics Institute (Stevens INI) at the Keck School of Medicine of USC have found that a key Alzheimer’s disease risk factor may influence Hispanic older adults differently than non-Hispanic white adults. Analysing brain imaging and clinical data from more than 17,000 participants across five major ageing and Alzheimer’s disease studies, the team discovered that although greater amyloid buildup was linked to cognitive impairment and the APOE ε4 genetic variant in both groups, Hispanic participants generally had lower amyloid levels than non-Hispanic white participants with similar characteristics. The findings were published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.

Amyloid plaques are a hallmark biological feature of Alzheimer’s disease. At the same time, APOE ε4 is the strongest common genetic risk factor for late-onset Alzheimer’s and is typically associated with increased amyloid accumulation. However, the study suggests this relationship may not be equally strong across populations. “APOE ε4 is a major Alzheimer’s disease genetic risk factor, but our results suggest its relationship to amyloid buildup may be more nuanced in Hispanic populations,” said lead author Cally Xiao, PhD, a researcher at the Stevens INI. She noted that the findings could improve how researchers interpret risk, understand cognitive decline, and develop treatments for diverse communities.

The research was made possible through the Global Alzheimer’s Association Interactive Network (GAAIN), a data-sharing platform developed at the Stevens INI with support from the Alzheimer’s Association. GAAIN enabled the team to identify and combine compatible datasets using the Centiloid scale, a standardised measure of brain amyloid levels across different imaging methods. Data were drawn from five major studies, including the Alzheimer’s Disease Neuroimaging Initiative and the Health and Aging Brain Study–Health Disparities, allowing researchers to analyse patterns that would have been difficult to detect in any single study.

The researchers examined data from 17,017 older adults, including 1,427 Hispanic participants, while accounting for factors such as age, sex, education, and cognitive performance. As expected, individuals with mild cognitive impairment or dementia generally had higher amyloid levels than cognitively healthy participants, and APOE ε4 carriers in both ethnic groups showed greater amyloid burden. However, Hispanic participants consistently had lower average amyloid levels than non-Hispanic white participants across diagnosis groups. Among APOE ε4 carriers with normal cognition or mild impairment, Hispanic participants also had lower amyloid levels.

The team found that while APOE ε4 remained associated with amyloid pathology in both groups, its effect was weaker in Hispanic participants. Non-Hispanic white APOE ε4 carriers were more than four times as likely to show evidence of amyloid pathology, compared with about two and a half times among Hispanic carriers. Xiao emphasised that these findings do not suggest Hispanic adults face a lower risk of dementia. Instead, they indicate that cognitive decline in Hispanic older adults may not always be driven by amyloid to the same extent, with other biological, vascular, or social factors likely contributing to disease risk.

The findings have important implications as anti-amyloid therapies become increasingly central to Alzheimer’s treatment. Because these medications target amyloid plaques, understanding how amyloid accumulation varies across populations is essential for ensuring equitable and effective care. The authors stress that further research involving larger and more diverse Hispanic populations, more detailed ancestry information, and long-term follow-up is needed. Senior author Arthur W. Toga, PhD, said large-scale resources such as GAAIN are helping researchers better understand the complexity of Alzheimer’s disease and move towards more precise, inclusive approaches to diagnosis and treatment.

More information: Cally Xiao et al, Association of cognitive impairment and APOE ε4 with Centiloids in Hispanic and non-Hispanic White cohorts, Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association. DOI: 10.1002/alz.71586

Journal information: Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association Provided by Keck School of Medicine of USC

Cleveland Study Pinpoints Major Driver of Cognitive Decline With Age

Leave a Reply

A research team from University Hospitals, Case Western Reserve University, and the Louis Stokes Cleveland VA Medical Center has identified a key molecular driver of age-related cognitive decline. This discovery could lead to new treatments to preserve brain health in older adults. The findings, led by the Pieper Laboratory and published in the Proceedings of the National Academy of Sciences, point to a protein called KLF4 as a critical factor in maintaining the health of the blood-brain barrier (BBB). This protective network shields the brain from harmful substances while supporting normal brain function.

