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PubMed2026

Prevalence and chronology of colibactin-associated mutational processes and their microbiome spectra in Japanese colorectal cancer.

The incidence of colorectal cancer (CRC) has risen in recent decades, with a disproportionate increase observed among younger individuals in Japan and other countries. The etiological contribution of the gut microbiota to CRC pathogenesis is recognized, yet the mechanisms involved remain to be fully clarified. Here we integrated whole-genome sequencing (WGS) and transcriptome profiling of CRC with whole-genome metagenomic sequencing of fecal samples to interrogate host-microbiome interactions at high resolution. Application of interpretable artificial intelligence enabled the stratification of CRC into four distinct microbiome-informed subtypes. WGS analysis identified mutational signatures SBS88 and ID18, linked to colibactin exposure, as early clonal events detected in 44.8% of non-hypermutated patients. Notably, these signatures were significantly more frequent among patients born after the 1960s. Microbiome-based subclassification revealed subtype-specific clinical and molecular features. Collectively, our findings indicate that colibactin exposure constitutes a prevalent and potentially modifiable risk factor for CRC in the Japanese population.

Humans↗

PubMed2026

Comparing genome-wide significant and chemosensory variants as instruments for dietary patterns in Mendelian randomization.

BACKGROUND: Diet is a modifiable risk factor for cardiometabolic disease, yet establishing causality remains challenging. Mendelian randomization (MR) leverages genetic variants as instrumental variables (IVs) to enable causal inference. METHOD: Using two-sample MR, we assessed the causal effects of four principal component-derived dietary patterns (DPs)-Unhealthy, Healthy, Meat-based, Pescatarian-on cardiometabolic outcomes including body mass index, coronary artery disease, blood lipids, blood pressures, type 2 diabetes, fasting glucose and insulin, and glycated haemoglobin. Two sets of IVs were employed: conventional genome-wide significant variants associated with each DP, filtered for pleiotropy and directionality; and biologically informed variants in chemosensory receptor genes, given the role of taste and smell perception in food choice. RESULTS: Using conventional IVs, the Pescatarian DP was associated with reduced fasting insulin (βIVW = -0.10 pmol/L per SD increase in the Pescatarian DP score, 95% confidence interval -0.15, -0.04; P = 1.19 × 10-3), surviving multiple sensitivity analyses. Associations between the Unhealthy DP and elevated blood pressure and glycated haemoglobin should be interpreted cautiously; one of the two filtered IVs was strongly associated with caffeine intake, limiting the attribution of these findings to the DP itself. Chemosensory Receptor IVs yielded null findings, reflecting insufficient power. CONCLUSION: Evidence for causal effects of DPs on cardiometabolic traits was limited, with the strongest support for a protective effect of the Pescatarian DP on fasting insulin. Chemosensory IVs demonstrated limited utility for DPs, likely reflecting the heterogeneous and complex sensory profiles of overall diets. Future efforts should consider guideline-based dietary indices to facilitate interpretability and translation.

Humans↗

PubMed2025

Proteomic signatures and predictive modeling of cadmium-associated anxiety in middle-aged and elderly populations: an environmental exposure association study.

