The research drew on the Ma’anshan Birth Cohort, a long-running population study in Anhui Province, China, and focused on 1,234 children at age ten. Rather than estimating exposure indirectly, the investigators measured it directly. Urine samples were analyzed using Laser Direct Infrared spectroscopy, or LDIR, a technique that fires an infrared laser across a sample and reads the characteristic absorption fingerprints of the polymers present. This allowed the team not only to count particles but to identify which types of plastic they were, from polyethylene terephthalate and polypropylene to polyamide and polytetrafluoroethylene, the nonstick polymer better known as PTFE.

The headline number is striking: microplastics were detected in 91.41 percent of the children tested, with a median abundance of 250 particles per milliliter of urine. That figure alone underscores how thoroughly plastic pollution has penetrated the human body, even in a cohort of children who have lived barely a decade. Scientists have previously found microplastics in blood, lungs, placenta and breast milk, but quantifying exposure in school-aged children, and connecting it to neurodevelopmental outcomes, remains rare. The authors note that empirical research on how microplastic exposure might interact with diet is especially scarce, a gap this study was designed to address.

To assess emotional and behavioral development, the researchers used the Child Behavior Checklist, a widely validated parent-report instrument that generates standardized T-scores across syndromes such as Anxious/Depressed, Withdrawn/Depressed, Social Problems, Thought Problems, Attention Problems, Rule-Breaking Behavior and Aggressive Behavior, which combine into broader Internalizing, Externalizing and Total Problems scales. Dietary patterns were scored with the KIDMED index, the Mediterranean Diet Quality Index for Children and Adolescents, which rewards consumption of fruit, vegetables, fish and olive oil and penalizes processed snacks and sugary drinks. Statistical models, built with a directed acyclic graph to guide confounder selection, tested the effects of exposure and diet independently and then examined how they interacted.

The results revealed a pattern that differed sharply by sex. In boys, higher urinary abundance of PTFE was positively correlated with T-scores for Rule-Breaking Behavior, with a regression coefficient of 0.165 (95 percent confidence interval 0.026 to 0.305), and with Externalizing Problems, at 0.249 (95 percent CI 0.001 to 0.496). In plain terms, boys carrying more PTFE particles tended to score higher on parent-reported rule-breaking and outwardly directed behavioral problems. PTFE is ubiquitous in modern kitchens, found in nonstick cookware coatings, food packaging and water-repellent textiles, making it one of the more difficult polymers to avoid in daily life.

Diet, meanwhile, emerged as a meaningful counterweight in its own right. Higher adherence to the Mediterranean diet was significantly associated with lower Total Problems scores, with a coefficient of −0.383 (95 percent CI −0.620 to −0.146). Significant negative associations also appeared for the Withdrawn/Depressed, Thought Problems, Attention Problems, Internalizing Problems and Externalizing Problems scales, and these protective patterns were more pronounced in girls. The Mediterranean diet, rich in antioxidants, omega-3 fatty acids, fiber and anti-inflammatory compounds, has long been linked to better cognitive and mental health outcomes, and the authors suggest such nutritional properties may plausibly interact with the inflammatory and oxidative stress pathways that microplastics are suspected of activating.

The interaction analysis sharpened the picture further. When the team stratified children by level of dietary adherence, a troubling association appeared in the low and moderate adherence groups: polyamide, a nylon-type plastic used in textiles, kitchen utensils and food packaging, was significantly positively associated with Total Problems, at 0.244 (95 percent CI 0.015 to 0.473). Significant positive associations were also observed for Anxious/Depressed scores at 0.126 (95 percent CI 0.007 to 0.245), Social Problems at 0.199 (95 percent CI 0.071 to 0.326), Rule-Breaking Behavior at 0.156 (95 percent CI 0.041 to 0.271) and Externalizing Problems at 0.246 (95 percent CI 0.036 to 0.455). These diet-dependent associations were more pronounced in boys, mirroring the sex-specific pattern seen with PTFE.

The authors conclude that microplastic exposure was associated with sex-specific differences in children’s emotional and behavioral development, and that higher adherence to the Mediterranean diet was associated with a reduced magnitude of these adverse associations. The sex-specificity is biologically intriguing. Boys and girls differ in hormonal environments, body composition, metabolic handling of xenobiotics and even behavioral expression of distress, and the finding that PTFE tracked externalizing behavior in boys while the Mediterranean diet’s protective signal was stronger in girls suggests that exposure and resilience may follow partly distinct pathways in each sex.

As with any cross-sectional study, caution is warranted before drawing causal conclusions. The measurements of exposure, diet and behavior were taken at a single point in time, so the data cannot establish whether microplastics cause behavioral problems, whether children with certain behavioral profiles accumulate more plastics through their habits, or whether unmeasured factors such as household income, housing quality or overall environmental chemical load drive both exposure and outcomes. Urinary microplastics also represent a snapshot of what the body is currently excreting, not necessarily the total body burden, and particle counts near detection limits carry inherent measurement uncertainty. The authors themselves note that the impact of microplastic exposure on children’s emotional and behavioral development remains unclear, positioning this study as an early contribution rather than a definitive verdict.

Even so, the study breaks new ground in combining direct polymer-specific exposure measurement with a rigorous dietary interaction analysis in a large pediatric cohort. If the findings are replicated in longitudinal and experimental settings, they would add a neurodevelopmental dimension to the growing list of health concerns attributed to microplastics and would elevate diet from a general health habit to a potential modifiable shield for children growing up in a plastic-saturated world. For parents, the practical takeaway is twofold: reduce plastic contact with food and drink where feasible, and lean into the Mediterranean pattern of vegetables, fruit, fish and olive oil, a prescription that is already well supported on other grounds and now, tentatively, may help children’s minds as well as their bodies.

Subject of Research: Associations between urinary microplastic exposure, emotional and behavioral development, and Mediterranean diet adherence in school-aged children

Article Title: Impact of microplastic exposure on emotional and behavioral development in school-aged children: the moderating role of diet

Article References: Impact of microplastic exposure on emotional and behavioral development in school-aged children: the moderating role of diet. (n.d.). https://doi.org/10.1186/s12916-026-05185-0

Image Credits: AI Generated

DOI: 10.1186/s12916-026-05185-0

Keywords: microplastics, children, Mediterranean diet, Child Behavior Checklist, PTFE, polyamide, urine biomonitoring, behavioral development, sex differences, LDIR spectroscopy, public health, Ma'anshan Birth Cohort

The scale of the synthesis matters because most previous work on diet and the developing brain has concentrated on younger children, leaving adolescence surprisingly underexplored. Adolescence is a period of profound neural remodelling, when the prefrontal cortex, the brain region responsible for executive function, impulse control and planning, continues to mature well into the twenties. It is also the life stage when many psychiatric conditions first emerge, with depression and anxiety frequently taking root during the teenage years. Understanding whether nutrition influences these trajectories could therefore have enormous public health consequences, given that dietary habits established in adolescence often persist into adulthood.

To capture the evidence, the team searched ten electronic databases and applied strict inclusion criteria. Only full-text, peer-reviewed English-language publications were eligible, and studies had to examine the relationship between adolescent dietary intake, whether measured as overall dietary patterns, dietary quality indices or specific nutrient intakes, and validated measures of cognition, mental health or wellbeing. The researchers deliberately excluded studies focused solely on eating behaviours such as breakfast skipping, as well as nutritional supplement interventions and animal or laboratory-based research, ensuring that the review captured real-world dietary exposure in free-living adolescents. Two independent reviewers screened every retrieved article and assessed methodological quality using the Joanna Briggs Institute critical appraisal tools, before conducting a narrative synthesis of the findings.

The fifty included studies divided into three overlapping domains: five examined cognition, thirty-three examined mental health and twenty examined wellbeing, with some studies reporting on both mental health and wellbeing outcomes. Methodologically, the evidence base was heavily weighted towards snapshot research. Forty-four of the studies were cross-sectional, measuring diet and psychological outcomes at a single point in time, while only seven were longitudinal, following participants across months or years. That imbalance, the authors note, is one of the most important caveats attached to their conclusions.

Despite those limitations, the patterns were remarkably consistent. Adherence to a Mediterranean diet, characterised by high consumption of vegetables, fruits, whole grains, legumes, nuts and olive oil, was positively associated with higher cognitive performance, greater attention capacity and stronger learning processes. This aligns with a broader body of nutritional neuroscience suggesting that the anti-inflammatory and antioxidant properties of Mediterranean-style eating patterns may protect neural tissue and support the metabolic demands of developing brains. Nutrients abundant in such diets, including omega-3 fatty acids, polyphenols and B vitamins, participate in neurotransmitter synthesis, myelination and the regulation of neuroinflammation, all processes that remain active during adolescent brain maturation.