The blood-brain barrier is formed by tightly connected endothelial cells that line blood vessels in the brain. These cells regulate which molecules enter the brain, remove certain waste products generated by normal brain activity, and ensure blood flow is directed to the areas of the brain that need it most. Although deterioration of the BBB has long been associated with ageing, scientists had not established whether this breakdown directly contributes to cognitive decline or identified the molecular mechanisms responsible for its deterioration.

The researchers found that ageing endothelial cells gradually lose their ability to produce KLF4, a protein essential for maintaining the integrity of the blood-brain barrier. To investigate its role, the team reduced KLF4 levels in the endothelial cells of mice and monitored changes using advanced two-photon microscopy throughout the animals’ lifespan. Mice with accelerated KLF4 loss developed leaky blood vessels, fewer small blood vessels in the brain, and impaired regulation of blood flow in response to neuronal activity.

These vascular changes had widespread consequences. Even in middle-aged mice, reduced KLF4 triggered oxidative damage, neuroinflammation, nerve cell injury, anxiety-like behaviours, and measurable cognitive decline—changes typically seen only in much older animals. According to senior author Dr. Andrew A. Pieper, the loss of endothelial cell KLF4 accelerated every major feature of brain ageing examined in the study, suggesting that preserving KLF4 function could help protect the brain from age-related deterioration.

The team also used single-cell RNA sequencing to understand the underlying biology better. Their analysis showed that KLF4 loss disrupted multiple gene programmes involved in maintaining the blood-brain barrier and regulating immune responses, providing further evidence that the protein plays a central role in preserving brain health. These findings help explain how declining KLF4 levels contribute to the progressive breakdown of the BBB during ageing.

The discovery identifies KLF4 as a promising therapeutic target for slowing or preventing age-related cognitive decline. Future research will focus on understanding why KLF4 levels decrease with age and whether drugs can safely restore or enhance its activity in endothelial cells. If successful, such treatments could help maintain the integrity of the blood-brain barrier, protect the ageing brain, and reduce the risk of cognitive impairment later in life.

More information: Matasha Dhar et al, Endothelial KLF4 depletion drives age-related neurovascular dysfunction and neuropsychiatric impairment, Proceedings of the National Academy of Science. DOI: 10.1073/pnas.2426990123

Journal information: Proceedings of the National Academy of Science Provided by University Hospitals Cleveland Medical Center

Early-Onset Cancer Rise Associated with Faster Ageing in Younger Generations

Leave a Reply

Cancer has long been considered a disease associated with ageing, as the risk of developing cancer increases with the accumulation of cellular damage over time. However, the growing incidence of early-onset cancers among younger adults has prompted researchers to investigate whether biological ageing is occurring more rapidly in recent generations. A new study led by researchers at Washington University School of Medicine in St. Louis suggests that younger generations are indeed experiencing accelerated biological ageing, which may contribute to rising cancer rates before the age of 55.

The researchers found that individuals born in more recent decades tend to have a greater gap between their biological age—the age reflected by the condition of their body—and their chronological age. This larger “age gap” was associated with an increased risk of developing early-onset cancers, providing evidence that accelerated ageing may help explain the rising cancer burden observed across successive generations.

The study also revealed that ageing within specific organs may influence the risk of particular cancers. An immune system that appeared biologically older than expected was linked to an increased risk of early-onset lung cancer, while accelerated ageing of adipose (fat) tissue was associated with a higher risk of early-onset colorectal cancer. These findings suggest that ageing processes affecting different organ systems may contribute to distinct cancer types.

Published in Nature Medicine, the study highlights the potential value of biological ageing measures in identifying individuals at elevated cancer risk before symptoms appear. Such measures could eventually support more personalised approaches to cancer prevention, screening, and early detection by identifying those most likely to benefit from targeted interventions.

Led by molecular epidemiologist Dr Yin Cao, the research builds on previous work identifying lifestyle and environmental factors—including obesity, metabolic dysfunction, poor diet, alcohol use, sedentary behaviour, and other exposures—that influence cancer risk throughout life. Rather than examining these factors individually, the researchers sought to understand how their combined effects may accelerate biological ageing and increase susceptibility to cancer.

