The study, published in BMC Public Health by Ruixin He of Shanghai Jiao Tong University School of Medicine and colleagues at the University of Oxford and Peking University, took advantage of the second resurvey of the China Kadoorie Biobank, conducted in 2013 and 2014. Participants were drawn from five urban and five rural regions of China, an unusually broad geographic and social spread for personality research. Neuroticism was measured with the 23-item Eysenck Personality Questionnaire, a classic psychometric instrument in which respondents answer yes-or-no questions about mood, worry and emotional reactivity. Answers were converted into a neuroticism score, or N-score, ranging from 0 to 23, with higher values indicating a stronger tendency toward anxiety, irritability and emotional instability.

The average N-score in the cohort was 2.52, a comparatively low figure that the authors interpret in light of cultural and response-style differences. Yet the patterning across the population was anything but flat. Women scored higher than men on average, and urban residents scored higher than their rural counterparts. Perhaps most intriguingly, the trait showed a pronounced downward trend with age: older participants reported consistently fewer neurotic symptoms than younger ones. This age gradient echoes findings from Western cohorts and supports the idea of a maturational curve in emotional stability, in which people tend to become calmer and more resilient as they move through adulthood, though longitudinal data would be needed to confirm that individuals actually decline in neuroticism rather than the pattern reflecting generational differences.

Socioeconomic circumstances left an equally strong fingerprint on the trait. Higher N-scores were strongly associated with social disadvantage: participants who were not married and those from households with lower incomes scored significantly higher than their wealthier, married peers. The relationship between neuroticism and deprivation is almost certainly bidirectional. Chronic financial stress and social isolation can heighten emotional reactivity, while a temperament prone to worry and distress can undermine relationships, job performance and economic advancement. Disentangling cause from consequence in such data is notoriously difficult, but the consistency of the association across a cohort of this size strengthens the case that personality and social position are deeply intertwined.

The cross-sectional health findings were dramatic. Compared with participants who scored zero on the neuroticism scale, those with an N-score of 4 or higher showed substantially higher prevalence of mental health problems and poor self-rated general health, with adjusted risk ratios ranging from 1.52 to 41.01 depending on the condition examined. The upper end of that range reflects the near-universal co-occurrence of very high neuroticism scores with certain psychological conditions, which is expected given that the trait itself measures emotional distress. Even the more conservative end of the range, however, indicates a meaningful excess burden of psychological suffering among people with elevated scores, reinforcing the trait’s status as one of the most robust psychological predictors of mental ill health.

What elevates the study above a simple snapshot is its prospective component. By linking participants to electronic health registries, the researchers tracked who went on to develop major diseases after the personality assessment. Using Cox regression models that adjusted for confounding factors, they found that people in the highest neuroticism category had significantly higher risks of several serious conditions than those in the lowest category, with hazard ratios between 1.17 and 1.81. The list of affected outcomes is strikingly broad: ischaemic heart disease, stroke, mental and behavioural disorders, and diseases of the nervous system and digestive system all appeared at elevated rates among highly neurotic participants.

The cardiovascular findings deserve particular attention because they speak to a long-standing debate in psychosomatic medicine. Proposed mechanisms run along several plausible pathways. Chronically heightened emotional reactivity is associated with sustained activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, which can raise blood pressure, promote inflammation and disturb metabolic regulation. People high in neuroticism are also more likely to smoke, sleep poorly, remain sedentary and neglect medical care, behaviours that mediate part of the observed risk. The digestive system association is similarly biologically credible, given the dense neural communication between the gut and the brain and the established role of stress in functional gastrointestinal disorders.

The authors are careful to frame their results as associations rather than proof of causation. Reverse causation remains a possibility, since subclinical disease may itself heighten emotional distress, and residual confounding by unmeasured lifestyle or environmental factors cannot be excluded. Nevertheless, the sheer scale and diversity of the China Kadoorie Biobank, combined with registry-based outcome ascertainment, give the findings a weight that smaller clinic-based studies cannot match. The work also fills a conspicuous gap: most large-scale personality epidemiology has been conducted in Europe and North America, and it was genuinely uncertain whether the trait’s health correlates would replicate in a population with very different cultural norms around expressing emotion and answering questionnaire items.

