The study, led by Jie Ding, Ben Schöttker, Hermann Brenner and Michael Hoffmeister, exploited the prospective design of the UK Biobank, a cohort of more than half a million middle-aged and older adults recruited across England, Wales and Scotland between 2006 and 2010. After excluding people with prevalent cancer at recruitment, incomplete lifestyle data or less than two years of follow-up, the researchers followed 287,745 participants through national cancer and death registries for a median of 11.5 years. During that window, 12,947 participants received a first cancer diagnosis. Because the cohort was healthy at baseline and the cancers emerged afterwards, the analysis captures genuine temporal sequence rather than retrospective recall.

The technical heart of the study is the healthy lifestyle score, or HLS, a previously benchmarked instrument that assigns one point to each of five healthy behaviours: non-smoking, moderate alcohol intake, a healthy diet, adequate physical activity and a healthy body mass index. Non-smoking was defined as never having smoked regularly or having been a former smoker with fewer than 30 pack-years. Moderate drinking meant no more than 12 grams of alcohol per day for women and 24 grams for men. Diet quality was assessed by placing participants in the highest 40 percent of a cohort-specific healthy diet score distribution. Adequate physical activity required at least 500 MET-hours per week of walking, moderate or vigorous activity, and a healthy BMI meant more than 18.5 but less than 25 kilograms per square metre. Scores were grouped into low (0–1), medium (2–3) and high (4–5) categories.

Cox proportional hazards models, adjusted for age, sex, ethnicity, region, deprivation, household income, education, cancer screening history, family history of cancer, hypertension, diabetes and height, revealed a 29 percent lower risk of overall cancer for the high versus the low HLS group. But the site-specific results are where the story becomes dramatic. After correction for multiple comparisons using the Benjamini-Hochberg procedure, strong adherence was associated with reduced risks of oral cancer (hazard ratio 0.57), pharyngeal cancer (0.41), laryngeal cancer (0.12), oesophageal cancer (0.41), stomach cancer (0.49), colorectal cancer (0.65), liver cancer (0.44), pancreatic cancer (0.52), lung cancer (0.19), soft tissue sarcoma (0.61), kidney cancer (0.73), bladder cancer (0.52) and postmenopausal breast cancer (0.79). The laryngeal figure is extraordinary: an 88 percent risk reduction, meaning that people with four or five healthy behaviours almost never developed this tumour in the cohort.

The researchers went one step further and calculated population attributable fractions, or PAFs, a statistical measure of the proportion of cancer cases that would be attributable to incomplete adherence to a healthy lifestyle. Using the graphPAF R package with 1000 bootstrap replications, they found significant PAFs for 14 of the 27 cancer types. The highest fractions clustered in the upper aerodigestive and respiratory tracts: 65.5 percent for laryngeal cancer, 51.9 percent for lung cancer and 30.2 percent for pharyngeal cancer. Digestive cancers also carried heavy burdens, with 29.9 percent for oesophageal, 25.9 percent for stomach, 24.0 percent for pancreatic, 22.3 percent for liver and 16.6 percent for colorectal cancer. In plain terms, if everyone in the cohort had achieved four or five healthy behaviours, roughly two-thirds of laryngeal cancers and half of lung cancers might never have occurred.

When the team dissected the score into its individual components, smoking and overweight emerged as the dominant contributors. Non-smoking was significantly associated with 12 of the 27 cancers, with hazard ratios ranging from 0.13 to 0.82, including an 87 percent lower risk of lung cancer, an 82 percent lower risk of laryngeal cancer and a 67 percent lower risk of pharyngeal cancer. Normal BMI was linked to reduced risks of seven cancers: oesophageal, colorectal, pancreatic, kidney, central nervous system, postmenopausal breast and uterine. The other components, including diet, physical activity and moderate alcohol intake, showed associations with fewer cancer types. Smoking showed significant PAFs for 12 cancer types and overweight for 10, far more than any other factor, leading the authors to conclude that smoking cessation and weight control should be prioritised in cancer prevention strategies.

The analysis also uncovered some counterintuitive patterns that demand careful interpretation. A healthy lifestyle was associated with an increased risk of prostate cancer (hazard ratio 1.11), and non-smoking was linked to higher risks of melanoma, uterine and prostate cancer. Normal BMI showed positive associations with pharyngeal and lung cancer, a paradox previously reported in the literature and often attributed to confounding by smoking, although the evidence remains inconclusive. Moderate alcohol intake was associated with reduced risks of kidney cancer and multiple myeloma, consistent with some prior studies, and one proposed mechanism is that alcohol may increase insulin sensitivity. The authors caution that these paradoxical results require further study before any biological conclusions can be drawn.

Subgroup analyses revealed that the protective associations varied by age and sex. The link between a healthy lifestyle and reduced pancreatic cancer risk was stronger in participants under 60, while the associations with kidney and postmenopausal breast cancer were stronger in those aged 60 and over, suggesting that healthy behaviours may accumulate over time and have a more pronounced effect at older ages. Oesophageal and colorectal cancer showed stronger protective associations in men than in women, in line with prior European cohort evidence. For laryngeal cancer, no cases at all were observed among women with a high HLS, an outcome so rare that the hazard ratio for that group could not even be defined.

The study has notable strengths, including its simultaneous investigation of a broad spectrum of cancers within the same population, which enhances the comparability of cancer-specific results, its large sample size, its prospective design and its detailed lifestyle assessment. But the authors are candid about limitations. The UK Biobank population is predominantly White and healthier than the general population, which may limit generalisability. The dietary component was based on a cohort-specific diet quality score rather than a validated dietary index. Most lifestyle factors were self-reported, leaving room for measurement error and residual confounding. Lifestyle changes during follow-up may have caused regression dilution bias, which would actually mean the true effect sizes are stronger than estimated. And for rare cancers, statistical power may have been insufficient to detect relevant associations.

What makes this analysis resonate is its scope and its clarity. Global cancer incidence is projected to reach 28.4 million cases by 2040, and while age-standardised rates in the UK have been relatively stable since 1993, less common cancers such as liver, oral and melanoma skin cancer have shown notable increases. By demonstrating that a simple five-point checklist is associated with lower risks of both common and rare cancers, and by quantifying how much of the cancer burden is attributable to incomplete adherence, the study provides a technical foundation for targeted prevention. The message for public health is unambiguous: if the goal is to prevent the greatest number and the widest variety of cancers, the first priorities are keeping cigarettes out of reach and keeping weight in check, with the remaining healthy behaviours reinforcing the effect across a remarkable range of tumour types.

Subject of Research: Cancer epidemiology

Article Title: Healthy lifestyle and cancer risk: a pan-cancer analysis in the UK Biobank prospective cohort

Article References: Ding, J., Schöttker, B., Brenner, H., & Hoffmeister, M. (2026). Healthy lifestyle and cancer risk: a pan-cancer analysis in the UK Biobank prospective cohort. British Journal of Cancer. https://doi.org/10.1038/s41416-026-03613-9

Image Credits: AI Generated

DOI: 10.1038/s41416-026-03613-9

Keywords: cancer prevention, healthy lifestyle, UK Biobank, smoking, obesity, population attributable fraction, pan-cancer analysis, cancer epidemiology, Healthy, lifestyle, cancer, risk

The study, led by Haibo Huang of Peking Union Medical College Hospital and Guangliang Shan of the Chinese Academy of Medical Sciences, drew on the China National Health Survey 2023, a cross-sectional survey that included 6,291 participants aged 20 to 88 years. Rather than asking people whether they thought their hearing was slipping, the researchers measured it directly using air-conduction pure-tone audiometry, the standard clinical technique in which listeners respond to tones delivered through headphones at specific frequencies. This objective measurement matters, because self-reported hearing problems are notoriously unreliable and tend to understate the true scale of the problem.