On the mental health side, the review found that healthier diets were generally associated with better psychological outcomes and a reduced risk of conditions such as depression and anxiety. Conversely, a so-called Western diet, defined by high intakes of processed foods, added sugars and saturated fats, was associated with poorer mental health. One plausible biological mechanism runs through the gut-brain axis, the bidirectional communication network linking the gastrointestinal tract, its trillions of resident microbes and the central nervous system. Diets rich in fibre and plant-derived compounds promote the production of short-chain fatty acids, molecules with anti-inflammatory effects that can influence brain function, whereas highly processed diets may promote systemic and neural inflammation and disrupt the microbial balance implicated in mood regulation. The hypothalamic-pituitary-adrenal axis, which governs the body’s stress response, represents another plausible pathway through which nutrition could modulate adolescent mental health.

Wellbeing, a broader construct encompassing quality of life and day-to-day functioning, showed a similar gradient. Higher overall diet quality was associated with better wellbeing across diverse populations, while unhealthy eating patterns and lower diet quality were associated with poorer wellbeing. Because the included studies spanned multiple countries and used validated instruments such as established diet quality indices and standardised wellbeing questionnaires, the consistency of this association across different cultural and dietary contexts lends weight to the finding, even though the observational nature of most of the underlying research prevents firm causal claims.

That caveat deserves emphasis. Cross-sectional data cannot establish which comes first: poor diet or poor mental health. The authors highlight the possibility of reverse causality, in which mental health symptoms drive poor dietary choices, as low mood, fatigue or anxiety can reduce motivation to prepare nutritious meals and increase reliance on convenient, energy-dense foods. Residual confounding presents a further challenge, since factors such as socio-economic status, physical activity, sleep and family environment influence both what adolescents eat and how they feel, and may not be fully accounted for in statistical models even when researchers attempt to control for them. The review’s conclusions are therefore framed as associations rather than causal effects, a distinction that is scientifically essential but easily lost in public reporting.

The authors argue that the field now requires more longitudinal and intervention studies to establish causal pathways definitively. Randomised trials of dietary improvement in adolescents, though logistically difficult, would provide far stronger evidence than further cross-sectional surveys. They also call for greater standardisation of dietary definitions, noting that the heterogeneity of how studies define and measure dietary patterns, from food frequency questionnaires to composite quality indices, complicates comparison across the literature, alongside consistent controls for important confounders. Such improvements would allow future syntheses to move beyond narrative description towards quantitative meta-analysis and, ultimately, evidence-based dietary guidance tailored to this age group.

Even with those caveats, the review arrives at a moment when adolescent mental health is a mounting global concern and ultra-processed foods occupy an expanding share of teenage diets worldwide. The work was undertaken as part of a PhD project funded by the National Institute for Health and Care Research School for Public Health Research, and the research questions were co-created with young people themselves, reflecting a growing commitment to involving adolescents in shaping the science that concerns them. If future longitudinal and intervention studies confirm the associations documented here, the implications would extend well beyond the clinic, reaching school food policy, family mealtime habits and the regulation of food marketing aimed at young people. For now, the message is one of cautious optimism: the food on a teenager’s plate appears to be entangled with the health of a maturing brain, and science is only beginning to untangle how deeply that connection runs.

Subject of Research: Associations between adolescent dietary intake and cognition, mental health and wellbeing

Article Title: Effect of diet on cognition, mental health and wellbeing among adolescents: a systematic review

Article References: Coombes, J. P., Russell, A., Murphy, M., Turner, A., Ansell, E., Algaai, E., & Pallan, M. (2026). Effect of diet on cognition, mental health and wellbeing among adolescents: a systematic review. BMC Pediatrics. https://doi.org/10.1186/s12887-026-07596-7

Image Credits: AI Generated

DOI: 10.1186/s12887-026-07596-7

Keywords: adolescents, diet, nutrition, cognition, mental health, wellbeing, Mediterranean diet, Western diet, systematic review, gut-brain axis, depression, diet quality

The research team, led by investigators at the Aging Research Center of Karolinska Institutet and Stockholm University, set out with a specific and technically ambitious goal. Rather than examining a single disease endpoint, they wanted to identify the blood biomarkers most strongly associated with adherence to several well-established dietary patterns and to describe the pathophysiological domains those markers belong to. To do this, they drew on fifty-four blood biomarkers spanning four major domains: metabolic, inflammatory, vascular, and neurodegenerative. This breadth matters, because aging is not driven by any single pathway. It is the product of interacting processes, from glucose regulation and lipid transport to chronic low-grade inflammation and neural injury, and a diet’s biological fingerprint may be scattered across all of them.

Dietary intake in the study was assessed using validated food frequency questionnaires, the standard instrument for capturing what people eat over extended periods. The researchers then scored diet quality in three complementary ways. The first was adherence to the Alternative Mediterranean Diet, or AMED, a scoring system that rewards high consumption of vegetables, legumes, fruits, nuts, whole grains, fish, and monounsaturated fats, with moderate alcohol intake and limited red and processed meat. The second was the Alternative Healthy Eating Index, or AHEI, a broader index developed to capture foods and nutrients most strongly linked to lower chronic disease risk. The third was a reverse-transformed Empirical Dietary Inflammatory Index, or rEDII, which quantifies the inflammatory potential of the diet; higher rEDII scores in this transformation indicate a less pro-inflammatory, and therefore more favorable, dietary pattern.

On the statistical side, the team used quantile regression to examine cross-sectional associations between dietary adherence and standardized biomarker levels, adjusting for sociodemographic and lifestyle factors. Quantile regression is a technically deliberate choice: by modeling the median of each biomarker distribution rather than only the mean, the approach is less sensitive to extreme values and outliers, which are common in biological data from older populations. The researchers also corrected for multiple comparisons, a safeguard against the false positives that inevitably arise when dozens of biomarkers are tested simultaneously. Associations were expressed per one standard deviation increment in dietary adherence, allowing effects to be compared across different diets and biomarkers on a common scale.

The results were striking in their specificity. Higher adherence to the Mediterranean-style AMED pattern was directly associated with higher blood levels of folic acid, with a beta coefficient of 0.066, and inversely associated with glial fibrillary acidic protein, or GFAP, a marker of astrocyte activation that is increasingly studied as an indicator of neurodegenerative processes in the brain. The inverse association with GFAP, at a coefficient of -0.018, is particularly intriguing because it hints that a Mediterranean-style diet may be linked to a quieter profile of glial activity, the cellular inflammation within the brain that is thought to accompany cognitive aging. The AHEI showed a nearly identical association with folic acid, at 0.068, and was additionally inversely associated with growth differentiation factor 15, or GDF15, a circulating protein that rises with mitochondrial stress, inflammation, and biological aging more broadly.

The rEDII analysis told a complementary story. Higher adherence to the reverse-transformed inflammatory index, meaning a diet with lower inflammatory potential, was inversely associated with leptin, insulin, GDF15, alkaline phosphatase, tumor necrosis factor receptor superfamily member 1B, and leukocyte counts. The coefficients ranged from -0.047 for TNFRSF1B, a receptor shed during tumor necrosis factor signaling, to -0.094 for leptin, the hormone produced by fat tissue that regulates appetite and energy balance. In practical terms, older adults whose diets carried a lower inflammatory burden showed lower levels of hormones and signaling molecules tied to adiposity, insulin action, inflammatory cascades, and cellular stress responses. Leukocytes, the circulating immune cells that often rise with systemic inflammation, were also lower, at a coefficient of -0.058.

What makes this pattern biologically coherent is that the affected markers cluster into recognizable physiological narratives. Folic acid, elevated in those following Mediterranean-style and healthy eating patterns, is a B vitamin central to one-carbon metabolism, DNA synthesis, and the regulation of homocysteine, an amino acid implicated in vascular and neurological damage. GDF15, reduced among those eating less inflammatory diets, has emerged in geroscience as one of the most compelling blood-based indicators of biological age, rising steadily with tissue stress and chronic disease. TNFRSF1B and leukocytes sit squarely within the inflammaging framework, the slow-burning, low-grade inflammation that accumulates with age and is implicated in frailty, cardiovascular disease, and dementia. Alkaline phosphatase, meanwhile, is an enzyme associated with liver and bone metabolism that has been linked to metabolic and vascular risk in prior research.