To investigate this relationship, the team analysed data from more than 154,000 participants in the UK Biobank and over 10,000 individuals enrolled in the U.S. National Institutes of Health’s All of Us Research Program. Biological ageing was assessed using established clinical biomarkers, metabolic indicators, and blood protein profiles that estimate ageing across the whole body and within individual organs. Younger birth cohorts consistently showed older biological profiles than older cohorts of the same chronological age.

The researchers found that accelerated systemic ageing was associated with an 8% higher risk of developing early-onset solid cancers, particularly lung, gastrointestinal, and uterine cancers. Participants with the highest levels of biological ageing had a 15% greater risk of early-onset solid cancers than those with the lowest levels, even after accounting for inherited genetic risk factors and genetic susceptibility to accelerated ageing. These findings strengthen the evidence that biological ageing plays an important role in cancer development beyond genetics alone.

Although the precise causes of accelerated biological ageing remain unclear, researchers believe modern environmental, lifestyle, and societal changes may collectively leave lasting biological effects that increase cancer susceptibility. Ongoing international collaborations, including Cancer Grand Challenges Team PROSPECT, aim to uncover how these influences accumulate across the life course. Ultimately, the goal is to identify individuals at greatest risk earlier and develop personalised prevention strategies that shift cancer care from treating disease after it develops to preventing it before it begins.

More information: Ruiyi Tian et al, Biological aging and generational shifts in early-onset cancer risk, Nature Medicine. DOI: 10.1038/s41591-026-04448-w

Journal information: Nature Medicine Provided by WashU Medicine

The Hidden Link Between Food and Gene Activity: Scientists Discover a Biological “Pencil”

Leave a Reply

A new international clinical intervention study published in Clinical Nutrition has uncovered molecular evidence explaining how diet may beneficially influence gene activity. Led by Prof. Iris Shai and Dr. Hila Zelicha Peer of Ben-Gurion University of the Negev, in collaboration with researchers from Leipzig University, the Leipzig Center of Metabolism (LieCeM), and Harvard University, the study suggests that certain plant-derived nutrients may act as an “epigenetic pencil,” helping shape cellular health by influencing gene expression through nutrition.

The researchers found that participants following a Green Mediterranean (Green-MED) diet experienced significantly higher circulating folate levels than those following either a traditional Mediterranean diet or standard healthy eating guidelines. Rather than serving only as a nutritional marker, the elevated folate appeared to enhance one-carbon metabolism—a key biochemical pathway that supports DNA methylation, regulates gene expression, maintains DNA integrity, and contributes to overall metabolic health.

The Green-MED diet emphasises polyphenol-rich foods, including green tea, walnuts, and a daily shake containing the aquatic plant Mankai (Wolffia globosa), while reducing red and processed meat intake. Participants on this dietary pattern showed marked increases in serum folate, which were associated with improved insulin sensitivity, lower inflammatory marker IL-6 levels, a healthier triglyceride-to-HDL cholesterol ratio, and reductions in visceral and liver fat.

The study also advances the growing field of Nutri-Omics by demonstrating how precision nutrition may help offset inherited genetic risk. Researchers focused on a common variant of the MTHFR gene (rs1801133), which reduces the activity of an enzyme essential for folate metabolism. People carrying the high-risk TT genotype typically have lower folate levels throughout life, making them more susceptible to metabolic complications.

Among TT carriers, those with low Mankai consumption experienced an increase in cardiovascular risk based on the Framingham Risk Score. In contrast, participants with the same genetic variant who closely followed the Mankai-enriched Green Mediterranean diet achieved an average 7.74-point reduction in cardiovascular risk, highlighting how dietary choices may help overcome inherited metabolic vulnerabilities.

Transcriptomic analyses revealed one of the study’s most significant findings. Increased consumption of plant-derived nutrients appeared to trigger adaptive biological reprogramming in TT carriers. Blood mRNA analyses showed increased expression of alternative folate-pathway genes, including MTHFD2 and DHFR, allowing cells to compensate for reduced inherited enzyme activity and utilise dietary folate more effectively.