To characterize hearing loss in detail, the team calculated pure-tone averages, known as PTAs, across three frequency ranges. Low and mid-frequency hearing loss was defined as an average threshold above 20 decibels at 0.5, 1, and 2 kilohertz, the frequencies that carry much of the energy of everyday speech. Speech-frequency hearing loss added the 4 kilohertz tone to that average, while high-frequency hearing loss was assessed at 4, 6, and 8 kilohertz, the region where age-related damage typically appears first and where consonants become hard to distinguish. In every case, the definition used the better ear, reflecting the hearing that actually matters for communication in daily life.

The central innovation of the study lies in its statistical framing. Instead of simply asking which risk factors are associated with hearing loss, the researchers estimated population attributable fractions, or PAFs, for a set of socioeconomic and cardiometabolic factors. The PAF answers a deceptively simple question: if this risk factor were eliminated from the entire population, what percentage of hearing loss cases would disappear? The estimates were derived from multivariable logistic regression models, which adjust for the influence of other measured variables, and were reported with 95 percent confidence intervals to convey the precision of each figure. The analysis was then stratified by age, sex, and menopausal status to reveal how the burden attributable to each factor shifts across different groups.

The headline result is that roughly 10 to 19 percent of hearing loss in this population could be attributed to the socioeconomic and cardiometabolic risk factors studied. That may sound modest next to the enormous contribution of noise exposure and aging, but it represents millions of people when scaled to a country the size of China, and it points to levers that public health systems can actually pull. Crucially, the ranking of risk factors and the size of their attributable fractions were broadly consistent across low, speech, and high-frequency hearing loss, suggesting the same underlying mechanisms may be at work regardless of which part of the cochlea is examined.

Two factors stood out at the top of the list. Abnormal body mass index accounted for approximately 3.0 to 6.5 percent of hearing loss, and low educational attainment accounted for roughly 2.7 to 5.5 percent, making these the leading attributable risk factors in the analysis. Hypertension also carried a substantial attributable fraction, particularly among older adults and men. The connection between cardiometabolic health and hearing is biologically plausible: the delicate hair cells of the inner ear and the tiny vessels that feed them are exquisitely sensitive to blood flow, and the same vascular damage that elevates the risk of heart attack and stroke may quietly starve the cochlea over decades.

The stratified results add a layer of nuance that could reshape how prevention campaigns are targeted. The attributable fractions of the selected risk factors were generally higher in younger adults than in older adults, higher in men than in women, and higher in premenopausal women than in postmenopausal women. In other words, the same risk factor does not carry the same weight everywhere. In younger people, whose hearing loss is less likely to be driven by age alone, modifiable factors account for a larger share of the disease burden, which means interventions aimed at weight and blood pressure in early and mid-adulthood could pay outsized dividends later in life.

The sex and menopausal patterns hint at possible biological modulation. Estrogen is thought to have protective effects on cochlear function and vascular health, and the lower attributable fractions observed among postmenopausal women may reflect a shift in the dominant causes of hearing loss in that group, with aging and other unmeasured factors taking a larger role. The researchers are careful to frame these as observations that suggest priorities rather than definitive causal proofs. Cross-sectional data capture a single moment in time, so they cannot establish that changing a risk factor today will change hearing tomorrow, and residual confounding by factors such as occupational noise exposure cannot be excluded.

Even with those caveats, the practical implications are striking. Weight management and blood pressure control are already cornerstones of cardiovascular prevention, supported by decades of evidence and existing health infrastructure. If the same interventions also preserve hearing, the case for investing in them becomes stronger still, and hearing preservation could be added to the long list of benefits that clinicians cite when counseling patients about diet, exercise, and antihypertensive treatment. The finding that low education is a leading attributable factor also underscores that hearing loss is not purely a biomedical problem; socioeconomic circumstances shape health trajectories in ways that policy, not just medicine, must address.

For a condition long treated as an inevitable companion of growing old, the message from this study is quietly radical: a measurable slice of the world’s hearing loss is tied to risks we already track in every routine checkup. The authors conclude that the disparities in how risk factors contribute across age, sex, and menopausal status should guide prevention priorities, and they identify weight and blood pressure management as logical initial targets for hearing loss prevention strategies. With more than 1.5 billion people affected globally and numbers expected to rise as populations age, even a ten to twenty percent reduction in preventable cases would represent a public health victory measured in hundreds of millions of ears.

Subject of Research: Population attributable fractions of socioeconomic and cardiometabolic risk factors for hearing loss in a Chinese national health survey

Article Title: Priorities for hearing loss prevention based on population attributable fraction estimates: a cross-sectional analysis within the China national health survey 2023

Article References: Huang, H., Fan, Y., Yan, F., Hu, Y., He, H., Liu, Y., Xu, T., Zhu, X., Zhu, Y., Diao, W., Xia, X., Tu, J., Li, A., Lin, B., Liu, Q., Lu, Z., Wang, W., Xu, D., Chen, Z., … Shan, G. (2026). Priorities for hearing loss prevention based on population attributable fraction estimates: a cross-sectional analysis within the China national health survey 2023. BMC Public Health. https://doi.org/10.1186/s12889-026-28506-7

Image Credits: AI Generated

DOI: 10.1186/s12889-026-28506-7

Keywords: hearing loss, population attributable fraction, body mass index, hypertension, pure-tone audiometry, China National Health Survey, cardiometabolic risk factors, public health prevention, cross-sectional study, BMC Public Health, low education, menopausal status

The research team set out to test a framework that has become a cornerstone of dementia prevention policy worldwide. In prior work, the Lancet Commission identified fourteen modifiable risk factors across the life course that are collectively responsible for up to 45 percent of dementia cases in the general population. These factors span early life, midlife, and later life, and include limited education, hearing loss, elevated low-density lipoprotein cholesterol, depression, a history of traumatic brain injury, physical inactivity, diabetes, smoking, hypertension, obesity, excess alcohol use, social isolation, exposure to air pollution, and vision loss. The 45 percent figure is expressed as a population attributable fraction, a statistical measure representing the proportion of disease in a population that could theoretically be eliminated if a given risk factor were removed.

Population attributable fraction is a powerful tool for public health planning because it weights both the strength of the association between a risk factor and a disease and how common that factor is in the population. A factor that doubles risk but affects only a small fraction of people may contribute less to the overall disease burden than a modest risk elevation that touches nearly everyone. By calculating population attributable fractions for dementia risk factors in American Indian communities, the Boston University researchers could identify which interventions might deliver the greatest benefit in this specific population, rather than relying on estimates derived from very different demographic and socioeconomic contexts.

When the researchers validated the Lancet Commission model among older American Indians, the results diverged sharply from the global pattern. Of the fourteen established factors, ten could be evaluated in the cohort, and only four showed statistically significant associations with vascular and Alzheimer’s dementias: limited education, hypertension, social isolation, and depression. The population attributable fractions for these four factors were striking. Limited education accounted for 19 percent, hypertension for 11 percent, and social isolation for 13 percent of dementia risk in the population. Depression stood out with an attributable fraction of 60 percent, though the researchers cautioned that this figure may be an overestimate, because depression can also be an early symptom of dementia rather than a purely causal factor, a form of reverse causation that complicates interpretation.

Together, these four factors may represent the highest-impact targets for dementia prevention programs designed for Native American populations. The pattern itself is informative. Some of the factors that loom large in global models, such as hearing loss, diabetes, and smoking, did not reach statistical significance in this cohort, while others were more or less prevalent than in the general population. The researchers concluded that American Indian communities may carry a complex and unique constellation of contributing factors that elevate risk of both vascular dementia, which stems from impaired blood flow to the brain, and Alzheimer’s dementia, the most common neurodegenerative form of the disease.