The associations held up under scrutiny. The authors report that the findings remained consistent across multiple sensitivity analyses, a robustness check designed to test whether the results were artifacts of particular modeling choices or subgroups. The biomarker quantification itself was supported by the Affinity Proteomics-Stockholm unit at SciLifeLab, reflecting the kind of high-throughput proteomic infrastructure that has transformed what population-based aging studies can measure. Where earlier cohorts might have tracked a handful of clinical chemistry values, this study could interrogate dozens of proteins and metabolites simultaneously, then map the survivors of statistical correction back onto known pathophysiological domains.

It is worth being precise about what the study does and does not show. The design is cross-sectional, meaning diet and biomarkers were measured at the same point in time, so the analysis cannot establish that eating well causes favorable biomarker levels. Reverse causation remains possible: people with higher biological burden may eat differently, and underlying illness can reshape both appetite and blood chemistry. The effect sizes, while statistically robust after correction, are modest, as is typical for dietary epidemiology in free-living populations. Yet the consistency of the domain-specific signals, the use of validated dietary indices, and the population-based sampling all strengthen the case that the observed signature reflects genuine biology rather than statistical noise. The study was approved by the Regional Ethical Review Board in Stockholm, and all participants or their next of kin provided written informed consent.

For the field of geroscience, the work lands at a moment of growing interest in identifying modifiable levers over the biology of aging. Diet is among the most tractable of these levers, and the new findings suggest that its influence is legible in the blood, distributed across metabolic hormones, inflammatory receptors, and even markers of glial activity in the brain. If future longitudinal and interventional studies confirm that shifting dietary patterns moves these biomarkers in the directions observed here, the humble food frequency questionnaire may become an even more powerful clinical tool, one that connects everyday eating choices to the molecular machinery of healthier aging.

Subject of Research: Associations between dietary patterns and blood-based biomarkers of aging in older adults

Article Title: Biological signature of dietary patterns in older adults: findings from a population-based study

Article References: DaCosta, R. A., Gregorio, C., Calderón-Larrañaga, A., Ornago, A. M., Mrhar, A., Ortolá, R., Fredolini, C., Vetrano, D. L., & Carballo-Casla, A. (2026). Biological signature of dietary patterns in older adults: findings from a population-based study. BMC Medicine, 24(1), Article 520. https://doi.org/10.1186/s12916-026-05202-2

Image Credits: AI Generated

DOI: 10.1186/s12916-026-05202-2

Keywords: nutrition, biomarkers, aging, Mediterranean diet, inflammation, GDF15, GFAP, folic acid, geroscience, diet quality, older adults, population-based study

The Mediterranean diet has accumulated one of the strongest evidence bases in nutritional science. An influential umbrella review by Dinu and colleagues, published in the European Journal of Clinical Nutrition in 2018, synthesized meta-analyses of both observational studies and randomized trials and found consistent associations between Mediterranean-style eating patterns and multiple favorable health outcomes. The dietary pattern, characterized by high intakes of fruits, vegetables, whole grains, legumes, nuts, and olive oil, moderate consumption of fish and dairy, and limited intake of processed foods and added sugars, has become a benchmark against which other dietary patterns are measured. For children and adolescents specifically, the evidence has continued to grow in recent years, prompting researchers to ask not simply whether the diet matters, but how adherence is distributed across real populations of young people.

That distribution question is more important than it might initially appear. Traditional studies of diet and health often compute a single average adherence score for a population and then correlate it with an outcome such as mood, academic performance, or cardiometabolic health. Averages, however, can conceal as much as they reveal. If a school class contains a handful of students who follow a near-ideal Mediterranean pattern, a larger group with mediocre eating habits, and a substantial cluster who regularly skip breakfast and rely on ultra-processed snacks, the population average may land somewhere in the middle and describe no actual student at all. Latent class analysis addresses this problem directly by using probability models to sort individuals into unobserved categories based on their patterns of responses, allowing researchers to describe the genuine diversity of dietary behavior rather than flattening it into a single number.

The technique has a long pedigree in the social and health sciences. At its core, latent class analysis assumes that the observed variables, in this case indicators of dietary habits and breakfast consumption, are generated by an underlying categorical variable that cannot be measured directly. Statistical model-fitting procedures, typically evaluated with information criteria and related diagnostics, are used to determine how many classes best explain the observed data. Each adolescent is then assigned a probability of belonging to each class, and the classes are characterized by their response patterns. In the context of nutrition research, this means the method can distinguish, for example, a group of consistent breakfast eaters with high diet quality from a group of breakfast skippers with poor overall adherence, even when both groups exist within the same dataset and the same average score.

Why focus on breakfast? The meal has a distinctive status in adolescent nutrition research. It is the easiest dietary behavior to skip, particularly as sleep schedules shift later during puberty and morning time pressure increases. Decades of observational work have linked regular breakfast consumption to better concentration, improved nutrient intakes, and healthier body weight trajectories, although causal questions remain debated because breakfast eating correlates with many other favorable characteristics. By placing breakfast behavior at the center of a latent class framework, the new study positions the meal as a potential marker that helps define distinct dietary subgroups among adolescents, rather than as an isolated habit to be studied on its own.

The well-being dimension of the research connects to a rapidly expanding literature. A systematic review published in Nutrition Reviews in 2025 by Camprodon-Boadas and colleagues examined the relationship between Mediterranean diet and mental health in children and adolescents, adding to earlier work on physical health outcomes. In parallel, a 2024 systematic review and meta-analysis in JAMA Network Open by Lopez-Gil and colleagues assessed Mediterranean diet adherence against cardiometabolic biomarkers in young populations. Together, these strands of evidence suggest that diet quality in adolescence may matter not only for long-term physical health but for psychological functioning during a developmental window when mood disorders often first emerge. A method that can identify which adolescents deviate most from the protective dietary pattern could therefore sharpen both research and intervention design.

The methodological contribution of the Mitchell and Biasini paper lies in its explicit framing of heterogeneity. The authors argue, in effect, that adolescent adherence to the Mediterranean diet is not a single continuum but a set of distinguishable behavioral profiles, and that breakfast habits are woven into those profiles in ways that average-based analyses miss. This perspective has practical consequences. Public health messaging that treats all teenagers alike may resonate with the moderate majority while failing to reach the subgroups whose eating patterns diverge most sharply from recommendations. If latent class analysis can characterize those subgroups reliably, interventions can be tailored to the students who skip breakfast and consume few Mediterranean-style foods, rather than diluted across an entire school population.

It is worth emphasizing what the latent class approach does and does not establish. Like most dietary research in free-living humans, studies of this kind rest on observational data, and associations between eating patterns and well-being can be shaped by confounding factors such as family environment, socioeconomic status, sleep, physical activity, and mental health itself. A teenager who feels low may skip breakfast, and a teenager who skips breakfast may subsequently feel low; cross-sectional data cannot fully separate these directions. What the class-based approach offers is a more faithful descriptive map of the behavioral landscape, one that future longitudinal and experimental studies can use to test whether moving adolescents between classes, for example by supporting regular breakfast consumption, produces measurable improvements in well-being.

The publication also reflects a broader shift in nutritional epidemiology toward person-centered rather than variable-centered analysis. As datasets grow larger and richer, researchers increasingly recognize that population averages obscure the very variation that matters most for policy and clinical practice. The work by Mitchell and Biasini, published without external funding support and with the authors declaring no competing interests, contributes to this shift by applying a rigorous classification framework to a question of everyday relevance: who eats breakfast, who follows a Mediterranean pattern, and how those behaviors cluster together in adolescence. For parents, educators, and health professionals, the underlying message is familiar but newly precise. The teenagers who most need support are not an abstraction hidden inside an average; they are identifiable groups with characteristic habits, and better statistical tools are making them visible.

Subject of Research: Latent class analysis of adolescent breakfast habits and Mediterranean diet adherence in relation to well-being

Article Title: Linking breakfast to well-being: unmasking heterogeneity in adolescent adherence to the mediterranean diet using latent class analysis

Article References: Mitchell, W. B., & Biasini, B. (2026). Linking breakfast to well-being: unmasking heterogeneity in adolescent adherence to the mediterranean diet using latent class analysis. Pediatric Research. https://doi.org/10.1038/s41390-026-05425-2

Image Credits: AI Generated

DOI: 10.1038/s41390-026-05425-2

Keywords: adolescent health, Mediterranean diet, breakfast, latent class analysis, well-being, nutrition, pediatric research, diet quality, mental health, nutritional epidemiology, heterogeneity, public health

The research team, led by Lucía Camacho-Barcia and Fernando Fernández-Aranda of Bellvitge University Hospital and the Bellvitge Biomedical Research Institute in Barcelona, together with Jordi Salas-Salvadó of Universitat Rovira i Virgili, analysed data from 448 participants enrolled in the PREDIMED-Plus Cognition sub-study. Participants had a mean age of 65.3 years and were randomly assigned to one of two groups. The intensive intervention group received an energy-reduced Mediterranean diet combined with a physical activity programme and behavioural support, while the control group was advised to follow a Mediterranean diet ad libitum, meaning without any deliberate calorie restriction or structured support. The researchers tracked food addiction symptomatology using the Yale Food Addiction Scale 2.0, a validated instrument that applies criteria analogous to those used for substance-related disorders in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, alongside anthropometric measurements, diet and physical activity adherence, and quality of life at baseline and at one and three years.

