Author Archives: support

Can Eating Less Protein Promote Healthy Ageing?

Protein-fortified foods are now common, appearing in products ranging from breakfast cereals and coffee to protein water. Yet a new review published on July 31 in Cell Press Blue suggests that consuming less protein may, for many people, offer greater health benefits and even help extend lifespan. Reviewing more than 350 studies on protein restriction and ageing, researchers found consistent evidence that lower protein intake may slow biological ageing by improving metabolism, altering how cells respond to nutrients, reducing cellular damage, and preserving healthy cell function.

“It’s absolutely crystal clear that there are benefits of protein to muscle growth and exercise response of active individuals,” says Dudley Lamming, the review’s corresponding author from the University of Wisconsin–Madison. “But because most people are relatively sedentary, many people are likely consuming more protein than they actually need, which probably has negative health consequences.” While calorie restriction has long been shown to extend lifespan and reduce age-related diseases in many species, maintaining a low-calorie diet is difficult. Protein restriction, however, may provide many of the same benefits without reducing total calorie intake.

Evidence from animal studies has shown that reducing protein intake can extend lifespan in flies and rodents, even when calorie consumption remains unchanged. Human clinical trials have also found that protein-restricted diets can reduce body weight, lower fat mass, and improve fasting blood sugar, despite participants often consuming more calories overall. Together, these findings suggest that the quality and quantity of protein consumed may influence health independently of total energy intake.

At the same time, research has demonstrated that higher protein intake, particularly when combined with regular exercise, can promote weight loss and help preserve muscle mass in older adults. These findings contributed to updated U.S. dietary recommendations encouraging adults to consume 1.2–1.6 grams of protein per kilogram of body weight each day—substantially higher than previous guidelines. Against this backdrop of increasing protein consumption, the researchers sought to understand better how protein restriction influences healthy ageing.

The review identifies several biological mechanisms that may explain these benefits. A key factor is fibroblast growth factor 21 (FGF21), a hormone that increases when protein intake is low. Higher FGF21 levels are associated with greater energy expenditure, improved blood sugar regulation, and reduced inflammation. In animal studies, elevated FGF21 has been linked to longer lifespan, with stronger effects observed in male mice. The review also highlights specific amino acids—including methionine, isoleucine, and valine—that may accelerate ageing-related processes when consumed in excess by stimulating pathways associated with obesity, inflammation, and chronic disease.

The authors emphasise that protein requirements should be individualised. Although athletes, pregnant women, and some older adults often benefit from higher protein intake, protein-fortified foods may provide little advantage for the average sedentary adult and could even have unintended health consequences. Lamming suggests that regular physical activity may protect athletes from the metabolic effects of a high-protein diet by directing protein towards muscle growth. “We probably need to personalise protein recommendations based not just on age, but also on how physically active people are,” he says.

More information: Bailey A. Knopf et al, The hallmarks of protein and amino acid restriction in aging and longevity, Cell Press Blue. DOI: 10.1016/j.cpblue.2026.100079

Journal information: Cell Press Blue Provided by Cell Press

Why Keeping a Doctor Is Becoming Harder

If it feels harder to keep the same doctor, you are not imagining it. Across many healthcare systems, retirements, burnout and changing workforce expectations are making it increasingly difficult to retain experienced clinicians. A new study published in the Joint Commission Journal on Quality and Patient Safety suggests that the challenge extends beyond workforce shortages. Interviews with leaders from four major healthcare systems in the Dallas–Fort Worth region reveal that generational shifts are changing who enters healthcare, who stays and why clinicians leave. According to study co-author Dr. William Sage, healthcare organisations are no longer facing simply a staffing problem, but the challenge of supporting five generations of clinicians with different expectations about work, well-being and career longevity.

The study involved 17 senior leaders who consistently identified clinician turnover as one of their greatest concerns. They described the growing number of younger physicians leaving earlier in their careers, while many experienced clinicians have few options between full-time practice and complete retirement. Several participants noted that replacing a seasoned physician may require hiring multiple younger clinicians because of changes in productivity expectations and the way healthcare systems measure performance.

The consequences of clinician turnover extend well beyond filling vacant positions. Co-author Keegan Warren explained that when experienced clinicians leave, organisations lose valuable institutional knowledge, mentoring relationships and practical expertise that can take years to rebuild. Physician departures also carry high financial costs while disrupting continuity of care. The researchers argue that recognising clinicians as individuals with meaningful careers and lives is essential to building a stable workforce and protecting high-quality patient care.

Burnout and evolving workplace expectations were also identified as major drivers of turnover. Younger physicians and nurses increasingly prioritise mental health, work-life balance, flexible scheduling and supportive workplace cultures, expecting employers to address these needs actively. However, the researchers emphasise that these findings should not be viewed as a conflict between generations. Instead, workplace expectations have evolved through broader changes, including work-hour regulations for medical trainees, the shift from physician-owned practices to large healthcare organisations, and the lasting effects of the COVID-19 pandemic.