Corresponding author Astrid Suchy-Dicey, PhD, associate professor of medicine at Boston University Chobanian & Avedisian School of Medicine, emphasized that the findings call for careful consideration of exposures and tailored prevention programs across the life course when assessing cognitive risk for Indigenous populations. She noted that later-life factors such as social isolation and depression are likely to provide efficient targets for community interventions, while public health programs designed to improve the treatment and control of hypertension and cardiovascular conditions are critically needed to address persistent health inequities. Structural improvements to educational systems, learning resources, and skills training for rural communities, she added, may result in better life-course trajectories for everyone living in those communities.

The distinction between midlife and later-life interventions carries practical weight. Hypertension is a classic midlife target: elevated blood pressure damages the small vessels of the brain over decades, contributing to both stroke-related vascular injury and the accumulation of Alzheimer’s pathology. Controlling it requires sustained clinical infrastructure, medication access, and cardiovascular care, resources that have historically been unevenly distributed in rural and Tribal communities. Social isolation and depression, by contrast, are potentially more amenable to community-level programs that strengthen social connection, mental health support, and cultural engagement, interventions that can be designed and delivered within the communities themselves.

The researchers also observed that because of the high burden of some risk factors, this population may develop neurodegenerative and vascular brain injury earlier in life, or progress toward dementia more rapidly once injury begins. This possibility has implications for how future studies are designed. Suchy-Dicey noted that future research should evaluate risk in younger groups, perhaps as young as 35 to 45 years of age, in order to observe the conversion from healthy cognition to symptomatic disease and to evaluate risk with lower potential for bias due to selective survival. Selective survival is a well-known problem in aging research: individuals with the heaviest burden of risk factors may die before they can be enrolled in studies of older adults, making surviving cohorts appear healthier than the population truly was and understating the true contribution of those risks.

The evidence base for the new analysis comes from the Strong Heart Study, a large cohort of American Indians aged 45 to 95 years residing in Tribal communities in the U.S. Southwest, Southern Plains, and Northern Plains. Participants attended multiple examination visits from midlife into late life and underwent cognitive assessment, allowing the researchers to track changes over time. Using regression models, the team estimated the prevalence of each risk factor, the relative risk of dementia associated with each, and the population attributable fraction for the cohort. This longitudinal design, spanning decades of adult life, is essential for distinguishing factors that precede cognitive decline from those that merely accompany it.

Equally notable is how the research was conducted. Strong Heart Study research is carried out in collaboration with the participating Tribal communities under a community-participatory research model, which centers research participants and Tribes throughout the research process, from study design through interpretation and dissemination. This approach stands in contrast to a long history of extractive research practices in Indigenous communities and reflects a growing recognition that trustworthy science requires genuine partnership. The authors argue that their findings underscore the importance of including many groups in population research, because models built on one population can mislead when applied to another. For the most valid understanding of health and disease in all peoples, dementia prevention science must reflect the diversity of the populations it aims to serve, and the four factors identified here, limited education, hypertension, social isolation, and depression, offer a starting point for prevention strategies built by and for American Indian communities.

Subject of Research: Modifiable dementia risk factors and population attributable fractions in American Indian populations

Article Title: BU researchers identify risk factors for dementia among American Indians

Article References: BU researchers identify risk factors for dementia among American Indians. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: dementia, American Indians, Alzheimer's disease, vascular dementia, population attributable fraction, hypertension, social isolation, depression, education, Strong Heart Study, Boston University, public health

The headline numbers reveal a striking asymmetry between absolute scale and population-adjusted rates. In 2023, China recorded approximately 103,000 pancreatic cancer cases, substantially more than the 66,000 cases documented in the United States. Yet when the researchers adjusted for age structure, the picture inverted: China’s age-standardized prevalence stood at 4.51 per 100,000 people, compared with 11.19 in the United States, and its age-standardized mortality rate was 4.97 per 100,000 against 9.56 in the American population. This contrast reflects the interplay of population size, demographic aging, and underlying exposure to risk factors, and it underscores why raw case counts alone can mislead when comparing disease burden across countries with very different demographic profiles.

Trends over time added further nuance to the comparison. Between 1990 and 2023, the absolute burden of pancreatic cancer grew in both countries, a trajectory shaped by aging populations, population growth, and shifting exposures to known and suspected risk factors. However, when the researchers examined age-standardized DALYs, a metric that corrects for changes in population size and age composition, they found that China experienced a slight decline of 0.15 percent, while the United States saw a modest increase of 0.12 percent. Though these percentage changes appear small, they point in opposite directions and suggest that the two nations may be traveling along different epidemiological paths, with China potentially benefiting from earlier stages of its demographic and lifestyle transition and the United States confronting the cumulative consequences of metabolic disease.

Age distribution emerged as another point of divergence. In China, the burden of pancreatic cancer peaked among people aged 60 to 74, whereas in the United States the peak had shifted to an older bracket, ages 70 to 84. This difference in age patterning has practical consequences for health systems. It means that in China, pancreatic cancer strikes a working-age and recently retired population, amplifying the socioeconomic cost of each case through lost productivity and years of life lost, while in the United States the disease increasingly concentrates among the very old, placing demands on geriatric oncology services, palliative care infrastructure, and long-term support systems for elderly patients and their families.

Perhaps the most consequential finding of the study concerns the changing hierarchy of modifiable risk factors. In the United States, high fasting plasma glucose has overtaken tobacco use as the leading attributable risk factor for pancreatic cancer DALYs. In China, high fasting glucose has risen to become a major contributor, now roughly comparable to tobacco in its population-attributable impact. The researchers measured this using population attributable fractions, or PAFs, which quantify the proportion of disease burden that could theoretically be eliminated if a specific risk factor were removed at the population level. The ascent of metabolic risk factors in both countries signals a fundamental shift in the prevention landscape, one that moves pancreatic cancer control increasingly into the domain of diabetes management, obesity prevention, and metabolic health.

This shift is biologically plausible and fits within a broader scientific understanding of pancreatic carcinogenesis. Chronic hyperglycemia, insulin resistance, and type 2 diabetes have been repeatedly associated with elevated pancreatic cancer risk in epidemiological studies, and the pancreas is an organ exquisitely sensitive to metabolic stress. At the same time, the decline of tobacco as the dominant attributable factor in the United States reflects decades of successful smoking control, a public health achievement that has reduced smoking prevalence substantially since the 1960s. The Chinese trajectory differs: smoking remains widespread, particularly among men, so tobacco continues to exert a heavy toll even as metabolic risk factors rise rapidly alongside economic development, dietary change, and increasing rates of overweight and diabetes.

The study also examined the socioeconomic dimensions of pancreatic cancer burden, and here the findings were sobering. Globally, the burden of the disease remained concentrated in regions with a high socio-demographic index, a composite measure of income, education, and fertility that serves as a proxy for overall development. More troubling still, absolute socioeconomic inequality in pancreatic cancer burden increased over the study period. This pattern suggests that as some populations gain access to better diagnostics, registration, and care, the measured and actual burden accumulates disproportionately among wealthier and more developed settings, while gaps between the best-off and worst-off regions widen rather than narrow. For a disease that is already difficult to diagnose early and harder still to treat, such inequities compound the challenge of mounting an effective global response.

The methodological backbone of the analysis deserves attention, because it illustrates how modern burden-of-disease research works. The Global Burden of Disease Study synthesizes data from vital registration systems, cancer registries, and modeling approaches to produce comparable estimates across countries and years, complete with 95 percent uncertainty intervals that convey the precision of each figure. By combining these estimates with population attributable fractions for individual risk factors, the researchers could rank the drivers of pancreatic cancer DALYs in each country and track how those rankings changed between 1990 and 2023. This framework transforms raw epidemiological surveillance into actionable intelligence, allowing policymakers to see not just how much disease exists but which modifiable exposures contribute most to it and how those contributions are evolving.