These molecular discoveries help explain earlier findings from the internationally recognised DIRECT-PLUS trial, one of the world’s most comprehensive nutrition and imaging studies. The Green Mediterranean diet has previously been linked to regression of carotid atherosclerosis, reduced aortic stiffness, improved blood sugar control, lower visceral and liver fat, and favourable effects on biomarkers associated with brain ageing. The new findings provide a biological mechanism for these benefits, suggesting that folate-driven methylation acts as an “epigenetic pencil” that influences protective cellular pathways without altering DNA itself.

Mankai appears to play a central role in these effects. This nutrient-dense aquatic plant contains more than 45% protein, essential amino acids, fibre, minerals, and naturally occurring bioavailable folate. Participants consuming the highest amounts of Mankai demonstrated the greatest increases in folate, the strongest gene expression changes, and the most pronounced clinical improvements. According to Prof. Shai and Dr. Zelicha Peer, the findings strengthen the scientific basis for personalised nutrition, suggesting that folate is not only a marker of deficiency but also a biomarker of dietary quality, metabolic health, and the body’s ability to activate protective epigenetic mechanisms.

More information: Hila Zelicha et al, Effect of green mediterranean diet on serum folate and its interaction with genetic variation in folate metabolism: The DIRECT PLUS 18-month dietary randomized controlled trial, Clinical Nutrition. DOI: 10.1016/j.clnu.2026.106701

Journal information: Clinical Nutrition Provided by Ben-Gurion University of the Negev

Living Environment May Affect Women’s Heart Health for Decades, Study Suggests

Leave a Reply

Women who live in socially disadvantaged neighbourhoods may face poorer heart health for decades and experience a faster decline as they approach menopause, according to a long-term study led by the Harvard Pilgrim Health Care Institute. The findings suggest that where women live can have a lasting influence on cardiovascular health beyond individual lifestyle choices.

Researchers tracked more than 1,200 women in eastern Massachusetts for over 20 years, following them from pregnancy into midlife. Published in Circulation: Population Health and Outcomes, the study assessed heart health at five different time points using a score based on eight measures, including blood pressure, cholesterol, diet, sleep, physical activity, and other key health factors.

Women living in the most socially vulnerable neighbourhoods consistently recorded heart health scores around 6 to 10 points lower than those living in the least disadvantaged areas. These differences appeared within three years of joining the study and remained evident throughout more than two decades of follow-up. Participants in disadvantaged neighbourhoods also experienced a steeper decline in heart health before menopause, a stage of life when cardiovascular risk naturally begins to rise.

Individual socioeconomic factors also influenced outcomes. Women with lower incomes, lower educational attainment, or who identified as Non-Hispanic Black generally had lower heart health scores throughout the study, highlighting the combined effects of personal and community-level circumstances on long-term cardiovascular wellbeing.

Heart disease remains the leading cause of death among women, making these findings particularly significant. Previous research has shown that even modest reductions in heart health scores are linked to a greater risk of cardiovascular disease and premature death, suggesting that relatively small differences can have important long-term consequences.

“Our study shows that heart health in midlife is shaped by more than personal choices,” said senior author Izzuddin Aris, associate professor at Harvard Medical School and the Harvard Pilgrim Health Care Institute. “Income, education, and neighbourhood conditions may all play a role.” Researchers also found that neighbourhood disadvantage continued to affect heart health even after accounting for income and education, indicating that long-term exposure to under-resourced communities has an independent impact on cardiovascular health.

Aris added that the years leading up to and surrounding menopause may represent a critical opportunity to improve women’s cardiovascular health. He noted that targeted support could be especially beneficial for women living in neighbourhoods with fewer resources, where persistent social and environmental challenges may contribute to worsening heart health over time.