Food addiction is not a formal diagnosis in current psychiatric classification manuals, but the construct has gained traction among researchers because it captures a cluster of behaviours that many patients with obesity describe: loss of control over eating, continued consumption despite negative consequences, unsuccessful attempts to cut down, and withdrawal-like distress when palatable foods are unavailable. The Yale Food Addiction Scale 2.0 operationalises these symptoms and allows researchers to quantify both the presence of a food addiction phenotype and the severity of symptoms on a continuous scale. Critics have long argued that the label risks medicalising ordinary overeating, while proponents counter that a subset of patients genuinely exhibits an addictive-like relationship with food, particularly with ultra-processed products engineered for high palatability. The new trial is notable because it examines this phenotype not in a laboratory or a specialist eating disorders clinic, but within one of the largest and most rigorous nutrition intervention trials ever conducted.

The results on symptom change were nuanced. Food addiction severity declined in both study arms over the three-year follow-up, which the authors interpret as partly reflecting the natural fluctuation of symptoms and the effects of study participation itself. However, only the intensive intervention group sustained those reductions to the three-year mark, and at that final assessment the intensive group had significantly lower food addiction scores than the control group, a difference that reached statistical significance at p equals 0.011. In other words, simply being advised to eat a Mediterranean diet freely was not enough to produce lasting change in addictive-like eating, whereas a structured, energy-restricted, behaviourally supported programme was. This pattern mirrors what addiction science would predict: sustained change in compulsive behaviours typically requires active, repeated intervention rather than passive advice.

Where the trial becomes particularly striking is in the stratified analysis by baseline food addiction status. Among participants who did not meet criteria for food addiction at the start of the study, the intensive intervention dramatically increased the odds of achieving clinically meaningful outcomes. The likelihood of losing at least eight percent of body weight was nearly tripled, with an odds ratio of 2.87 and a 95 percent confidence interval of 1.99 to 4.14. The odds of achieving at least a five percent reduction in waist circumference, a proxy for visceral adiposity and cardiometabolic risk, were similarly elevated, with an odds ratio of 3.01 and a confidence interval of 2.20 to 4.11. Improvements in adherence to the Mediterranean diet were even more pronounced, with participants without food addiction in the intensive arm showing an odds ratio of 5.82 for meaningful adherence gains, significant at p less than 0.001.

For participants with food addiction at baseline, the picture was considerably less encouraging. The intensive intervention still produced some benefit, and food addiction symptoms did improve, but the magnitude of weight loss, waist circumference reduction, and dietary adherence gains was attenuated compared with their counterparts without the phenotype. The researchers used structural equation modelling, a statistical technique that allows researchers to test hypothesised networks of causal pathways in observational and trial data, to explore how these variables related over the three-year period. The models indicated that improvements in Mediterranean diet adherence mediated, or statistically explained, the long-term improvements in body weight, waist circumference, and quality of life, but only in individuals without food addiction. In the food addiction group, that mediating pathway was absent or substantially weakened, suggesting that the behavioural mechanism through which the diet programme usually works was disrupted.

These findings have immediate implications for how clinicians and researchers think about personalised obesity medicine. If food addiction marks a subgroup of patients who respond less well to standard lifestyle interventions, then screening for it at the outset of treatment could identify who needs additional or different support, perhaps drawing on techniques from addiction treatment such as cognitive behavioural therapy, motivational interviewing, or pharmacological approaches that target craving and reward circuitry. The study’s authors frame food addiction as a clinically relevant behavioural phenotype, and the trial provides the kind of longitudinal, randomised evidence that has been largely missing from a debate often fuelled by cross-sectional studies and self-selected samples. It is one thing to show that people with addictive-like eating differ cross-sectionally from others; it is quite another to show, in a randomised framework over three years, that the phenotype predicts differential adherence and differential benefit from a specific intervention.

The trial also speaks to the ongoing scientific controversy over ultra-processed foods and their role in addictive eating. Although the published report focuses on the intervention effects rather than on specific food categories, the food addiction construct is closely entwined with research on ultra-processed products, which are typically high in refined carbohydrates and fats and are thought to hijack reward pathways in ways that whole foods do not. The Mediterranean diet, rich in olive oil, nuts, legumes, fish, vegetables, and whole grains, represents almost the nutritional opposite of the ultra-processed food environment, and the marked adherence improvements in the intensive group suggest that replacing the food environment, with support, is feasible even in older adults. That feasibility matters, because much of the food addiction literature has been criticised for documenting the problem without testing solutions.

Several limitations deserve attention when weighing the findings. The participants were older adults with metabolic syndrome enrolled in a cardiovascular prevention trial, so generalisation to younger populations or to patients with severe obesity remains untested. Food addiction was measured by self-report questionnaire rather than clinical interview, and the construct itself remains scientifically contested. The structural equation models, while sophisticated, describe statistical associations consistent with mediation rather than proving causal chains. The trial was registered with the International Standard Randomized Controlled Trial Number registry as ISRCTN 89898870 in July 2014, and the analysis was embedded within the broader PREDIMED-Plus Cognition sub-study, meaning the food addiction assessment was added to a trial designed primarily for other endpoints. None of these caveats undermines the central result, but they do bound the conclusions.

What makes the study resonate beyond the specialist literature is its reframing of a familiar clinical frustration. Weight-loss programmes fail for many people, and clinicians have long observed that some patients seem unable to sustain adherence no matter how well-designed the programme. This trial provides prospective, randomised evidence that one measurable psychological phenotype, food addiction, predicts exactly that pattern of attenuated response, while simultaneously showing that the phenotype itself is not fixed: symptoms improved under intensive intervention. The dual message, that food addiction both limits standard treatment response and can itself be treated, points toward a future in which obesity care begins with a brief behavioural assessment and routes patients toward the intensity and type of support their profile requires. For a field searching for ways to move beyond one-size-fits-all dietary advice, that is a genuinely consequential step.

Subject of Research: The effect of an intensive energy-reduced Mediterranean diet lifestyle intervention on food addiction symptoms and weight-loss outcomes in older adults with overweight or obesity and metabolic syndrome

Article Title: Targeting food addiction through an intensive energy-reduced Mediterranean diet lifestyle intervention: evidence from the 3-year PREDIMED-plus trial

Article References: Camacho-Barcia, L., Jimenez-Murcia, S., Granero, R., de la Torre, R., Babio, N., Pintó, X., Corella, D., Gazzoli, S., Frances, F., Riera-Mestre, A., Fitó, M., Cuenca-Royo, A., Gómez-Martínez, C., Gearhardt, A. N., Forcano, L., Salas-Salvadó, J., & Fernández-Aranda, F. (2026). Targeting food addiction through an intensive energy-reduced Mediterranean diet lifestyle intervention: evidence from the 3-year PREDIMED-plus trial. BMC Medicine. https://doi.org/10.1186/s12916-026-05283-z

Image Credits: AI Generated

DOI: 10.1186/s12916-026-05283-z

Keywords: food addiction, Mediterranean diet, PREDIMED-Plus, obesity, weight loss, metabolic syndrome, Yale Food Addiction Scale 2.0, lifestyle intervention, dietary adherence, quality of life, randomized controlled trial, personalised nutrition

The research team, led by Zoltan Ungvari of the University of Oklahoma Health Sciences Center and Semmelweis University together with colleagues across Hungary, Italy, Spain, and the United States, pooled data from 34 observational studies identified through a systematic search of PubMed, Web of Science, and Scopus covering publications through September 2025. From an initial haul of 12,530 records, the investigators winnowed the field down to studies that measured adherence to a Mediterranean-style dietary pattern using validated scoring instruments and reported quantitative risk estimates for one of the three cancer types. The final dataset encompassed 4,286,835 participants, making it one of the largest syntheses ever assembled on diet and these malignancies.