The research was led by investigators including Dr. Yifei Hu of the School of Public Health at Capital Medical University in Beijing and Dr. Wenming Wu of the Department of General Surgery at Peking Union Medical College Hospital, and it was funded by the Beijing Natural Science Foundation and the National Natural Science Foundation of China. The authors conclude that tailored, country-specific prevention strategies will be essential to curb the growing burden of pancreatic cancer in the coming decades, with particular emphasis on addressing the rising tide of metabolic risk factors. For the United States, that means treating glycemic control and diabetes prevention as cancer prevention, while for China it demands a dual strategy that confronts both the entrenched tobacco epidemic and the accelerating metabolic transition simultaneously.

The broader lesson of this study extends beyond two countries. Pancreatic cancer is projected to remain a leading cause of cancer death worldwide, and its resistance to early detection and treatment makes prevention the most powerful available lever. As populations age and metabolic diseases proliferate across the globe, the findings from China and the United States offer a preview of what many nations may face: a rising tide of pancreatic cancer whose risk profile is shifting from behavioral exposures like smoking toward metabolic conditions like hyperglycemia. Health systems that anticipate this shift, investing in diabetes prevention, metabolic screening, and equitable access to care, may be better positioned to blunt the impact of one of medicine’s deadliest diseases before its burden becomes unmanageable.

Subject of Research: Comparative burden and risk factors of pancreatic cancer in China and the United States, 1990–2023

Article Title: Pancreatic cancer burden rises in both China and the US, but patterns diverge

Article References: Pancreatic cancer burden rises in both China and the US, but patterns diverge. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: pancreatic cancer, Global Burden of Disease, DALYs, high fasting glucose, tobacco use, China, United States, population attributable fraction, metabolic risk factors, age-standardized mortality, socioeconomic inequality, cancer prevention

The significance of the study lies less in its absolute figures than in the fact that they exist at all. Mental health research across Central Asia has been critically under-prioritized, according to a recent scoping review cited by the authors, and empirical data on youth aged 15 to 24 in the region have remained sparse. This gap is particularly concerning given the epidemiological context. Globally, roughly 300 million people aged 5 to 24 live with a mental health disorder, contributing nearly 30 million years lived with disability, and suicide remains a leading cause of death among those aged 15 to 29, with three quarters of these deaths occurring in low- and middle-income countries. In Eastern Europe and Central Asia, suicide is the foremost cause of mortality among young people. UNICEF has previously reported that the risk of suicidal behavior among Kazakhstani adolescents aged 15 to 19 is three times higher than the average across the Commonwealth of Independent States, making the absence of rigorous national data all the more striking.

The methodological machinery behind the new estimates is considerable. The 2024 MICS employed a two-stage, stratified cluster sampling design that generated representative estimates at national, regional, and urban-rural levels across all 17 regions and three major municipalities of Kazakhstan. In the first stage, census enumeration areas were systematically selected with probability proportional to size; in the second, households were systematically sampled within each area. The survey achieved a household response rate of 96.3 percent, with response rates of 97.4 percent among women and 94.4 percent among men aged 15 to 24. After excluding participants with more than half of the screening items missing, the analytical sample comprised 5,079 young people. Missing data were minimal, below 1 percent for all three outcomes, and were handled through multiple imputation by chained equations with five imputations. All analyses incorporated survey weights and clustering by enumeration district to preserve national representativeness.

Depression and anxiety were screened using two ultra-brief instruments: the two-item Patient Health Questionnaire, known as PHQ-2, and the two-item Generalized Anxiety Disorder Scale, GAD-2. The PHQ-2 asks about the frequency of depressed mood, defined as sadness and hopelessness, and anhedonia, the loss of pleasure in previously enjoyable activities, over the preceding two weeks. The GAD-2 probes feelings of nervousness, anxiety, or being on edge, together with the inability to stop or control worrying. Each item is rated on a four-point scale from zero to three, producing total scores from zero to six, with a cut-off of three or higher flagging potential depression or anxiety. Suicidality was assessed as a binary self-reported measure, classifying participants as positive if they had tried to harm themselves with intent to end their life in the past 12 months or had thought about doing so in the past two weeks. While formal validation of these instruments in Kazakhstan is limited, systematic reviews support the reliability of ultra-brief screeners across diverse cultural settings.

To identify independent risk factors, the researchers applied modified Poisson regression models, an approach chosen because it directly estimates risk ratios, which are more interpretable than odds ratios and align with the calculation of population attributable fractions, a statistic that quantifies how much of a condition’s burden in the population could theoretically be eliminated if a risk factor were removed. The results were unambiguous. In fully adjusted models, female sex was the strongest predictor of both potential depression, with an adjusted risk ratio of 2.72, and potential anxiety, with an adjusted risk ratio of 2.80. Non-Kazakh ethnicity remained significantly associated with both outcomes, at 1.88 for depression and 1.99 for anxiety. The population attributable fractions were striking: female sex alone accounted for 45.6 percent of the population risk of depression and 46.8 percent of the risk of anxiety, while non-Kazakh ethnicity contributed 19.5 percent of depression risk.

Anxiety showed a further wrinkle that sets it apart from depression: a U-shaped relationship with household wealth. Both lower wealth, with an adjusted risk ratio of 1.89, and higher wealth, at 2.20, were associated with elevated anxiety risk, and the corresponding attributable fractions were 33.0 percent for low wealth and 21.7 percent for high wealth. The authors suggest that the mechanisms at the two ends of the wealth spectrum may differ. At the lower end, financial hardship and material deprivation act as persistent stressors that erode mental health, a relationship well documented in longitudinal research. At the upper end, evidence indicates that parents with higher socioeconomic status tend to hold higher expectations for their children’s achievement, and that pressure to perform can breed worry about failure and fear of disappointing parents, feeding internalizing problems. In other words, scarcity and pressure may converge on the same anxious outcome through very different routes.

Stratified analyses reinforced how pervasive the gender gap is. Among 15 to 19 year olds, females reported significantly higher prevalence of potential depression, 1.8 percent versus 0.8 percent in males, and anxiety, 1.9 percent versus 0.6 percent. The disparity widened in the 20 to 24 age group, where depression reached 3.5 percent in females against 1.0 percent in males, and anxiety 3.0 percent versus 1.2 percent. The same pattern held in both rural and urban settings, suggesting that gender-specific vulnerabilities operate independently of residential context. The authors frame this within the internalizing-externalizing framework of psychopathology, which conceptualizes depression and anxiety as manifestations of a broader internalizing dimension to which females show greater liability, shaped by pubertal hormonal changes, differential exposure to stressors, adverse childhood experiences, gender inequity, and higher exposure to maltreatment, including childhood sexual abuse.

Geography mattered too. Regional prevalence varied significantly for depression and anxiety, though not for suicidality. North Kazakhstan recorded the highest prevalence of potential depression at 5.44 percent, while West Kazakhstan led on anxiety at 4.51 percent and also showed the highest, though statistically non-significant, suicidality figure of 2.35 percent. The authors point to regional heterogeneity in economic development, service access, and culture as plausible explanations: North Kazakhstan has experienced lower economic development and higher unemployment, potentially exposing residents to chronic stressors that manifest as depression, whereas West Kazakhstan is characterized by industrial activity, migration fluctuations, and relative social isolation, conditions that may heighten exposure to acute stress and uncertainty. Cultural factors, including stigma, help-seeking norms, and religiosity, may further shape which symptoms are experienced and reported in surveys.