The researchers say the findings highlight the importance of improving access to healthy food, safe places for physical activity, and quality healthcare in disadvantaged communities. The study drew on data from Project Viva. This ongoing research programme has followed women from pregnancy in the early 2000s into midlife, providing a rare long-term view of how neighbourhood environments can shape heart health across decades.

More information: Zhi Lin et al, Associations of Sociodemographic and Neighborhood Vulnerability With Cardiovascular Health in Midlife Women in the United States, Circulation. DOI: 10.1161/CIRCOUTCOMES.126.013433

Journal information: Circulation Provided by Harvard Pilgrim Health Care Institute

Study Shows How the Adolescent Brain Reshapes Memory

Leave a Reply

Scientists have long known that the brain continues developing well beyond the teenage years, with important changes in decision-making, emotional regulation and memory extending into the mid-to-late 20s. Now, researchers at Albert Einstein College of Medicine have identified a biological process in mice that sheds light on how memory circuits mature during this prolonged period of brain development. Published in PLOS Biology, the study found that a key memory region undergoes a surprising phase of remodeling during late adolescence, temporarily making earlier memories harder to access before they re-emerge later in adulthood, often with less precise detail.

The researchers focused on the retrosplenial cortex (RSP), a brain region involved in organising and retrieving long-term memories. They discovered that protective, mesh-like structures known as perineuronal nets, which help stabilise memory circuits, unexpectedly diminished during late adolescence before rebuilding in adulthood. This temporary decline was observed only in the RSP and not in the nearby hippocampus, another brain region critical for memory.

According to senior author Jelena Radulovic, M.D., Ph.D., the findings provide the first detailed picture of how one of the brain’s memory circuits continues developing after adolescence. She believes the reorganisation of these protective structures may help the brain prioritise memories formed in adulthood over those from early adolescence, allowing individuals to better adapt to new challenges at different stages of life.

The timing of these changes is particularly significant because it coincides with a period now recognised as one of continued brain maturation in humans. While adolescence was once thought to end around age 19, neuroscientists increasingly acknowledge that the brain continues developing into the mid-to-late 20s. Lead author Hui Zhang, Ph.D., said the behavioural changes closely mirrored the biological ones.

As the stabilising structures in the retrosplenial cortex temporarily weakened, access to memories formed earlier in life became less reliable, suggesting that memory retrieval naturally shifts as the brain continues to mature.

To examine how these changes affected memory, the researchers trained mice to associate a particular environment with a mild foot shock. Shortly afterwards, the mice remembered the experience and froze when returned to the same location. However, weeks later, many of the mice trained during early adolescence no longer displayed the fear response, whereas mice trained in adulthood retained stable memories. When the adolescent mice were later tested in a different environment, they once again responded to the original setting, indicating that the memories had become temporarily inaccessible rather than erased.

Further analysis revealed that the temporary loss of memory access was linked to reduced levels of proteins that maintain perineuronal nets, along with lower activity of TGFβ2, a growth factor that supports these protective structures. When researchers restored either the perineuronal nets or TGFβ2 activity, the mice regained access to memories formed earlier in life. By mid-adulthood, many of these memories returned naturally, although they were less specific, with the mice responding similarly in unfamiliar environments. The researchers note that this resembles the “reminiscence bump” seen in humans, in which adults tend to recall experiences from adolescence and early adulthood more readily than memories from other periods of life, while often remembering their emotional significance more clearly than the exact details.

Beyond advancing understanding of memory, the findings may also provide clues about mental health. Schizophrenia and major depression frequently emerge during late adolescence, the same developmental stage in which the researchers observed extensive remodeling of memory circuits in mice. The team suggests that disruptions to this normal developmental process could contribute to vulnerability to psychiatric disorders in genetically susceptible individuals. Although further studies are needed to determine whether the same mechanisms operate in people, the research offers an important new perspective on how the developing brain reshapes memories while preparing for adulthood.