The statistical approach was deliberately conservative. The team used random-effects models with the inverse variance method, which allows the true effect to vary from study to study rather than assuming a single fixed value. For head and neck cancer, fourteen cohorts yielded a pooled relative risk of 0.55, with a 95 percent confidence interval of 0.45 to 0.67. Thirteen studies of gastric cancer produced a pooled relative risk of 0.62 (95 percent CI 0.53 to 0.73), and eleven studies of liver cancer produced a relative risk of 0.59 (95 percent CI 0.53 to 0.67). All three estimates were statistically significant, and the confidence intervals for each excluded the null value of 1.0, indicating that the associations are unlikely to be explained by random variation alone.

Not every result was equally robust, however. The analysis revealed substantial statistical heterogeneity for head and neck cancer, with an I-squared value of 90 percent, meaning that nine-tenths of the variability among study results arose from real differences between studies rather than chance. Gastric cancer showed similarly high heterogeneity at 76 percent. In contrast, the liver cancer analysis was far more consistent, with only moderate heterogeneity (I-squared of 35 percent), suggesting that the protective association for hepatocellular carcinoma was remarkably uniform across populations, designs, and dietary assessment methods. This consistency, combined with a symmetric funnel plot and a non-significant Egger’s test for liver cancer, makes the hepatic findings arguably the most trustworthy of the three.

For head and neck and gastric cancers, the picture is more complicated. Funnel plot asymmetry and significant Egger’s tests pointed to potential publication bias or small-study effects, meaning that smaller studies reporting stronger protective associations may have been more likely to reach the published literature. The authors explicitly declined to apply trim-and-fill corrections, reasoning that funnel plot asymmetry can stem from genuine heterogeneity as well as selective publication, and that imputed bias-adjusted estimates would be unreliable given the limited number of studies. They caution that the true magnitude of protection for these two cancer types may be more modest than the headline numbers suggest.

Why would a single dietary pattern influence cancers as anatomically distinct as tumors of the mouth, throat, stomach, and liver? The answer likely lies in shared biology. Chronic inflammation and oxidative stress are central drivers of carcinogenesis across the digestive tract and upper aerodigestive system, and the Mediterranean diet is exceptionally rich in compounds that counter both: fiber, polyphenols, carotenoids, omega-3 fatty acids, and monounsaturated fats. For liver cancer specifically, metabolic dysfunction, insulin resistance, and fatty liver disease are key etiological pathways, and the Mediterranean diet has been shown to improve insulin sensitivity, reduce hepatic steatosis, and dampen systemic inflammation—offering a coherent mechanistic account for the particularly consistent association observed there.

The gut microbiome adds another layer of plausibility. A diet abundant in plant foods, fiber, and polyphenols reshapes microbial community structure and function, alters the production of microbial metabolites such as short-chain fatty acids, strengthens intestinal barrier integrity, and modulates systemic inflammatory signaling. These effects are directly relevant to gastrointestinal malignancies and, through the gut-liver axis, to hepatocellular carcinoma as well. From a geroscience perspective, the authors note that these same pathways—inflammaging, metabolic dysregulation, cellular senescence, immunosenescence, and epigenetic alteration—intersect with the biology of aging itself, positioning Mediterranean diet adherence as a single modifiable exposure that may simultaneously influence cancer susceptibility and other age-related chronic diseases.

For head and neck cancers, where tobacco and alcohol dominate the risk landscape, the diet may work both directly and indirectly. Mediterranean-style eating limits salt, processed meats, and refined foods while increasing protective bioactive compounds, but it also tends to cluster with broader healthy behaviors—lower smoking, moderate alcohol consumption, higher physical activity, and greater engagement with preventive healthcare. The authors are candid that this healthy-adherer phenomenon represents a serious residual confounding concern. Although individual studies adjusted for major measured confounders, adjustment strategies varied, and unmeasured lifestyle factors cannot be excluded. Some portion of the observed association may therefore reflect the overall phenotype of people who eat this way rather than the diet alone.

Methodological limitations temper the findings further. Dietary intake was assessed almost entirely through self-reported food frequency questionnaires, which are vulnerable to recall and measurement error, and the Mediterranean diet scoring systems varied across studies, from classic MedDiet scores to the Healthy Eating Index 2015. Pooling relative risks, odds ratios, and hazard ratios as approximations of a common association is reasonable for rare outcomes but introduces minor imprecision. The review protocol was not prospectively registered, though eligibility criteria and analytical plans were defined before the quantitative synthesis was completed, and reporting followed the PRISMA framework.

Even with these caveats, the public health implications are considerable. Unlike single-nutrient interventions, which have repeatedly disappointed in trials, the Mediterranean diet is a feasible, culturally adaptable framework with already established cardiometabolic benefits—and now growing evidence of oncologic protection that extends the earlier, robust findings for colorectal cancer. The convergence of cardiovascular, metabolic, and cancer-preventive effects within one dietary pattern makes it a uniquely efficient target for population-level prevention. The stakes are especially high in Central and Eastern Europe: Hungary, for instance, records among the highest cancer mortality rates in the European Union, with gastric cancer mortality exceeding the EU average and fruit and vegetable consumption among the lowest. In such high-burden settings, promoting Mediterranean-style eating could offer a scalable, cost-effective strategy against not only gastrointestinal cancers but also cardiovascular disease, stroke, and potentially dementia. The authors call for large prospective cohorts with repeated dietary assessments, standardized scoring systems, and objective biomarkers such as circulating fatty acid profiles and polyphenol metabolites to firm up the causal case. Until then, the message is one of cautious optimism: the same plate that protects the heart may, it appears, help guard the stomach, liver, and throat as well.

Subject of Research: Association between Mediterranean diet adherence and reduced risk of head and neck, gastric, and liver cancers

Article Title: Adherence to the Mediterranean diet is associated with reduced risk of head and neck, gastric, and liver cancers: a systematic review and meta-analysis

Article References: Ungvari, Z., Fekete, M., Varga, P., Lehoczki, A., Grosso, G., Godos, J., Murmu, A., Ocana, A., Kiss, C., & Győrffy, B. (2026). Adherence to the Mediterranean diet is associated with reduced risk of head and neck, gastric, and liver cancers: a systematic review and meta-analysis. GeroScience. https://doi.org/10.1007/s11357-026-02525-z

Image Credits: AI Generated

DOI: 10.1007/s11357-026-02525-z

Keywords: Mediterranean diet, head and neck cancer, gastric cancer, liver cancer, hepatocellular carcinoma, cancer prevention, meta-analysis, systematic review, nutritional epidemiology, dietary patterns, inflammation, gut microbiome

The review, published open access on 3 October 2026, set out to bring order to a literature that has produced stubbornly inconsistent results. Rather than running a new experiment, the authors conducted a comprehensive search of three major bibliographic databases, PubMed, Scopus, and Web of Science, hunting for quantitative studies published between 2000 and November 2024 that measured diet quality in adult immigrants and compared it against a meaningful reference group. That comparison could take one of three forms: immigrants versus the native-born population of the destination country, immigrants versus the native-born population of their country of origin, or the same individuals measured before and after migration. Only studies meeting these criteria, framed by the authors in a Population, Exposure, Comparator, Outcome, Study design, or PECOS, structure, were eligible.

Nineteen studies survived the screening process. That number may sound modest for a field as globally significant as migration and health, but it reflects how demanding the inclusion criteria were: the studies had to use validated quantitative indices of diet quality rather than loose proxies such as single food items or self-reported general eating habits, and they had to include an explicit non-migrant comparison group. Fifteen of the nineteen studies compared immigrants with the native-born population of their destination country. Within that group, seven studies found immigrants had higher diet quality, two found lower diet quality, and the remaining six reported mixed results, with outcomes differing either between immigrant groups or between the different diet quality indices used to score the same diets.

The second comparison strategy yielded a similarly nuanced picture. Five studies compared immigrants with the native-born residents of their countries of origin, effectively asking whether moving to a wealthier country improved the quality of what people ate relative to those who stayed behind. Three of those studies found immigrants eating better, one found them eating worse, and one found no significant difference at all. Finally, a single study took the most direct approach of all, tracking diets before and after immigration, and observed a decline in diet quality following the move. That lone longitudinal data point is a reminder that the aggregate statistics can conceal real individual trajectories of dietary deterioration.