The replication appears to have succeeded, and that has practical implications. If neuroticism reliably flags elevated risk for cardiometabolic and psychiatric disease in Chinese adults, it could in principle be incorporated into risk stratification tools, helping clinicians identify patients who might benefit from closer monitoring, stress-management interventions or earlier mental health support. The sociodemographic patterning adds another layer: because elevated scores cluster among people who are unmarried, poorer and, in some respects, already vulnerable, the trait may serve as a marker for compounded disadvantage, concentrating both psychological and physical health burdens in specific segments of the population.

For a trait once dismissed as a mere questionnaire curiosity, neuroticism is emerging as a genuine public health variable. The China Kadoorie Biobank analysis suggests that the emotional temperament of a population is not evenly distributed, that it tracks social circumstances closely, and that it foreshadows disease outcomes ranging from heart attacks to digestive disorders. As biobanks worldwide continue to link psychological measurements to long-term health records, the question is shifting from whether personality matters for health to how best to translate that knowledge into prevention. For the tens of millions of people worldwide who sit at the anxious end of the neuroticism spectrum, the new evidence offers both a warning and, potentially, an early opportunity for intervention.

Subject of Research: Sociodemographic patterns and disease associations of neuroticism in Chinese adults

Article Title: Patterns and health relevance of neuroticism in Chinese men and women: evidence from the China Kadoorie Biobank

Article References: He, R., Du, H., Clarke, J., Wang, B., Yang, L., Pei, P., Sun, D., Lv, J., Yu, C., Yang, X., Sun, X., Chen, J., Li, L., Chen, Z., Chen, Y., for the China Kadoorie Biobank Collaborative Group, Clarke, R., Collins, R., Peto, R., … Qu, C. (2026). Patterns and health relevance of neuroticism in Chinese men and women: evidence from the China Kadoorie Biobank. BMC Public Health. https://doi.org/10.1186/s12889-026-29670-6

Image Credits: AI Generated

DOI: 10.1186/s12889-026-29670-6

Keywords: neuroticism, China Kadoorie Biobank, personality, mental health, ischaemic heart disease, stroke, Eysenck Personality Questionnaire, epidemiology, public health, socioeconomic status, cohort study, psychometrics

The scale of the undertaking is what sets this research apart. Led by Eugenio Traini of the Netherlands Organisation for Applied Scientific Research and colleagues, the team assembled a cohort of 10,156,661 people aged 30 and older who were registered at a Dutch address on 1 January 2012. Rather than relying on sparse monitoring stations, the researchers used LOTOS-EUROS, an open-source chemistry transport model that simulates atmospheric chemistry, transport and deposition to estimate PM2.5 concentrations at a resolution of roughly two by two kilometres, every hour, across the entire country from 2006 to 2019. Those gridded estimates were aggregated to postal code areas and linked to each participant’s residential history, allowing the team to follow people as they moved through landscapes of shifting air quality.

PM2.5 refers to airborne particles smaller than 2.5 micrometres across, roughly a thirtieth of the width of a human hair. These particles are emitted directly from burning solid fuels, road transport and industry, or formed secondarily in the atmosphere from precursor emissions such as ammonia from agriculture and sulphur compounds from shipping. Because of their tiny size, they evade the lungs’ defences, penetrate deep into the respiratory tract, and can enter the bloodstream, where they trigger systemic inflammation, oxidative stress and vascular dysfunction. In the Netherlands, average annual concentrations fell from about 20 micrograms per cubic metre in 2006 to 13 micrograms per cubic metre in 2019, a decline reflecting European and national clean-air policies, yet the study suggests that these remaining, lower levels continue to exact a measurable toll.

The researchers tracked first-time hospitalisations for three cardiovascular outcomes: ischaemic heart disease, myocardial infarction, and stroke, together with a composite outcome capturing the first hospitalisation for any cardiovascular cause. Over the follow-up period ending in 2019, the cohort recorded 437,089 incident ischaemic heart disease hospitalisations, 205,663 strokes and 151,345 heart attacks, totalling 592,259 first cardiovascular hospitalisations. Because modelling time-varying exposure across ten million people is computationally punishing, the team used a nested case-control design: each person hospitalised was matched with four controls of the same sex and exact age who were still event-free at the moment of the case’s admission, a technique known to yield estimates comparable to full cohort analyses.

The short-term findings show how quickly dirty air can tip vulnerable patients into crisis. In fully adjusted models, a 10 microgram per cubic metre increase in PM2.5 averaged over the six days preceding admission was associated with a 5.8 percent higher risk of hospitalisation for ischaemic heart disease, a 5.3 percent higher risk for myocardial infarction, and a 4.7 percent higher risk for a first cardiovascular hospitalisation overall. Even exposure on the day of admission itself, lag zero, carried elevated odds. Stroke was the exception: its estimates pointed in a positive direction but the confidence intervals crossed the null, meaning the acute association could not be confirmed statistically in this population.