More information: Hui Zhang et al, Retrosplenial cortical reorganization during late adolescence introduces instability of contextual memory circuits, PLOS Biology. DOI: 10.1371/journal.pbio.3003908

Journal information: PLOS Biology Provided by Albert Einstein College of Medicine

Study Finds Frequent TV Watching Associated with Smaller Brain Structures

Leave a Reply

For decades, parents have warned that watching too much television would “rot your brain.” While that phrase may be an exaggeration, new research suggests the long-standing concern may contain some truth. A recent study published in Alzheimer’s & Dementia: Journal of the Alzheimer’s Association found that people who reported watching television very often during midlife were more likely to have smaller brain structures later in life. These included regions linked to memory, executive function and visual processing, along with greater damage to white matter—changes associated with ageing, stroke risk, cognitive decline and dementia. According to senior author David Raichlen of the USC Dornsife College of Letters, Arts and Sciences, the findings suggest that what people do while sitting may be just as important as how long they spend sitting.

The researchers analysed data from around 1,700 adults who joined the long-running Atherosclerosis Risk in Communities (ARIC) Study between 1987 and 1989. Participants, whose average age was 53, reported how frequently they watched television during their leisure time using a scale ranging from “never/seldom” to “very often.” They also provided information about how much of their working day was spent sitting. More than 20 years later, participants underwent MRI brain scans, allowing researchers to compare long-term brain health with earlier lifestyle habits.

People who reported watching television “very often” showed widespread structural differences in the brain compared with those who watched TV rarely. They had smaller brain volumes in regions commonly affected during the early stages of Alzheimer’s disease, as well as reduced frontal and occipital lobe sizes. They also displayed greater volumes of white matter hyperintensities, a marker of small blood vessel disease in the brain that has been linked to dementia and cognitive decline. Importantly, these associations remained even after researchers accounted for factors including physical activity, diabetes, body mass index, smoking and alcohol consumption.

One of the study’s most surprising findings was that sitting itself did not appear to explain the results. Participants who spent long periods sitting at work did not show the same brain changes. In fact, occupational sitting was associated with larger frontal and occipital lobes and lower levels of white matter abnormalities, suggesting better overall brain health. The researchers believe mentally stimulating work may help offset some of the negative effects commonly associated with prolonged sitting, highlighting that cognitive engagement could play an important protective role.

The study also found notable differences between men and women. When researchers analysed MRI scans separately by sex, most of the brain changes linked to both television viewing and occupational sitting were observed in men, suggesting they may be more susceptible to the neurological effects associated with these behaviours. However, the researchers caution that the reasons for these differences remain unclear and require further investigation before firm conclusions can be drawn.

Like any observational study, the research has limitations. Television viewing was self-reported rather than objectively measured, and participants did not receive brain scans at the beginning of the study, making it impossible to track structural changes over time directly. Even so, the findings raise important questions about how different sedentary activities affect long-term brain health. Rather than focusing solely on reducing sitting time, future public health advice may also encourage replacing passive activities such as television viewing with more cognitively engaging pursuits. As corresponding author Natan Feter notes, experts may need to broaden recommendations beyond simply moving more to include paying closer attention to how people spend their time while seated.

More information: Natan Feter et al, Associations of distinct sedentary behaviors with cortical, subcortical, and white matter hyperintensity volumes: Evidence from the ARIC study, Alzheimer’s and Dementia: Journal of the Alzheimer’s Association. DOI: 10.1002/alz.71582

Journal information: Alzheimer’s and Dementia: Journal of the Alzheimer’s Association Provided by University of Southern California

Overweight May Contribute to Cancer Risk More Than Previously Thought

Leave a Reply

Being overweight may contribute to far more cancer cases than previously thought, according to new research from the German Cancer Research Center (DKFZ). By using more accurate measures of body fat and accounting for methodological biases that may have distorted earlier findings, researchers estimate that more than 10% of all cancer cases could be attributed to excess body weight—almost double previous estimates. The findings suggest that obesity plays a much larger role in cancer development than has long been recognised.

To investigate the relationship between excess weight and cancer, the researchers analysed data from 458,543 adults enrolled in the UK Biobank. Participants were followed for a median of nearly 12 years, during which more than 50,000 new cancer cases were recorded. While overweight and obesity have long been established as risk factors for several cancers, earlier studies estimated they accounted for only around 2–8% of cases. Epidemiologist Hermann Brenner and his colleagues suspected these figures were underestimated because of limitations in the way body fat and cancer risk had been assessed.