Why would immigrants so often out-eat their new neighbors? The authors point to a cluster of mechanisms that researchers have been refining for decades. Many migrants arrive from food cultures built around home-cooked meals, fresh produce, legumes, and traditional dietary patterns that happen to align well with modern healthy eating indices such as the Alternative Healthy Eating Index, the Alternate Mediterranean Diet score, or the Healthy Eating Index. Compared with the highly processed, convenience-driven diets common in high-income destination countries, those inherited patterns can look remarkably protective. The review’s finding that most immigrant groups showed higher diet quality than non-migrants is consistent with this interpretation: the baseline diet a person brings with them can be better than the one waiting for them at the destination.

But the same review shows how quickly that advantage can erode, and for whom. The studies that reported poorer diet quality among immigrants concentrated in socioeconomically underprivileged groups, where the forces that shape eating are less about cultural heritage and more about budget, time, and access. The authors identify length of residence in the destination country as a key variable, reflecting the well-documented process of dietary acculturation: as migrants spend more years in a new food environment, their diets tend to converge toward local norms, and not always in a healthy direction. Educational attainment, financial status, and occupational conditions also emerged as contributing factors, as did food culture itself, the shared expectations and practices that determine what a family considers a proper meal.

Methodology matters too, and the review is unusually candid about this source of heterogeneity. Diet quality is not a single measurable quantity like blood pressure; it is a constructed score, and different indices weight different things. The studies included in the review used a wide array of instruments, among them the Healthy Eating Index, the Alternative Healthy Eating Index, the Alternate Mediterranean Diet score, the Diet Quality Index and its international variant DQI-I, the Dietary Diversity Score, the Food Variety Score, the Dietary Guidelines Index-2013, the Healthful Plant-based Diet Index, and the Pyramid-based Mediterranean Diet Score. A diet that scores well on a Mediterranean-style index might score only modestly on a diversity-based measure, and vice versa. Six of the fifteen destination-country comparisons reported mixed results precisely because different indices or different migrant subgroups produced different verdicts within the same study.

The practical implications reach well beyond academic taxonomy. Public health agencies in immigrant-receiving countries often design nutrition interventions on the assumption that migrants are a uniformly vulnerable population, and this review complicates that assumption in a useful way. If most immigrant groups eat better than their non-migrant neighbors, blanket dietary warnings aimed at migrant communities may miss the mark. The groups that genuinely need support are identifiable and specific: those facing economic precarity, those who have lived in the destination country long enough for dietary acculturation to take hold, and those whose food culture has been disrupted without being replaced by an equally healthy alternative. Targeted interventions grounded in socioeconomic status and length of residence, the review suggests, would be far more efficient than one-size-fits-all messaging.

There is also a broader scientific lesson in the paper’s structure. By explicitly separating the three comparison frames, destination-country natives, origin-country natives, and pre-migration baselines, the authors show that the question “do immigrants eat better or worse?” is not one question but three, and answers to one frame do not transfer to the others. An immigrant may eat better than a stay-at-home compatriot while eating worse than their new next-door neighbor, and both facts can be true simultaneously because the reference points measure different things: the effect of leaving versus the effect of arriving. The single before-and-after study, showing a decline in diet quality after migration, hints that the transition itself, with its stress, changed schedules, and unfamiliar food markets, may push diets downward even when the destination country offers greater abundance.

The review’s conclusion distills all of this into a single framing that is likely to shape future research: diet quality among immigrants is a function of multiple social, cultural, and economic factors, with socioeconomic status standing out as especially decisive. That is a more sophisticated picture than the simple narrative of migration as either dietary rescue or dietary ruin, and it sets a clear agenda. Future studies, the authors imply, should stop asking whether migrants eat well and start asking which migrants, under which conditions, measured with which instruments, and at what point in their migration journey. With international migration continuing to reshape the demographics of nearly every high-income country, the answer to that refined question will help determine whether the food systems of destination countries become a source of health for newcomers or another axis along which inequality is written into the body.

Subject of Research: Comparative diet quality of adult immigrants versus non-migrant populations

Article Title: Diet quality of adult immigrants compared with non-migrants: a systematic review of quantitative studies

Article References: Kohanmoo, A., & Mirfardi, A. (2026). Diet quality of adult immigrants compared with non-migrants: a systematic review of quantitative studies. BMC Public Health. https://doi.org/10.1186/s12889-026-29748-1

Image Credits: AI Generated

DOI: 10.1186/s12889-026-29748-1

Keywords: diet quality, immigrants, migration, systematic review, public health, nutrition, dietary acculturation, socioeconomic status, Healthy Eating Index, Mediterranean diet, food culture, BMC Public Health

The authors of the response, led by researchers affiliated with the Center for Epidemiological Studies in Health and Nutrition at the University of São Paulo, include Carlos A. Monteiro, the epidemiologist who first proposed the Nova classification in the late 2000s. Their critics contend that ultra-processed foods, or UPFs, lump together harmful and benign products in a way that makes causal inference and policy unreliable. The São Paulo team counters that this criticism rests on a fundamental misunderstanding of what Nova measures and how the epidemiological evidence has been generated.

Nova, they explain, does not classify foods by nutrient composition, biochemical coherence, or expected biological effects. Instead, it sorts foods into four groups according to the extent and purpose of industrial processing: fresh and minimally processed foods, processed culinary ingredients, processed foods, and ultra-processed foods. The standard exposure metric used in most prospective studies is the dietary share of UPFs, meaning the proportion of total energy intake derived from Group 4 products. This metric, the authors argue, captures the health effects of the ultra-processed dietary pattern as a whole, reflecting the real-world displacement of the first three Nova groups, which form the basis of traditional healthy diets, by industrially formulated products.

The response draws an analogy with the Mediterranean diet to defuse the charge of heterogeneity. Foods within the Mediterranean pattern differ widely in nutrient profiles, texture, palatability, and potential health effects when considered in isolation, yet they are routinely grouped as a single dietary exposure in epidemiological studies and dietary guidelines. Variability within a category, the authors insist, does not invalidate the category. The same logic applies to ultra-processed foods: heterogeneity within the pattern does not undermine its relevance as a dietary exposure or as a target for policy.

Central to the São Paulo group’s argument is the claim that harmful attributes co-occur systematically in ultra-processed foods as a consequence of the manufacturing processes and ingredients needed to achieve their commercial purpose. These attributes include disrupted food matrices and excessive energy density that accelerate eating and increase energy intake; engineered hyper-palatable formulations that override satiety signals; additives such as emulsifiers and non-sugar sweeteners that have been linked to gut and metabolic dysfunction; and toxic industrial contaminants, including chemicals that leach from plastic packaging. Nutrient imbalances, they argue, are largely a downstream consequence of the expansion of this dietary pattern rather than its defining feature, which is why a nutrient-by-nutrient approach is insufficient to explain or reverse the global rise of diet-related chronic disease.

The authors also reject the criticism that the mechanisms linking ultra-processed foods to health outcomes are too non-specific to be meaningful. Mechanisms linking dietary patterns to health outcomes, they note, do not need to be specific: the beneficial effects of the Mediterranean diet are not discounted simply because fibre, unsaturated fats, and antioxidant compounds also appear in other dietary patterns. What matters is that harmful attributes are more prevalent and more systematically combined in ultra-processed diets than in traditional diets based on Nova Groups 1 through 3. Beyond driving nutrient imbalances and energy-dense eating, ultra-processed food intake is inversely associated with health-protective compounds such as flavonoids and phytoestrogens, and directly associated with processing-generated toxic compounds and potentially harmful additives. Soft textures, reduced chewing frequency, and faster eating rates further facilitate excess energy intake, and some researchers have argued that many ultra-processed products meet established criteria for addictive substances.

Crucially, the response points to experimental evidence that directly tests whether the health effects of ultra-processed diets can be explained away by poor nutrient profiles. Dozens of prospective studies have found associations with chronic disease even after adjusting for fibre, sodium, sugar, and saturated fat. Randomised crossover trials have shown that ultra-processed diets lead to higher energy intake and weight gain even when meals are matched for key nutrients. A recent UK trial found that non-ultra-processed diets adhering to national dietary guidelines produced better cardiometabolic outcomes than ultra-processed diets modified to meet the same criteria, a result the authors say reinforces the conclusion that reformulation does not neutralise harm.

On the charge that epidemiological studies rely on unrealistic comparisons and are confounded by other dietary components, the authors argue that the criticism inverts the logic of nutritional epidemiology. Dietary pattern analyses are not designed to isolate the effects of specific foods or nutrients; they estimate the health effects of real-world diets with high versus low ultra-processed food intake, implicitly capturing the displacement of unprocessed and minimally processed foods. Paradoxically, they contend, analyses of specific ultra-processed subgroups are more vulnerable to confounding, because they attempt to compare individual products against their non-ultra-processed counterparts within complex diets. Measurement error, meanwhile, is mitigated by validated protocols and trained raters, and its non-differential nature tends to underestimate true associations rather than fabricate false ones.