Rather than focusing solely on recruiting more clinicians, the researchers recommend strategies to strengthen retention throughout the career span. These include expanding mentorship programmes that transfer knowledge from experienced clinicians, improving early-career support through professional development and flexible work arrangements, involving multiple generations in leadership and decision-making, strengthening workforce planning through human resources, creating flexible late-career roles, and improving communication across generations to reduce workplace tensions.

The researchers conclude that a stable clinical workforce is fundamental to ensuring patients have consistent access to high-quality care. Retention can no longer be treated as an afterthought. By designing workplaces that recognise clinicians as people first—with families, responsibilities and limits—healthcare organisations can foster stronger commitment, preserve valuable experience and create a more resilient healthcare system that benefits both clinicians and the patients they serve.

More information: Andrew A. White et al, Generational Change in the Healthcare Workforce: Perspectives from Health System Leaders, The Joint Commission Journal on Quality and Patient Safety. DOI: 10.1016/j.jcjq.2026.06.009

Journal information: The Joint Commission Journal on Quality and Patient Safety Provided by Texas A&M University

The Changing Science of Ageing: New Perspectives on the Biology of Growing Older

As recently as the mid-20th century, ageing was described by Nobel Prize laureate Peter Medawar as “an unsolved problem in biology”. Today, researchers can analyse the activity of thousands of genes in individual cells and identify genetic variants linked to longevity. These studies identify molecular pathways that influence lifespan, and estimate biological age using epigenetic clocks. Experimental treatments such as senolytics, which target senescent cells, have also emerged. Yet despite these remarkable advances, scientists increasingly recognise that ageing is far more complex than once imagined. A new paper by Dr Piotr Chmielewski of Wroclaw Medical University argues that a single universal mechanism does not drive ageing, but rather the interaction of numerous biological processes operating across different levels of organisation.

Published in Biogerontology, the paper, Ageing was never a singular problem in biology: implications for mechanisms, measurements and interventions, challenges the search for a single cause of ageing. Recent discoveries have identified key pathways, including mTOR, AMPK, FOXO and IGF-1, that regulate growth, metabolism and lifespan. At the same time, advances in DNA sequencing have made it possible to study ageing at the level of individual cells. According to Dr Chmielewski, these discoveries have deepened understanding of specific mechanisms but have also highlighted how many overlapping processes contribute to ageing, making it increasingly difficult to view it as one unified biological phenomenon.

For decades, researchers proposed oxidative stress, DNA damage, telomere shortening, mitochondrial dysfunction, epigenetic changes and chronic inflammation as possible primary drivers of ageing. While each contributes to age-related decline, none alone explains the full picture. Instead, the evidence increasingly supports the idea that ageing reflects the gradual disorganisation of a complex biological system. This perspective is reflected in the widely adopted concept of the “hallmarks of ageing”, a collection of interconnected biological characteristics that collectively influence the ageing process rather than a single underlying cause.

The growing use of epigenetic clocks illustrates both the promise and the uncertainty of modern ageing research. These tools estimate biological age by analysing DNA methylation patterns and have been linked to disease risk and mortality. However, researchers still do not know whether they measure mechanisms that actively drive ageing or reflect biological changes caused by other processes. As Dr Chmielewski notes, determining whether reversing epigenetic changes would genuinely rejuvenate the body or merely alter a biomarker remains one of the field’s most important unanswered questions.

The paper also highlights the limitations of translating laboratory discoveries into human medicine. While many interventions extend the lifespan of mice by 20 to 30 per cent, mice differ fundamentally from humans in lifespan, metabolism, tissue organisation, immune function and repair mechanisms. As a result, therapies that appear highly effective in animal models often fail to deliver comparable benefits in people. Increasingly, researchers believe that youth may depend less on avoiding biological damage—which occurs throughout life—and more on maintaining the ability to repair tissues, adapt to stress and preserve normal function.

According to Dr Chmielewski, this shift in thinking may represent one of the most important developments in biogerontology. Rather than asking what causes ageing, researchers are increasingly asking how some organisms preserve resilience, adaptability and function despite continuous damage. From this perspective, interventions such as regular physical activity, calorie restriction and intermittent fasting may promote healthy ageing not by stopping ageing itself, but by strengthening the body’s capacity to adapt and recover. If this view proves correct, future research may focus less on finding a single cure for ageing and more on helping people maintain health and functional independence for as long as possible.

More information: Piotr Paweł Chmielewski, Ageing was never a singular problem in biology: implications for mechanisms, measurements and interventions, Biogerontology. DOI: 10.1007/s10522-026-10436-x

Journal information: Biogerontology Provided by Wroclaw Medical University

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

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

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

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

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”

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

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

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

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