Most previous studies relied on body mass index (BMI), which is calculated using height and weight. However, BMI cannot distinguish fat from muscle or indicate where fat is stored. Fat accumulated around the abdomen is particularly metabolically active and is strongly linked to chronic inflammation and other biological processes that can promote cancer. To address this limitation, the DKFZ team also examined waist circumference and waist-to-hip ratio, finding that these measures of body fat distribution were considerably better predictors of cancer risk than BMI alone.

The researchers also addressed an important source of bias that may have weakened previous estimates. Many cancers cause unintentional weight loss years before diagnosis, meaning some participants who already had undetected tumours appeared leaner when they entered the study. This can reduce the apparent association between obesity and cancer. To minimise this effect, the team progressively excluded cancers diagnosed during the first years of follow-up, as these cases were more likely to have been present before the study began. Once this bias was accounted for, the relationship between excess weight and cancer became much stronger.

After incorporating these methodological improvements, the estimated proportion of cancers attributable to excess weight increased from approximately 5.5% to as high as 11.5%. In other words, more than one in ten cancer cases may be linked to excess body fat and could potentially be prevented through effective weight management. The analyses also indicated that the impact of obesity may be greater among women than men and may be particularly important in adults younger than 60 years.

According to Brenner, the findings highlight the growing public health challenge posed by rising obesity rates worldwide. As populations continue to age and obesity becomes increasingly common, the number of obesity-related cancer cases is expected to increase substantially. The researchers argue that more effective strategies to prevent and treat obesity could have a far greater impact on reducing the burden of cancer than previously believed, reinforcing the importance of maintaining a healthy body weight as part of long-term cancer prevention.

More information: Luna Kiran Adhikari et al, Excess Weight May Account for More Than 10% of All Cancers: The Underestimated Impact of the Obesity Epidemic, Cancer Communications. DOI: 10.34133/cancomm.0040

Journal information: Cancer Communications Provided by German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ)

New Analysis in Nature Reviews Microbiology Examines the Impact of Climate Change on Waterborne Diseases

Leave a Reply

Climate change is reshaping the spread of waterborne diseases worldwide, according to a comprehensive review published in Nature Reviews Microbiology. Led by researchers from the Colorado School of Public Health at the University of Colorado Anschutz and the University of Washington School of Public Health, the review is among the most comprehensive analyses to date of how climate change influences waterborne diseases. The authors warn that increasingly frequent extreme weather events could reverse decades of progress in controlling these illnesses, which contribute to nearly 1.2 million deaths from infectious diarrhoeal diseases each year.

The review shows that climate change does not affect all disease-causing microorganisms in the same way. Bacteria, viruses and parasites each respond differently to changing environmental conditions, highlighting the need for pathogen-specific public health strategies. “We want people to know climate change changes the conditions that allow pathogens to spread,” said co-author Elizabeth Carlton, PhD, professor and chair of the Department of Environmental and Occupational Health at the Colorado School of Public Health. “It’s making it harder to control some of the world’s most deadly infectious diseases by creating more favourable conditions for transmission.”

According to the researchers, climate change alters the environmental conditions that determine whether pathogens survive, spread and infect new hosts. Flooding and heavy rainfall can contaminate drinking water supplies by carrying pathogens into water sources. At the same time, droughts can also increase disease risk by reducing access to safe water and forcing changes in water use. Rising temperatures generally encourage the growth of many bacteria. In contrast, some viruses, including norovirus, rotavirus and adenovirus, spread more efficiently in cooler, drier conditions and may become less common as global temperatures rise.

To reduce the growing threat of climate-driven waterborne diseases, the review identifies several practical public health measures. Investing in climate-resilient water, sanitation and hygiene (WASH) infrastructure is among the most effective ways to prevent disease, particularly as floods, hurricanes and other extreme weather events increasingly damage water and sanitation systems. The authors stress that strengthening these essential services will improve both current disease prevention and long-term resilience to climate change.