Perhaps the most enigmatic finding concerns suicidality. Despite the region’s alarming background rates of youth suicide, no sociodemographic factor, not sex, age, residence, education, marital status, wealth, or ethnicity, was significantly associated with potential suicidality in either unadjusted or adjusted analyses. The authors caution that the low prevalence of 0.96 percent may have limited statistical power to detect associations, and they stress that suicidal behavior may not simply be an extension of depression or anxiety but may involve complex, multidimensional interactions among social, psychological, and life-event factors. They also acknowledge the study’s limits: screening tools identify potential symptoms rather than confirmed clinical diagnoses, self-report in a stigma-laden context may drive underreporting, the cross-sectional design precludes causal inference, and the analysis was restricted to sociodemographic variables available in the survey, leaving room for residual confounding. Even so, the study delivers the first national benchmarks for youth mental health in Kazakhstan, and its implications are clear. Prevalence rates lower than global averages should not obscure the concentration of risk among young women and ethnic minority youth. Meeting Sustainable Development Goal Target 3.4, which mandates the promotion of mental health and well-being across the lifespan, the authors argue, will require culturally sensitive, targeted interventions and strengthened early detection for precisely these vulnerable subgroups.

Subject of Research: National prevalence and sociodemographic correlates of depression, anxiety, and suicidality among young people in Kazakhstan

Article Title: National prevalence and sociodemographic correlates of potential depression, anxiety, and suicidality among the young population in Kazakhstan: a national population-based study

Article References: Li, X., Stickley, A., Cai, Y., Gai, Y., Bjørklund, G., Li, Y., Jiang, F., & Chen, S. (2026). National prevalence and sociodemographic correlates of potential depression, anxiety, and suicidality among the young population in Kazakhstan: a national population-based study. BMC Psychology, 14(1), Article 1421. https://doi.org/10.1186/s40359-026-05618-8

Image Credits: AI Generated

DOI: 10.1186/s40359-026-05618-8

Keywords: Kazakhstan, youth mental health, depression, anxiety, suicidality, PHQ-2, GAD-2, MICS survey, gender disparities, ethnicity, population attributable fraction, Central Asia

The study, known as the Tianshan Community Cohort, enrolled participants between January 2019 and December 2023 through 12,520 primary healthcare institutions across the Xinjiang Uyghur Autonomous Region, a territory of roughly 1.66 million square kilometers. The cohort is ethnically diverse, comprising approximately 53 percent Uyghur, 33 percent Han, and 14 percent other minority participants, with 52 percent women. Annual health examinations mandated by China’s National Basic Public Health Services Program provided repeated measurements of six metabolic risk factors: obesity, hepatic steatosis, hypertension, hyperlipidemia, diabetes, and renal dysfunction. Cardiovascular events were objectively ascertained from inpatient records at 163 tertiary hospitals and 63 traditional Chinese medicine hospitals, coded according to the tenth revision of the International Classification of Diseases.

Among the 7,513,828 participants included in the primary analysis, who had a mean age of 44.4 years, the researchers tracked 669,995 incident cardiovascular events over a median follow-up of 4.5 years, including 442,120 cases of coronary heart disease and 398,300 strokes. As expected, cardiovascular incidence rose steeply with age, from 1.8 per 1,000 person-years in adults under 40 to 107.5 per 1,000 person-years among the very old. But the striking discovery was not the raw incidence; it was how the strength of the link between each metabolic abnormality and cardiovascular risk transformed across the age spectrum, with a rigor that had never before been achieved at this scale.

The central message is that metabolic abnormalities exert their most potent cardiovascular effects in young adults, and the strength of these associations steadily attenuates with advancing age. Hypertension showed the most dramatic pattern: in adults under 40, it was associated with a 3.60-fold increase in cardiovascular risk, but in those aged 80 and older, the hazard ratio fell to just 1.21. Diabetes showed a similar attenuation, from a hazard ratio of 2.48 in the youngest group to 1.31 in the oldest, as did hyperlipidemia, which fell from 1.65 to 1.05, and renal dysfunction, from 1.69 to 1.12. Notably, hypertension in young adults carried an exceptionally strong association with stroke specifically, with a hazard ratio of 4.84. When multiple metabolic abnormalities coexisted, the risk compounded: young adults with three or more risk factors had a 3.16-fold higher cardiovascular risk compared with metabolically healthy peers, whereas the excess risk among the very old with equivalent multimorbidity was only 1.50-fold.

The study also uncovered a striking age-dependent sexual dimorphism in metabolic health. In young adulthood, women enjoyed a clear metabolic advantage, being more likely to be metabolically normal and less likely to carry three or more simultaneous metabolic abnormalities. However, this female advantage reversed around age 45, when women became less likely to be metabolically normal than men, and a second reversal occurred around age 50, when the prevalence of multimorbidity in women surpassed that of men. The underlying factors crossed over at different ages: obesity and hepatic steatosis became more prevalent in women around age 40, hypertension around 50, and hyperlipidemia around 55. The researchers suggest that reproductive transitions, pregnancy-related hormonal shifts, childrearing-related lifestyle changes, and the perimenopausal reshaping of body composition likely drive this midlife reversal, making women a uniquely vulnerable population during this period.

Sex also mattered for the strength of metabolic risk itself. In adults under 40, hypertension was associated with a stronger cardiovascular impact in women than in men, with a hazard ratio for stroke of 6.41 in young women compared with 4.22 in young men, a clinically meaningful disparity that the researchers flagged using a predefined ratio-of-hazard-ratios threshold. Conversely, renal dysfunction carried a stronger cardiovascular penalty for men than women in the two youngest age groups. These sex-specific patterns largely faded in older groups, suggesting that the physiological vulnerability of young women to hypertension-related vascular damage has been substantially underappreciated in a literature dominated by middle-aged and elderly cohorts.

To translate individual risk into population impact, the team calculated population attributable fractions, the proportion of cardiovascular disease cases that could be attributed to each metabolic factor, using a method that permutes each risk factor through every possible position in the statistical hierarchy to account for correlations and shared causal pathways. The combined metabolic burden showed an inverted U-shaped pattern across the lifespan, peaking in midlife at 37.89 percent among adults aged 40 to under 60, compared with 29.78 percent in young adults, 25.24 percent in those aged 60 to 80, and 15.85 percent in the very old. Obesity was the single largest contributor to cardiovascular burden in every age group, potentially explaining between 6.07 and 11.86 percent of incident cardiovascular cases across adulthood, followed by hypertension and hepatic steatosis. For coronary heart disease, obesity’s attributable fraction reached 13.91 percent in the middle-aged group, while for stroke, hypertension was the predominant contributor at every age. The researchers attribute obesity’s outsized regional prevalence partly to northwestern China’s distinctive climate, ethnic composition, and dietary habits, and they argue that its dual role as an upstream driver of other metabolic disorders makes obesity prevention the most consequential public health lever available.

Perhaps the most actionable finding came from analyzing what happens when metabolically abnormal people change their metabolic state. Among 3,712,053 participants with at least one metabolic risk factor at baseline, the researchers tracked transitions between the first and second health examinations, separated by a median of roughly one year. The results showed a clear dose-response relationship: each additional risk factor gained increased cardiovascular risk, and each one lost decreased it. Critically, the benefit of improvement was strongly age-dependent. Young adults who brought three or more metabolic risk factors under control within about a year experienced a 55 percent lower subsequent cardiovascular risk, compared with only a 17 percent reduction among the very old. The authors interpret this asymmetry through the lens of disease biology: metabolic derangements in the young are typically nascent and largely reversible, with minimal cumulative end-organ damage, whereas in the very old, metabolic control often represents long-term maintenance rather than true reversal, frequently accompanied by multimorbidity and polypharmacy.

The time-series analysis of 1,649,758 participants with five consecutive annual examinations added an alarming temporal dimension. In the youngest age group, obesity prevalence climbed from 36.0 percent in 2019 to 48.5 percent in 2023, while the proportion of metabolically normal individuals fell from 50.9 percent to 38.8 percent in just five years, a pace of deterioration far exceeding that seen in older groups. The authors note that metabolic abnormalities in young adults are chronically under-recognized and under-treated, and that without prompt intervention these abnormalities can progress into a self-reinforcing vicious cycle of insulin resistance and inflammation. In a region where cardiovascular disease causes an estimated 19.2 million deaths and 437 million disability-adjusted life years globally each year, and where 42 percent of incident cardiovascular cases in China are attributable to four major metabolic risk factors, the implications are stark.