The authors concede a nuance on comparators: in countries such as the United Kingdom and the United States, where traditional diets based on Nova Groups 1 through 3 are no longer the default, comparisons between ready-to-consume processed and ultra-processed products may be relevant, and a more incremental policy approach starting with feasible targets may be warranted. But they stress that the Lancet Series was not designed for these settings alone. In most countries, cooked meals still predominate, and the evidence on the health effects of displacing traditional diets with ultra-processed products is particularly relevant. Early comprehensive policies targeting all ultra-processed foods, they argue, could help other nations avoid the dietary crises observed in the UK and US.

The policy implications are stark. The authors acknowledge that nutrient-focused interventions, such as trans-fat bans, sodium front-of-package warnings, and taxes on sugar-sweetened drinks, are valuable but insufficient, because they operate within the existing corporate food system and encourage reformulation without addressing the underlying production model. Removing trans fat does not eliminate other industrial contaminants; reducing salt does nothing to address energy density, soft texture, and engineered hyper-palatability; and cutting sugar often means increasing amounts of harmful additives. Several countries have already incorporated Nova into their dietary guidelines and implemented policies targeting ultra-processed foods, actions the authors say are justified by more than one hundred prospective studies, randomised trials, and mechanistic investigations. Scientific uncertainty, they conclude, should always be acknowledged, but it should not be conflated with complexity, nor should heterogeneity within a meaningful category justify inaction. In their view, the case for treating ultra-processed foods as a systemic driver of the pandemic of diet-related chronic disease is robust, and policy responses should reflect that reality.

Subject of Research: Scientific debate over the Nova classification of ultra-processed foods and the evidence linking them to human health outcomes

Article Title: Response to: Debate in relation to “Ultra‑processed foods and human health: the main thesis and the evidence”

Article References: Rezende, L. F. M., da Costa Louzada, M. L., Martinez-Steele, E., Cannon, G., Levy, R. B., Jaime, P. C., & Monteiro, C. A. (2026). Response to: Debate in relation to “Ultra‑processed foods and human health: the main thesis and the evidence”. BMC Medicine, 24(1), Article 525. https://doi.org/10.1186/s12916-026-05217-9

Image Credits: AI Generated

DOI: 10.1186/s12916-026-05217-9

Keywords: ultra-processed foods, Nova classification, dietary patterns, nutritional epidemiology, public health policy, chronic disease, food industry, randomised trials, food additives, Mediterranean diet, BMC Medicine, dietary guidelines

The research involved 171 school-aged children drawn from five primary schools in Spain, assessed between January and March 2025. The design was deliberately comprehensive. Each child underwent standardized anthropometric assessment following the International Standards for Anthropometric Assessment, including weight, height, and calculation of BMI-for-age z-scores referenced against World Health Organization growth data and CDC growth charts. Blood pressure was measured and interpreted according to the fourth report of the National High Blood Pressure Education Program Working Group, the reference standard for pediatric hypertension screening. Dietary quality was captured with the KIDMED index, a sixteen-point instrument developed by Serra-Majem and colleagues that scores adherence to the Mediterranean dietary pattern, long considered the gold-standard model of healthy eating in the region. Parents and children also reported dietary intake, which the researchers converted into percentages of recommended energy and nutrient targets using the Spanish food composition database BEDCA and European Food Safety Authority dietary reference values.

On the headline question, the results were mixed but informative. Children attending the school cafeteria scored a mean of 5.55 points on the KIDMED Mediterranean diet index, compared with 4.80 among non-attendees, with standard deviations of 3.32 and 3.69 respectively. That difference, while directionally favorable to the cafeteria group, was modest in absolute terms and sits against a sobering backdrop: both scores fall well below what would indicate strong adherence to a dietary pattern associated with lower cardiovascular and metabolic risk. Recent meta-analyses of Spanish youth have documented a worrying decline in Mediterranean diet adherence, and this study’s numbers, hovering near the middle of the scale, are consistent with that national trend. In other words, the cafeteria may nudge children in the right direction, but neither group of children is eating particularly well by the standards of the traditional Mediterranean pattern.

Perhaps the most counterintuitive finding concerns what the children who ate at home were actually consuming. Non-attendees reported higher energy intake, at 108.3 percent of recommended levels compared with 94.4 percent for cafeteria users, and markedly higher lipid intake, at 128.5 percent of recommendations versus 105.9 percent, a difference that reached statistical significance with a p-value of 0.006. The home-fed group also reported higher intakes of several micronutrients, with differences significant at p below 0.05. The authors interpret this pattern as suggestive of a more energy-dense dietary profile among children eating at home, one that delivers abundant calories and fat alongside certain micronutrients. That combination is precisely the signature epidemiologists associate with the modern obesogenic diet: plentiful energy and fat, often from processed and palatable foods, rather than the balanced, lower-energy-density pattern the Mediterranean model prescribes.

Yet when the researchers turned to the physical measurements, the expected differences largely failed to materialize. BMI-for-age z-scores and blood pressure did not differ significantly between cafeteria attendees and non-attendees, with p-values above 0.05. The one anthropometric exception was weight percentile, which did differ significantly between the groups at p below 0.001, though the cross-sectional design of the study makes it impossible to determine whether cafeteria attendance influenced weight, whether families with children of different weights choose cafeteria use differently, or whether some third factor, such as household income or parental work schedules, drives both. This is the fundamental limitation of cross-sectional evidence: it captures a snapshot, not a causal pathway, and self-selection into school meal programs is well documented in the international literature.

Where the study truly broke new ground was in its analysis of the school menus themselves, and specifically their cost. The researchers assessed the nutritional composition of the menus on offer and the daily cost per child, then tested whether these variables related to children’s intake and health indicators. The results were emphatic. Menu cost and school type, whether public, state-funded private, or fully private, were significantly associated with nutrient intake, anthropometric percentiles, and Mediterranean diet adherence, all at p below 0.001. In plain terms, the price tag attached to a school’s lunch program appeared to travel through the food on the plate and into the bodies and health markers of the children eating it. This is a socioeconomic gradient rendered in nutrients and percentiles, and it echoes a growing body of European and global evidence that school food quality varies systematically with the resources behind it.

The implications of that finding reach well beyond Spain. A 2026 review of school meal quality across twenty-nine countries published in Public Health Nutrition documented wide international variation in what schools actually serve, and a 2025 scoping review in Obesity Reviews found that affordability was a recurring fault line in European school food policy. Spain itself has made childhood obesity a national priority, with a strategic plan running from 2022 to 2030 and the long-standing NAOS strategy on nutrition, physical activity, and obesity prevention. The ALADINO 2023 national survey continues to document substantial rates of childhood overweight and obesity, with socioeconomic status among the strongest predictors. Against that backdrop, the Cordoba team’s suggestion that minimum per-child spending on school menus might need to be standardized is a policy proposal with real teeth, because it targets the resource gap that their data suggest is shaping what children eat.

The international evidence on school meals more broadly supports the idea that these programs can be powerful equity tools, particularly for food-insecure children. Systematic reviews of universal free school meal policies in the United States, including a 2024 review in JAMA Network Open and a 2021 synthesis in Nutrients, have found benefits for diet quality, food security, and school participation, with more limited and inconsistent effects on body mass index. Studies of the Healthy, Hunger-Free Kids Act published in JAMA in 2020 showed measurable improvements in dietary quality among participants in the US National School Lunch Program. Reviews spanning low- and middle-income countries have documented benefits for both educational and health outcomes. The Spanish study fits neatly into this literature: it finds dietary signals consistent with benefit, no dramatic anthropometric effects, and a strong suggestion that the quality of what is served, not merely whether it is served, determines the outcome.

Several caveats deserve emphasis before the findings are translated into policy. The sample of 171 children from five schools is small and geographically concentrated, and the cross-sectional design cannot establish that cafeteria meals caused the observed differences in diet quality or weight percentiles. Dietary intake data relied on reported consumption, a method inherently vulnerable to recall and social desirability bias, particularly in children. The KIDMED index, while widely used, is a screening tool rather than a full dietary assessment. And the significant differences in micronutrient intakes favoring the home-fed group complicate any simple narrative that cafeteria eating is uniformly healthier; the pattern more likely reflects overall dietary volume and composition than the cafeteria meal itself. Longitudinal and intervention studies, ideally with objective dietary measures and sufficient power to detect changes in growth trajectories, would be needed to confirm causal pathways.