The researchers also recommend expanding pathogen-specific disease surveillance and strengthening vaccination programmes. Early detection systems can help health officials identify which pathogens are circulating and respond with targeted interventions rather than relying on one-size-fits-all approaches. Increasing coverage of vaccines against diseases such as cholera, rotavirus, polio, hepatitis A and typhoid can further reduce disease burden. However, climate-related disasters may disrupt vaccine delivery by damaging infrastructure and interrupting cold-chain storage.

The authors describe these measures as “no-regrets” investments because they protect public health today while preparing communities for future climate risks. Carlton noted that although climate change is altering how waterborne diseases spread, many effective prevention tools already exist. The challenge, she said, is ensuring they are designed and deployed for current and future climate conditions. The review concludes that no single strategy will prevent every waterborne disease, and that successful climate adaptation efforts must account for the different ways individual pathogens respond to changing environmental conditions.

More information: Karen Levy et al, Waterborne diseases and climate change, Nature Reviews Microbiology. DOI: 10.1038/s41579-026-01338-3

Journal information: Nature Reviews Microbiology Provided by University of Colorado Anschutz

Common myths about water intake and spicy foods debunked

Leave a Reply

Researchers are challenging two long-standing pieces of nutrition advice: that drinking water during meals helps you eat less, and that spicy foods encourage overeating. A new study from Cornell University found little evidence that water at mealtimes promotes fullness. Instead, people who drank more water during a meal tended to eat more. At the same time, a separate experiment showed that adding extra spice to a snack slowed eating and reduced how much participants consumed overall.

The researchers found that for every additional 100 grams of water participants drank during a meal, they ate about 39 more grams of food, or roughly 49 extra calories. People who frequently alternated between bites of food and sips of water also ate more, with each additional switch linked to about 4.4 extra grams of food consumed. The team believes this may be because alternating between food and water delays sensory-specific satiety – the natural decline in a food’s appeal as you continue eating – helping meals stay enjoyable for longer.

“There’s been this widespread advice that if we drink water, it fills us up,” said Paige Cunningham, assistant professor in Cornell’s Division of Nutritional Sciences and corresponding author of the study, published in Appetite. “But water is emptied quickly from the stomach, so it likely doesn’t fill us up for long. Instead, water may increase how much we eat, providing lubrication which can speed up eating, and preventing a dry mouth which can prolong enjoyment of the food.” The analysis combined data from two previous laboratory studies involving 86 adults who ate as much beef chilli or chicken tikka masala as they wanted. At the same time, every bite and sip was recorded.

One unexpected finding was that participants who drank water more quickly during their meals actually ate less. Cunningham said the reason remains unclear and may be related to how long water stays in the mouth or reflects the overall length of a meal. “This was a secondary analysis looking at associations,” she said. “We are following up on this right now so we can make those causal inferences.”

In a separate study published in Food Quality and Preference, 49 adults ate tortilla chips with either a mild or spicy salsa, with the only difference being the amount of cayenne pepper. Participants consumed 28% less of the spicy snack and ate about 30% more slowly than when eating the mild version. Water intake remained unchanged, suggesting the reduction in food consumption was linked to the slower eating pace rather than increased thirst. “The takeaway is that adding spice to one part of the snack can significantly influence how much people eat overall,” Cunningham said.

Together, the studies suggest that common assumptions about water and spicy foods may need rethinking. Drinking more water during meals was associated with eating more, while adding spice appeared to slow eating and reduce overall food intake. However, the researchers caution that both experiments were conducted under controlled laboratory conditions using a limited range of foods, including chilli, tikka masala, tortilla chips and salsa. More research is needed to determine whether the same effects occur with different foods and in everyday eating situations.

More information: Paige Cunningham et al, Water intake, switching between bites and sips, and drinking behavior are associated with food intake across meals varying in spiciness: A secondary analysis of two randomized crossover studies, Appetite. DOI: 10.1016/j.appet.2026.108698

Journal information: Appetite Provided by Cornell University