The most sophisticated part of the analysis went beyond simple averages. Using distributed lag models, a statistical framework that estimates how risk is distributed across each individual day or year of past exposure, the researchers uncovered distinct temporal fingerprints for each condition. For ischaemic heart disease, the risk signal was clearest in the one to six days immediately before hospitalisation, consistent with the idea that pollution can acutely trigger events in people whose arteries are already compromised. For myocardial infarction, the effect emerged beginning one day after exposure. For stroke, however, a suggestive increase in risk appeared two to three weeks before admission, hinting that cerebrovascular events may follow more prolonged inflammatory and coagulation pathways rather than an immediate trigger.

The long-term results were even more striking in magnitude. A 10 microgram per cubic metre increase in annual PM2.5 averaged over the two years spanning the hospitalisation year and the year before was associated with a 39.8 percent higher risk of ischaemic heart disease admission, a 22.2 percent higher risk of stroke, a 13.4 percent higher risk of heart attack, and a 32.5 percent higher risk of a first cardiovascular hospitalisation overall. Distributed lag analysis showed that risk rose with cumulative exposure up to roughly three years before hospitalisation for ischaemic heart disease and the composite outcome, then plateaued or declined. For heart attack, the cumulative effect peaked around four years before admission. These estimates are larger than those reported in some earlier European studies, possibly because the time-varying exposure assignment reduced misclassification compared with the common practice of anchoring exposure to a single baseline year.

Several mechanisms and caveats frame how these numbers should be read. Effect estimates were consistently slightly higher in men than women, and higher among people aged 65 and older than those aged 30 to 64, though the differences were modest. Sensitivity analyses in a subset of about 305,000 participants with lifestyle data on smoking, alcohol, body mass index and education broadly supported the main results, although with wider uncertainty due to the smaller sample. The study adjusted extensively for individual socioeconomic factors such as income, civil status and country of origin, plus neighbourhood-level indicators including urbanisation and deprivation, and estimates attenuated with adjustment while remaining consistently positive. The authors note that their exposure model explained 72 percent of the variance in monitored concentrations, meaning residual prediction error could blur some lag-specific findings, and that hospitalisation registry completeness declined over part of the study period, a form of misclassification that would likely push the true effects down rather than up.

The researchers also caution that the analysis focused on PM2.5 alone and did not disentangle correlated co-pollutants such as nitrogen dioxide and ozone, which would require multipollutant mixture methods still under active methodological development. Nor did it capture exposures outside the home, at workplaces or during commuting, which would tend to understate rather than exaggerate the true associations. Looking ahead, the LOTOS-EUROS framework offers a promising capability the study did not yet exploit: source apportionment, or attributing particulate mass to specific emitters such as agriculture, industry and traffic, which could reveal which sources drive the greatest cardiovascular harm.

The message that emerges is sobering for a country that has largely cleaned up its air. Average Dutch PM2.5 levels were moderate by European standards and fell steadily throughout the study, yet both short bursts and years of accumulated exposure were consistently linked to hospitalisations at concentrations well below the World Health Organization’s historical guideline limits, echoing pooled European evidence that found no clear threshold below which cardiovascular effects vanish. The outcome-specific timing, acute for coronary events, more drawn-out for stroke, argues for epidemiological studies that treat exposure as a living, changing history rather than a single snapshot. For policymakers, the findings suggest that further reductions in fine particulate pollution, even from already low baselines, would translate directly into fewer heart attacks, strokes and cardiac hospital beds filled.

Subject of Research: Associations between short- and long-term exposure to ambient PM2.5 and cardiovascular disease hospitalisation in a nationwide Dutch cohort

Article Title: Short- and long-term exposure to ambient PM 2.5 and risk of cardiovascular disease hospitalisation: A nationwide cohort study in the Netherlands

Article References: Traini, E., Shen, Y., de Crom, T. O., Pekel, F., Henzing, B., Zhang, J. J., Pseftogkas, A., Ge, C., Timmermans, R., & Pronk, A. (2026). Short- and long-term exposure to ambient PM2.5 and risk of cardiovascular disease hospitalisation: A nationwide cohort study in the Netherlands. Environmental Advances, 26, Article 100756. https://doi.org/10.1016/j.envadv.2026.100756