Even with those limitations, the study lands at a consequential moment. Global analyses from the NCD Risk Factor Collaboration published in The Lancet in 2024 documented that more than 370 million children and adolescents worldwide now live with obesity, a figure that has risen relentlessly since 1990, and pediatric obesity is firmly linked to long-term cardiovascular, metabolic, and psychological consequences. School food environments remain one of the few settings where nearly all children, regardless of family circumstances, can be reached daily. The Spanish findings refine the message for policymakers: simply having a cafeteria is not enough, and the modest dietary advantage observed among attendees suggests that well-designed school meals can gently steer children toward better patterns. But the strong associations between menu cost, school type, and nearly every nutritional outcome measured indicate that the deeper variable is investment. If school meals are to function as an equity instrument, the authors’ case for guaranteeing a minimum standard of per-child spending may prove to be the study’s most important contribution.

Subject of Research: Associations between school cafeteria attendance, dietary intake, and nutritional status in Spanish primary school children

Article Title: Associations between school meal attendance, dietary intake and nutritional status in Spanish school-aged children: a cross-sectional study

Article References: Uclés-Torrente, M. D. M., Ruiz-Gamarra, G. E., Alcalde-Llergo, J. M., Vaquero-Álvarez, M., Blancas-Sánchez, I. M., Aparicio-Martínez, P., & Vaquero Abellán, M. (2026). Associations between school meal attendance, dietary intake and nutritional status in Spanish school-aged children: a cross-sectional study. Pediatric Research. https://doi.org/10.1038/s41390-026-05442-1

Image Credits: AI Generated

DOI: 10.1038/s41390-026-05442-1

Keywords: school meals, childhood obesity, Mediterranean diet, pediatric nutrition, school cafeteria, dietary intake, nutritional status, menu cost, socioeconomic gradient, KIDMED index, Spain, public health

Obesity has long been recognized as a state of chronic low-grade inflammation, a smoldering immune activation that contributes to insulin resistance, fatty liver disease, and cardiovascular risk. At the same time, obesity is marked by circadian disruption: the molecular clocks that orchestrate daily cycles of metabolism, hormone secretion, and immune activity fall out of sync. What has remained unclear is whether these two phenomena are merely parallel consequences of excess weight or whether they are mechanistically intertwined, and, crucially, whether a dietary intervention can pull both back into alignment at the same time.

The new study, led by Claudia Pivonello and senior author Annamaria Colao, set out to address exactly that question. Thirty-eight adults with obesity completed a twelve-week hypocaloric Mediterranean diet program. Before and after the intervention, the researchers collected detailed anthropometric and metabolic measurements, including body weight, body mass index, waist circumference, fat mass percentage, fat-free mass, muscle mass, and HDL cholesterol. They also assessed each participant’s chronotype using the Morningness–Eveningness Questionnaire, a validated instrument that captures whether a person’s natural tendencies lean toward morning or evening activity.

The most technically ambitious part of the study involved the participants’ peripheral blood mononuclear cells, or PBMCs, a mixed population of immune cells that includes lymphocytes and monocytes. Blood samples were drawn at two fixed time points, eight in the morning and four in the afternoon, allowing the researchers to track how gene expression shifted across the day. Using quantitative reverse-transcription PCR, they measured the expression of five core clock genes: BMAL1, PER1, PER2, CRY1, and CRY2. These genes form the interlocking feedback loops that constitute the molecular circadian oscillator, with BMAL1 acting as the positive driving element and the PER and CRY proteins as the negative limbs that restrain its activity on a roughly twenty-four-hour cycle. Alongside the clock genes, the team quantified expression of two innate immune receptors, TLR4 and TLR8, members of the Toll-like receptor family that detect microbial components and trigger inflammatory signaling.

The metabolic results were consistent with what clinicians have come to expect from a well-executed Mediterranean diet intervention. Participants showed significant reductions in body weight, body mass index, waist circumference, and fat mass percentage, together with increases in fat-free mass, muscle mass, and HDL cholesterol. Their MEQ scores also rose significantly, indicating a shift toward greater morningness, although the distribution of chronotype categories did not change in a statistically significant way. In other words, participants drifted somewhat toward morning preference without crossing into a new chronotype classification.

The molecular findings were more striking. At baseline, before any dietary change, expression of TLR4 and TLR8 in PBMCs was significantly higher in the afternoon than in the morning, a diurnal pattern in innate immune receptor expression that the researchers documented for the first time in this cohort. After twelve weeks of the Mediterranean diet, the picture had changed in a coordinated fashion. BMAL1 expression increased significantly in the morning samples, while PER1, TLR4, and TLR8 expression decreased significantly in the afternoon samples. Moreover, all five clock genes examined, BMAL1, PER1, PER2, CRY1, and CRY2, displayed a more pronounced morning-to-afternoon expression pattern following the intervention, which the authors interpret as evidence of improved diurnal organization of the peripheral clock.

Perhaps the most intriguing observation was the correlation structure linking the two systems. The researchers found significant positive correlations between BMAL1 expression and both TLR4 and TLR8 expression at both sampling time points. This statistical relationship supports the hypothesis of a bidirectional interaction between the molecular clock and innate immune pathways, a connection that has been suggested by animal and cellular studies but rarely examined in the context of a human dietary intervention. If BMAL1 activity helps govern the daily rhythm of Toll-like receptor expression, then dietary signals that strengthen the clock could, in principle, dampen the inappropriate immune activation that characterizes obesity.

The authors frame their results as evidence of partial restoration of diurnal–immune homeostasis. Increased morning BMAL1 together with reduced afternoon TLR4 and TLR8 suggests that the intervention did not simply suppress inflammation indiscriminately but instead rebalanced the temporal architecture of immune readiness. They propose that dietary modulation of what they call the BMAL1–TLR axis may represent a mechanism linking metabolic improvement to diurnal regulation, and they identify peripheral clock gene expression as a potential translational biomarker of response to lifestyle interventions. If validated, such a biomarker could allow clinicians to monitor, at the level of gene expression in a simple blood draw, whether a patient’s body clock and immune system are responding to dietary therapy.

Important caveats temper these conclusions. The study lacked a comparator arm, meaning there was no control group of patients with obesity who did not receive the intervention or who received an alternative diet. Without such a group, the findings must be interpreted as associations rather than proof of causation, and the authors are explicit on this point, calling for confirmation in randomized controlled studies. The sample size of thirty-eight participants, while adequate for an exploratory interventional design, is modest, and the two-time-point sampling strategy captures only a coarse snapshot of the full twenty-four-hour rhythm. The study was registered at ClinicalTrials.gov as NCT06236932 and was approved by the Ethical Committee of Federico II University of Naples, and it was funded by the Italian Ministry of University and Research through a Projects of Relevant National Interest grant.

Even with those limitations, the study adds a compelling piece to a rapidly growing body of work on the circadian–immune axis. It suggests that the Mediterranean diet, already celebrated for its cardiovascular and metabolic benefits, may exert part of its influence by entraining the peripheral clocks embedded in immune cells and by smoothing out the aberrant daily oscillations of innate immune receptors. For patients with obesity, the practical message is familiar but now carries deeper mechanistic weight: what you eat, and presumably when you eat it, may help decide not only how much you weigh but how well your body’s internal timekeeping and immune surveillance work together. For researchers, the message is that the blood-borne clock may be a readable, and potentially modifiable, target of nutritional therapy.

Subject of Research: Effects of a hypocaloric Mediterranean diet on circadian clock gene and innate immune receptor expression in patients with obesity

Article Title: A 12-week hypocaloric Mediterranean diet is associated with metabolic improvement and modulation of diurnal clock gene and innate immune receptor expression in peripheral blood mononuclear cells of patients with obesity

Article References: Pivonello, C., Magnacca, N., Graziadio, C., Negri, M., Vetrani, C., Amatrudo, F., Vozza, E., Vecchio, G. D., Tini, S., Celano, S., Prodam, F., Auriemma, R. S., Pivonello, R., & Colao, A. (2026). A 12-week hypocaloric Mediterranean diet is associated with metabolic improvement and modulation of diurnal clock gene and innate immune receptor expression in peripheral blood mononuclear cells of patients with obesity. Journal of Translational Medicine. https://doi.org/10.1186/s12967-026-09013-0

Image Credits: AI Generated

DOI: 10.1186/s12967-026-09013-0

Keywords: Mediterranean diet, obesity, circadian rhythm, clock genes, BMAL1, Toll-like receptors, TLR4, TLR8, peripheral blood mononuclear cells, inflammation, chronotype, nutritional intervention