Taken together, the study argues for a fundamental reallocation of preventive attention toward people under 60, and particularly toward young adults, who have been almost entirely absent from the evidence base that shapes current guidelines. Despite the persistently high metabolic burden in older adults, the window of maximal cardiovascular benefit from metabolic management appears confined to early and middle adulthood. The findings also call for age-specific and gender-sensitive strategies: intensified screening for hypertension in young women, obesity control as the universal top priority, and vigilant monitoring of midlife women as their metabolic advantage erodes through reproductive and menopausal transitions. The researchers acknowledge limitations, including the use of an indirect index rather than imaging to define hepatic steatosis, the absence of systematic medication data, self-reported lifestyle covariates, and the relatively short five-year follow-up, but extensive sensitivity analyses, including competing-risk regression, landmark analyses, and multiple imputation, consistently supported the primary conclusions. As the dual epidemics of youthful metabolic deterioration and population aging accelerate, this unprecedented cohort provides both a warning and a roadmap: the earlier metabolic health is restored, the greater the lifetime cardiovascular dividend.

Subject of Research: Metabolic risk factors and their age- and sex-specific impact on cardiovascular disease across the adult lifespan

Article Title: A landscape of metabolic burden and its cardiovascular impact across the adult lifespan: a prospective cohort study of 7.5 million people in Northwestern China

Article References: Liu, Z.-Y., Yang, J., Lyu, J.-Q., Miao, M.-Y., Qin, L.-Q., Wang, H.-P., Wan, Z., Huang, Q., Tao, J., Yang, Y., Di, Q., Yang, Y., Gu, K., & Chen, G.-C. (2026). A landscape of metabolic burden and its cardiovascular impact across the adult lifespan: a prospective cohort study of 7.5 million people in Northwestern China. The Lancet Regional Health – Western Pacific, 74, Article 101986. https://doi.org/10.1016/j.lanwpc.2026.101986

Image Credits: AI Generated

DOI: 10.1016/j.lanwpc.2026.101986

Keywords: cardiovascular disease, metabolic risk factors, obesity, hypertension, diabetes, hepatic steatosis, renal dysfunction, population attributable fraction, young adults, sex differences, prospective cohort, China

Hepatitis B virus (HBV) remains one of the world’s most consequential pathogens. An estimated 254 million people were living with chronic HBV infection in 2022, and roughly 1.1 million deaths were attributed to the virus that year. China carries the heaviest national burden, with approximately 75 million infected individuals. Chronic infection drives cirrhosis and hepatocellular carcinoma (HCC), but accumulating evidence also links chronic HBV to elevated risks of digestive system malignancies, kidney disease, and mortality from cardiovascular and cerebrovascular conditions compared with the general population. Against this backdrop, the World Health Organization has endorsed a global strategy to eliminate viral hepatitis by 2030, emphasizing both the prevention of new infections and the expansion of diagnosis and treatment to reduce mortality among those already infected.

Loss of HBsAg is the central therapeutic goal in chronic hepatitis B and underpins the treatment endpoint known as functional cure. Spontaneous HBsAg seroclearance also occurs during the natural course of infection, though infrequently — roughly 1 percent of patients per year. Prior research has consistently shown that patients who clear HBsAg experience substantially lower rates of cirrhosis and HCC. What remained uncertain, however, was whether seroclearance is also associated with overall survival and, in particular, with extrahepatic mortality from cancers and cardiovascular disease — a question of growing importance as the population of people living with chronic hepatitis B ages and accumulates comorbidities.

To address this gap, investigators drew on the Chronic Hepatitis B Infection and Liver Disease (HEPCARE) study, a multicenter, prospective, community-based cohort in Jiangsu Province. Participants were recruited through serological surveys conducted between September 2009 and November 2010 and were required to be HBsAg-positive, hepatitis C antibody-negative, and free of cirrhosis and liver cancer at enrollment. Because HBV DNA measurements began at the 2012 follow-up, the analysis defined 2012 as baseline and followed participants through December 2023, with assessments in 2012, 2013, 2014, 2016, 2018, 2020, and 2023. After exclusions, 6551 participants entered the analytical pool, and after propensity score matching on age, sex, region, and baseline antiviral treatment status, the final matched cohort comprised 1029 individuals who achieved sustained HBsAg seroclearance with HBV DNA below 100 IU/mL and 2931 who remained persistently HBsAg-positive.

A key methodological strength of the study lies in its handling of time. HBsAg seroclearance is a time-dependent event that occurs during follow-up, and conventional analyses that treat it as a fixed baseline characteristic are vulnerable to immortal time bias, which can distort survival estimates. By conducting regular interval surveillance and using time-dependent Cox regression, the researchers could allocate person-time accurately according to each participant’s changing serovirological status. The exposure itself was stringently defined: seroclearance required HBsAg negativity together with HBV DNA below the quantification limit of 100 IU/mL, confirmed at two or more consecutive follow-up visits, with participants whose profiles suggested occult hepatitis B infection excluded to avoid misclassification.

The results were striking across multiple outcome domains. Over a median follow-up of roughly 11 years, participants who achieved sustained seroclearance had significantly lower incidence rates of cirrhosis (2.02 versus 3.97 per 1000 person-years) and HCC (2.97 versus 4.97 per 1000 person-years). In fully adjusted time-dependent Cox models, seroclearance was associated with a 55 percent lower hazard of cirrhosis (adjusted hazard ratio 0.45) and a 48 percent lower hazard of HCC (adjusted hazard ratio 0.52). Mortality told a similar story: 64 deaths occurred in the seroclearance group compared with 405 in the persistent infection group, corresponding to incidence rates of 7.55 and 12.17 per 1000 person-years, and seroclearance was associated with a 53 percent lower hazard of all-cause mortality (adjusted hazard ratio 0.47).

Perhaps the most novel findings concerned cause-specific mortality. Among the 469 deaths in the matched population, 146 were attributed to extrahepatic cancers, 117 to cardiovascular disease, and 112 to liver-related causes. Sustained seroclearance was associated with lower hazards of liver-related mortality (adjusted hazard ratio 0.46), extrahepatic cancer-related mortality (0.51), and cardiovascular mortality (0.56), with the strongest association observed for digestive system cancer-related mortality. When competing risks were formally accounted for using Fine–Gray subdistribution hazard models, these associations persisted for cirrhosis, HCC, liver-related mortality, and extrahepatic cancer-related mortality, and model-standardized cumulative incidences at 10 years were consistently lower in the seroclearance state for all major endpoints examined.

The investigators then asked whether HBsAg loss carries prognostic information beyond viral DNA suppression alone — a clinically important question, since suppressing HBV DNA below 100 IU/mL is a conventional treatment goal. In an analysis treating serovirological status as a three-state time-varying variable, the HBsAg-negative state with very low HBV DNA was associated with lower hazards of cirrhosis, HCC, all-cause mortality, extrahepatic cancer mortality, and cardiovascular mortality compared with the HBsAg-positive state at similarly low viral loads. Conversely, isolated HBV DNA suppression without seroclearance was not associated with lower extrahepatic mortality. Additional weighting analyses incorporating baseline HBV DNA attenuated the HCC estimate somewhat, suggesting that part of that association depends on differences in baseline viral burden, but the associations with all-cause and extrahepatic cancer mortality remained statistically significant.

To translate the associations into population-level terms, the team estimated population attributable fractions and restricted mean survival time. Persistent infection was associated with attributable fractions of approximately 48 percent for cirrhosis, 47 percent for liver-related mortality, 42 percent for all-cause mortality, 41 percent for HCC, 40 percent for extrahepatic cancer mortality, and 35 percent for cardiovascular mortality. Using age as the time scale, restricted mean survival time was estimated at 83.21 years in the seroclearance state versus 78.04 years in the persistent infection state — a 5.17-year difference within the observed age range, with the survival advantage widening notably after age 60. Sex-stratified analyses suggested that these inverse associations were generally stronger in men, with statistically significant interactions for all-cause and liver-related mortality, echoing prior evidence that men with chronic hepatitis B tend to experience less favorable long-term outcomes than women.