Image Credits: AI Generated

DOI: 10.1016/j.envadv.2026.100756

Keywords: PM2.5, air pollution, cardiovascular disease, heart attack, stroke, ischaemic heart disease, hospitalisation, Netherlands, distributed lag models, LOTOS-EUROS, cohort study, environmental health

The study’s central innovation is methodological. Rather than relying on mortality rates alone, which can be misleading when disease prevalence differs sharply between countries and sexes, the team calculated the mortality-to-prevalence ratio, or MPR, dividing the age-standardised mortality rate by the age-standardised prevalence rate. Because ischaemic heart disease is a chronic condition, the population at risk of dying includes both newly diagnosed patients and the millions living with established disease, making prevalence a more appropriate denominator than incidence. A high MPR signals that, relative to the number of people living with the disease, deaths are excessive, a pattern that often points to weaknesses in prevention, treatment or both. The researchers also normalised risk-attributable mortality by prevalence to construct a case-fatality index, or CFI, which asks whether deaths attributable to a specific risk factor, such as tobacco or high blood pressure, are high or low among those actually living with the disease.

The headline numbers show genuine progress. Between 2011 and 2023, age-standardised mortality from ischaemic heart disease fell across the region in both sexes, with relative reductions of 2.6 percent in men and 3.7 percent in women, and regional mean MPRs declined from 5.32 percent to 4.32 percent in men and from 5.84 percent to 4.48 percent in women. Yet the averages conceal extraordinary heterogeneity. In 2023, mortality rates among men ranged from 216.93 per 100,000 in Hungary and 210.50 in Bulgaria down to just 63.55 in Slovenia, with women showing a parallel spread from 158.62 in Serbia to 29.17 in Slovenia. Slovenia’s case-fatality levels were statistically indistinguishable from those of the six founding members of the European Union, demonstrating that Western European outcomes are achievable within the region.

When the researchers applied formal Z-score testing to sex differences in MPR, a clear geography of inequality emerged. In 2011, women had significantly worse outcomes in Croatia, Serbia, Czechia and Bosnia and Herzegovina, while men fared worse in Poland and Bulgaria. By 2023, the disparities had narrowed but persisted in Croatia, Serbia and Czechia, with Z-scores of 5.55, 2.55 and 2.18 respectively, while Poland showed a significant reversal, with men now experiencing the higher mortality burden relative to prevalence. In Croatia and Serbia, women’s case-fatality was 46 percent and 38 percent higher than men’s, respectively. More modest but still meaningful female disadvantages appeared in Slovakia, Montenegro, North Macedonia and Bosnia and Herzegovina, whereas Bulgaria and Poland were the only countries where women-to-men ratios fell below one.

What drives these divergent patterns? The analysis points to two opposing domains of risk. In most countries, women exhibited higher case-fatality indices than men for the major metabolic risks, including elevated systolic blood pressure, fasting plasma glucose, LDL cholesterol and body mass index, with Croatia, Serbia and Slovakia showing the most pronounced female disadvantage, exceeding 20 percent for all four. Physical inactivity exerted a proportionally far greater impact on women, particularly in the Balkans, where the female-to-male CFI ratio reached 4.57 in Croatia and 4.11 in Serbia. Tobacco, by contrast, remained an overwhelmingly male hazard, with Albania’s tobacco-attributable male burden nearly six times that of women. In countries such as Croatia and Serbia, the female disadvantage domain of inactivity, metabolic vulnerability and dietary deficits predominates, while in Poland the absence of a strong female disadvantage leaves the universal male hazard from tobacco unopposed, helping to explain the reversal of the sex gap there.

Diet emerged as a critical and underappreciated component of the female disadvantage. Because dietary estimates carry wide uncertainty intervals, the team used Slovenia, the country with the lowest case-fatality, as an empirical benchmark, a choice validated by the finding that Slovenia’s MPR is statistically comparable to those of Belgium, France, Germany, Italy, Luxembourg and the Netherlands. This benchmarking revealed significant sex differences for seven dietary risks: low intake of whole grains, fruits, nuts and seeds, vegetables, seafood omega-3 fatty acids and fibre, along with high sodium intake. Low intake of nuts and seeds was the only dietary factor consistently associated with a significant female disadvantage in all three high-disparity countries, Croatia, Serbia and Czechia, suggesting a shared and potentially tractable population-level pattern. Country-specific deficits added further risk, most notably low fruit and vegetable intake in Croatia and low omega-3 intake in Romania, while male-specific dietary excesses were confined to isolated exposures such as high sodium in Romania and low whole grains in Bulgaria.