The authors caution that most seroclearance events in the cohort occurred spontaneously rather than through antiviral therapy, so the findings primarily reflect the prognosis associated with spontaneous HBsAg loss, which may partly reflect a favorable underlying viral-host profile and overall health status. Residual confounding from unmeasured factors such as socioeconomic status and healthcare utilization cannot be excluded, the assay’s quantification limit of 100 IU/mL may have classified some low-level viremia as undetectable, and the single-province, community-based design warrants validation in other populations, including cohorts enriched for treatment-induced functional cure. Biologically, the authors propose that persistent viral antigen exposure and chronic immune activation may impair tumor immune surveillance and promote systemic inflammation, whereas HBsAg clearance accompanies a marked reduction in antigen burden and partial restoration of HBV-specific immune responses — hypothesis-generating mechanisms that require further study. Nevertheless, the consistency of the associations across competing-risk models, three-state analyses, and extensive sensitivity analyses, combined with the substantial attributable burden and survival differences, positions sustained HBsAg seroclearance with very low HBV DNA as an informative long-term prognostic marker in chronic hepatitis B, and underscores the potential population health value of broader attainment of this serovirological state.

Subject of Research: HBsAg seroclearance and long-term hepatic and extrahepatic mortality risks in chronic hepatitis B

Article Title: HBsAg seroclearance with HBV DNA <100 IU/mL and long-term risks of adverse liver events, all-cause mortality, and cause-specific mortality in chronic hepatitis B: a prospective cohort study

Article References: Zhang, Y., Yao, W., Jiang, J., Qian, J., Chen, X., Jiang, Q., Yan, Y., Wang, S., Bai, H., He, C., Zhu, L., Jiang, T., Hu, Z., Shen, H., Zhai, X., & Song, C. (2026). HBsAg seroclearance with HBV DNA <100 IU/mL and long-term risks of adverse liver events, all-cause mortality, and cause-specific mortality in chronic hepatitis B: a prospective cohort study. The Lancet Regional Health – Western Pacific, 74, Article 101983. https://doi.org/10.1016/j.lanwpc.2026.101983

Image Credits: AI Generated

DOI: 10.1016/j.lanwpc.2026.101983

Keywords: hepatitis B, HBsAg seroclearance, functional cure, hepatocellular carcinoma, cirrhosis, all-cause mortality, extrahepatic cancer, cardiovascular mortality, HBV DNA, prospective cohort, population attributable fraction, chronic hepatitis B

The research team screened 21,418 references drawn from six major databases, including PubMed/MEDLINE, Scopus, Web of Science, SPORTDiscus, PsycINFO and Open Dissertations. From this vast pool, only 40 papers met the stringent inclusion criteria, which required studies to report total, direct or indirect monetary costs associated with at least one of the three movement behaviours in the general adult population. That small yield is itself revealing. Despite growing scientific consensus that physical activity, sedentary behaviour and sleep should be understood as a continuous, integrated 24-hour cycle of time use, the economic evidence base remains remarkably thin, fragmented and geographically skewed. Fully 77.5 percent of the included studies came from high-income countries, and an equally striking 77.5 percent addressed the costs of physical activity alone, leaving sedentary behaviour and sleep largely neglected in economic terms.

The methodological foundation of the review deserves attention because cost-of-illness studies vary enormously in how they count the money. Most of the included research, some 90 percent, relied on self-reported movement-behaviour data rather than device-based measurements, a choice that introduces well-documented recall and social desirability biases. People systematically overestimate how much they move and underestimate how long they sit. Many of the studies also employed the population attributable fraction approach, a technique borrowed from epidemiology that estimates what proportion of disease burden and associated costs could be avoided if exposure to a risk factor, such as insufficient exercise, were eliminated from the population. When applied to national data, PAF-based studies estimated the total annual cost of insufficient physical activity at between 1.94 and 9.78 billion US dollars, while the cost of excessive sedentary behaviour ranged from 1.82 to 1.97 billion dollars.

Sleep, the third pillar of the movement-behaviour triad, fared worst in terms of research attention. Only a single study in the review used the population attributable fraction approach to estimate the economic cost of inadequate sleep duration, placing Canada’s national bill at 0.44 billion US dollars per year. That figure, while substantial in absolute terms, is dwarfed by the estimates for physical inactivity, and the authors caution that it rests on a solitary data point rather than a robust, replicated body of evidence. The scarcity of sleep-cost studies is especially notable given the accelerating public health interest in sleep as a modifiable risk factor for cardiometabolic disease, mental illness, workplace accidents and lost productivity.

Perhaps the most consequential finding of the review is the relative ranking of the three behaviours. Across the included studies, the economic cost of insufficient physical activity was approximately two to four times higher than the cost of excessive sedentary behaviour and roughly sixteen times higher than the cost of inadequate sleep duration. On the basis of this cost hierarchy, the authors suggest that public health initiatives should focus primarily on promoting physical activity, while continuing to address sitting time and sleep within a broader 24-hour framework. The conclusion carries practical weight for policymakers forced to allocate finite prevention budgets: if the goal is to maximise the economic return on public health investment, getting populations moving appears to deliver the largest financial dividend.

The direct and indirect cost categories underlying these figures illuminate why unhealthy movement behaviours drain national economies so severely. Direct costs encompass healthcare expenditure, including hospital admissions, physician visits, medications and treatment for conditions attributable to inactivity, prolonged sitting or poor sleep, such as cardiovascular disease, type 2 diabetes, several cancers, depression and musculoskeletal disorders. Indirect costs capture productivity losses from absenteeism, presenteeism, premature mortality and unpaid informal care. Because movement behaviours influence such a wide array of chronic diseases, even modest shifts in population-level behaviour can translate into enormous aggregate expenditure changes. A behaviour that raises the risk of multiple conditions simultaneously multiplies its economic footprint across every disease pathway it touches.

The review’s global picture, however, remains frustratingly incomplete. The authors emphasise that while billions of dollars are cumulatively spent each year on the adverse consequences of unhealthy movement behaviours worldwide, the exact global cost could not be estimated because evidence exists only for a limited number of mostly high-income countries. This gap matters enormously. Low- and middle-income countries bear a growing share of the global burden of non-communicable disease, driven by rapid urbanisation, motorised transport, desk-based employment and changing dietary and sleep patterns, yet virtually no economic cost estimates exist for these settings. Without local cost data, governments in these countries lack the financial arguments needed to justify investment in physical activity infrastructure, workplace interventions or sleep health programmes.

The study also highlights a deeper conceptual challenge within the field. Public health research is increasingly shifting toward an integrative, compositional view of daily time use, in which physical activity, sedentary behaviour and sleep are treated as interdependent components constrained by the finite 24-hour day. Time spent in one behaviour necessarily displaces time in another, so the health and economic effects of any single behaviour depend on what it replaces. Yet the economic literature reviewed here remains overwhelmingly siloed, with most studies costing one behaviour in isolation and almost none examining the economic consequences of failing to meet the overall 24-hour movement guidelines that now appear in national and international recommendations. The authors explicitly call for more research exploring the costs of non-compliance with these integrated guidelines.

Looking forward, the research agenda outlined by the review is clear. Future studies should extend cost estimation to low- and middle-income countries, replace self-reported behaviour data with device-based measurements from accelerometers and other research-grade movement sensors, and address the glaring underrepresentation of sedentary behaviour and sleep in economic analyses. Until such work is done, the 9.2 billion dollar Canadian figure and the multi-billion dollar estimates for physical inactivity should be read as conservative, incomplete accounting of a problem whose true global scale remains hidden. What the review makes unambiguous is that unhealthy movement is not merely a personal health risk but a macroeconomic liability, and that the price of collective inactivity compounds year after year on national balance sheets.

Subject of Research: Systematic review of the economic costs of insufficient physical activity, excessive sedentary behaviour and inadequate sleep duration in adults

Article Title: Economic cost of movement behaviours: a systematic review

Article References: Chen, S., Matolic, T., Memon, A. R., Rachele, J. N., Grgic, J., Espinoza, M. A., & Pedisic, Z. (2026). Economic cost of movement behaviours: a systematic review. Journal of Activity, Sedentary and Sleep Behaviors. https://doi.org/10.1186/s44167-026-00108-z

Image Credits: AI Generated

DOI: 10.1186/s44167-026-00108-z

Keywords: physical activity, sedentary behaviour, sleep, economic cost, systematic review, public health, cost of illness, 24-hour movement behaviours, population attributable fraction, health economics, physical inactivity, chronic disease

H. pylori is a formidable public health adversary. More than 40 percent of adults worldwide carry it, and infection, typically acquired in childhood, generally persists for life unless deliberately eradicated. Most carriers never develop symptoms, so few seek testing or treatment, allowing a vast silent reservoir of chronic infection to accumulate. The International Agency for Research on Cancer estimates that roughly 850,000 cancer cases worldwide in 2020 were attributable to the bacterium, more than from any other cancer-causing infection, including human papillomavirus and the hepatitis B and C viruses. China, which accounts for about 35 percent of global gastric cancer cases, sits at the epicentre of this burden.

Earlier meta-analyses had reported that H. pylori prevalence in China fell from roughly 55 to 60 percent in 1990 to around 40 to 45 percent by 2020, fuelling optimism that the epidemic was receding on its own. The new study, led by Dianqin Sun of Erasmus MC in collaboration with researchers in the United States, Mexico, and the International Agency for Research on Cancer, argues that this optimism rested on shaky statistical ground. Previous pooled estimates ignored the age structure of the populations being surveyed, conflated distinct measures of infection, and failed to correct for the imperfect accuracy of diagnostic tests, biases that can make prevalence appear to fall faster than it truly does.

The team assembled an unusually deep evidence base. From six published meta-analyses and an updated search of PubMed, Embase, and Chinese databases, 741 original studies were initially identified; after rigorous screening for general-population relevance, adequate reporting, and acceptable detection methods, 180 unique studies covering 1983 to 2023 and all 31 provinces of mainland China qualified for meta-analysis, contributing 805 records of current infection or seroprevalence. One additional study measuring ever-infection was reserved for the transmission model, and a large nationwide survey was held back entirely as an independent validation target.

Crucially, the researchers recognised that the three main ways of measuring H. pylori are not interchangeable. Current-infection tests detect active bacteria, serology detects antibodies that can linger long after the infection has cleared or been treated, and ever-infection measures capture both. Pooling them together, as earlier reviews did, distorts trends. The team also applied the Rogan-Gladen correction to adjust each study’s observed prevalence for the sensitivity and specificity of the diagnostic test used, then pooled estimates separately by age, calendar period, and birth cohort using random-effects models on the logit scale.

The centrepiece of the analysis is a Bayesian catalytic model, a class of transmission model that infers the rate at which susceptible individuals acquire infection, known as the force of infection, from age-specific prevalence data. Individuals in the model begin uninfected, may become infected, and after treatment can clear the bacterium while remaining seropositive before eventually seroreverting. The model incorporated cohort-specific limits on lifetime infection risk, period-varying treatment rates, a constant rate of antibody waning, and diagnostic misclassification, and was fitted to the record-level data with Hamiltonian Monte Carlo. Four competing model structures were compared using leave-one-out cross-validation, and the selected model reproduced observed prevalence closely and passed external validation against the nationwide survey.

The model’s estimates tell a striking generational story. For the 1920 birth cohort, the annual force of infection was 3.21 percent at age 10; for the 2000 cohort it was just 1.72 percent at the same age, and childhood infection rates in recent cohorts now resemble those seen among young adults born in the 1910s. A clear inflection appears after the 1980 birth cohort, which the authors link to the sweeping improvements in water supply, sanitation, housing, and household hygiene that followed China’s reform and opening-up policy from 1978. Modernisation, in other words, reshaped transmission dynamics well before any medical intervention reached scale.

Yet the population-level picture is far less encouraging. Overall prevalence declined only modestly, from 43.1 percent in 1990 to 36.3 percent in 2023, and much of that apparent decline disappears once the ageing of the population is accounted for; age-standardised prevalence fell further than crude prevalence, indicating that demographic ageing has propped up the raw numbers. Because gastric cancer and peptic ulcer disease strike predominantly at older ages, the children who escaped infection have not yet reached the ages where disease risk peaks, while large, heavily infected cohorts continue to age into the danger zone. The population attributable fractions in 2023 remained 70.1 percent for non-cardia gastric cancer and 49.4 percent for cardia gastric cancer, using China-specific relative risks from the China Kadoorie Biobank and a ten-year latency window for cancer and a five-year window for ulcers.

The authors are careful about the limits of their estimates. Subtype-specific incidence data were unavailable, so they modelled bounding scenarios for the mix of cardia and non-cardia tumours and for duodenal versus gastric ulcers; the gastric ulcer attributable burden remained statistically compatible with zero. They also note that the synergy between H. pylori and nonsteroidal anti-inflammatory drugs was not modelled, which may underestimate the ulcer burden, and that substantial regional variation across China is masked by the national averages. Sensitivity analyses using alternative model structures produced similar attributable burden estimates, reinforcing the central conclusion.

The policy implications are pointed. The eradication benefits of treating H. pylori are well established, and guidelines from the World Health Organization, the Taipei Global Consensus, and Chinese expert bodies increasingly endorse organised screen-and-treat programmes and family-based approaches, which China’s expert consensus recommends but no national policy yet implements. Comparable efforts are advancing elsewhere: South Korea is trialling population screening within its national cancer programme, Japan reimburses eradication therapy for H. pylori gastritis, and the European Council has urged high-burden member states to consider screening. The study’s age- and cohort-specific estimates provide the quantitative foundation such programmes need, identifying which cohorts carry the heaviest infection load, how many people would be eligible for treatment, and what costs and antibiotic-use concerns each strategy would entail. The modelling framework, the authors add, is transferable to other high-burden countries undergoing similar epidemiological transitions, particularly in East and Southeast Asia, where declining childhood infection coexists with large infected adult cohorts moving into the gastric cancer risk window. Without active intervention, the analysis warns, China’s H. pylori-attributable disease burden is unlikely to decline rapidly for decades.

Subject of Research: Trends in Helicobacter pylori prevalence, force of infection, and attributable gastric cancer and peptic ulcer disease burden in China from 1990 to 2023

Article Title: Trends in Helicobacter pylori prevalence, force of infection, and attributable disease burden in China: a systematic review and Bayesian modelling study

Article References: Sun, D., Han, W., Alarid-Escudero, F., Roa-Contreras, J. A., Wang, S., Mülder, D. T., Huang, R. J., Ladabaum, U., Spaander, M. C., Camargo, M. C., Park, J. Y., Chen, W., Lansdorp-Vogelaar, I., & Hontelez, J. A. (2026). Trends in Helicobacter pylori prevalence, force of infection, and attributable disease burden in China: a systematic review and Bayesian modelling study. The Lancet Regional Health – Western Pacific, 74, Article 101979. https://doi.org/10.1016/j.lanwpc.2026.101979

Image Credits: AI Generated

DOI: 10.1016/j.lanwpc.2026.101979

Keywords: Helicobacter pylori, gastric cancer, peptic ulcer disease, Bayesian modelling, force of infection, systematic review, China, epidemiology, screen-and-treat, birth cohorts, population attributable fraction, public health