The biological plausibility of these dietary effects is well supported. Low intake of fruit, vegetables, nuts, seeds and omega-3-rich foods has been linked to higher blood pressure, impaired vascular function, inflammation and adverse cardiometabolic profiles, and these foods are foundational to the Mediterranean, DASH and Nordic dietary patterns with strong outcome evidence. The authors also point to possible physiological amplification in women, noting that the menopausal transition, with declining oestrogen levels, is associated with adverse lipid changes and vascular dysfunction that may heighten the impact of inadequate intake of omega-3-rich foods and micronutrient-dense sources such as nuts and seeds. Weight-promoting medications, including certain antidepressants, beta-blockers and insulin, may further compound cardiometabolic risk in midlife and older women, although medication use was not directly assessed in this ecological analysis.

Socioeconomic forces appear to compound these physiological vulnerabilities in a structural paradox: women with heart disease may experience relative deprivation of protective foods despite potentially greater nutritional needs. Croatia, though a high-income country, maintains one of the highest at-risk-of-poverty rates in the European Union at 21.7 percent, while upper-middle-income Serbia shows similarly high social vulnerability at 24.3 percent. Food insecurity, unequal household food allocation, gendered norms influencing food selection and time poverty from unequal domestic and caregiving responsibilities may all restrict women’s consistent access to nutrient-dense foods. Czechia offers a contrasting case, where excess female risk emerges despite low poverty levels of roughly 9.5 percent, suggesting that even a comparatively modest additional female shortfall in nuts and seeds, within a population-wide deficit of whole grains and fibre, may be sufficient to produce measurable sex differences in case-fatality.

Health-system capacity alone does not explain the patterns either. The researchers examined coronary revascularisation rates relative to disease prevalence and found that a country’s procedural capacity does not predict its pattern of sex disparity. Croatia and Bulgaria had among the highest procedure-to-prevalence ratios in the region, yet Croatia exhibited a significant disparity disadvantaging women while Bulgaria showed near-identical case-fatality between the sexes. This indicates that equitable outcomes depend not only on system capacity but on the fairness of clinical pathways determining who receives treatment. The findings align with individual-level data: Poland’s male disadvantage corresponds with registry evidence of higher sudden out-of-hospital cardiac arrest in men, while Serbia’s female disadvantage is consistent with Belgrade coronary care data showing higher in-hospital mortality in women with ST-elevation myocardial infarction even after adjustment for age and comorbidities.

The authors are careful to note the limitations of their approach. The analysis relies on modelled GBD estimates rather than primary clinical datasets, its ecological design precludes causal inference at the individual level, and the mortality and prevalence inputs of the MPR are structurally interrelated within the GBD modelling framework, meaning the ratio should be interpreted as a comparative indicator rather than a direct survival estimate. Nevertheless, the message for policymakers is clear: declining mortality does not automatically translate into equitable survival. The researchers call for cardiovascular surveillance systems to complement traditional mortality statistics with sex-specific, prevalence-adjusted indicators, and for a dual-track prevention strategy that confronts the pervasive male tobacco epidemic while addressing the female triad of physical inactivity, poor diet and metabolic risk. Slovenia demonstrates that low case-fatality is achievable in the region; the task now is to translate that benchmark into targeted, sex-sensitive action in the countries where preventable risks continue to drive excess deaths.

Subject of Research: Sex differences in ischaemic heart disease case-fatality and their dietary and lifestyle determinants across Central Europe

Article Title: Contributions of diet and lifestyle to sex differences in ischaemic heart disease burden in Central Europe: an analysis of the Global Burden of Disease Study 2023

Article References: Bugiardini, R., Rahaman, T., Badimon, L., Cenko, E., Anand, S. S., Manfrini, O., Merkely, B., Milicic, D., Townsend, N., Vaccarino, V., Gulati, M., & Gale, C. P. (2026). Contributions of diet and lifestyle to sex differences in ischaemic heart disease burden in Central Europe: an analysis of the Global Burden of Disease Study 2023. The Lancet Regional Health – Europe, 70, Article 101846. https://doi.org/10.1016/j.lanepe.2026.101846

Image Credits: AI Generated

DOI: 10.1016/j.lanepe.2026.101846

Keywords: ischaemic heart disease, Global Burden of Disease, Central Europe, sex disparities, case-fatality, dietary risk factors, physical inactivity, tobacco, hypertension, mortality-to-prevalence ratio, cardiovascular prevention, nutrition policy