BACKGROUND: Emerging evidence implicates environmental contaminants such as cadmium (Cd) as modifiable risk factors for anxiety. Despite growing recognition of heavy metal toxicity in neuropsychiatric disorders, the molecular mechanisms linking environmental exposure to anxiety pathogenesis remain poorly understood. METHODS: Based on the established cohort of individuals with cognitive impairment in cadmium-contaminated areas, this cross-sectional association study enrolled 50 middle-aged and elderly hospitalized patients from these regions, adhering to the STROBE guidelines. Blood concentrations of cadmium (Cd), lead (Pb), and mercury (Hg) were analyzed in relation to anxiety severity assessed via the Hamilton Anxiety Rating Scale (HAMA). Plasma proteomic profiling was performed using data-independent acquisition (DIA) quantitative technology with an LC-MS/MS platform (timsTOF Pro, Bruker Daltonics), systematically characterizing 2,531 proteins across all samples. Machine learning techniques, specifically XGBoost and LASSO, were employed to identify biomarkers that were subsequently validated through mediation analysis and animal experiments, allowing for the screening of key protein signatures. Finally, clinical variables were integrated to construct a comprehensive model, which was then thoroughly evaluated. RESULTS: Anxious individuals exhibited significantly higher blood Cd levels than controls (β = 0.50, 95% CI: 0.07-0.93, p < 0.01), with anxiety positively correlating with depression (r = 0.62, p = 0.003) and inversely with ApoE3 genotype prevalence. Proteomics identified 120 differentially expressed proteins in anxious patients, enriched in oxidative phosphorylation and neurodegenerative pathways. CCDC126 emerged as a cadmium-associated biomarker, validated in rat models exposed to Cd. Combining CCDC126, blood Cd, Pb, and hypertension, a clinical prediction model achieved robust discrimination (AUC = 0.80, validation cohort). CONCLUSIONS: This first integrative environmental-proteomic study highlights cadmium's synergistic role in anxiety pathophysiology and psychiatric comorbidity. The predictive model offers translatable potential for early risk stratification, while CCDC126 provides mechanistic insights for targeted interventions in populations exposed to environmental pollutants.

Cadmium↗

PubMed2026

Mendelian randomisation for rheumatology: beyond hype-what it's good for, what it can't do, and how to read it critically.

Mendelian randomisation (MR) has become abundant in the literature, with variation in quality and frequent overinterpretation of causality. This creates a problem for clinical readers, reviewers, and editors: some MR studies can sharpen causal thinking, prioritise drug targets, and challenge misleading observational claims, whereas others are little more than automated exposure-outcome scans with causal claims disproportionate to the evidence. MR can strengthen causal inference when randomised trials are impractical and conventional observational studies are vulnerable to confounding, reverse causation, or selection bias. In rheumatology, credible MR can contribute to questions about disease aetiology, modifiable risk factors, therapeutic target validation, adverse-effect anticipation, and phenotype validation. However, its interpretation depends on whether the exposure is plausibly instrumentable, whether the genetic instruments are biologically defensible, whether assumptions are interrogated in ways appropriate to the design, and whether findings are triangulated with clinical, observational, experimental, and mechanistic evidence. Instead of recapitulating all methodological issues of MR, this review aims to help rheumatologists distinguish robust MR from weak or overinterpreted analyses quickly. We provide an accessible framework for reading and triaging MR studies in rheumatology. Papers that use poorly justified instruments, treat medication use as drug-target evidence, interpret genetic liability as diagnosis, rely on mechanical sensitivity analyses, ignore prior evidence or ask no clinically meaningful question can often be passed over by readers. The goal is not to discourage MR in rheumatology, but to raise the standard; useful MR should clarify causal reasoning rather than simply generate another statistically significant association.

Journal Article↗

PubMed2025

The Role of Genomic-Informed Risk Assessments in Predicting Dementia Outcomes.

INTRODUCTION: By integrating genetic and clinical risk factors into genomic-informed dementia risk reports, healthcare providers can offer patients detailed risk profiles to facilitate understanding of individual risk and support the implementation of personalized strategies for promoting brain health. METHODS: We constructed an additive score comprising the modified Cardiovascular Risk Factors, Aging, and Incidence of Dementia Risk Score (mCAIDE), family history of dementia, APOE genotype, and an AD polygenic risk score in NACC and ADNI, and assessed its association with progression to all-cause dementia. RESULTS: 81% of participants had at least one high-risk indicator for dementia, with each additional risk indicator linked to a 34% increase in the hazard of dementia onset. DISCUSSION: We found that most participants in memory and aging clinics had at least one high-risk indicator for dementia. Furthermore, we observed a dose-response relationship where a greater number of risk indicators was associated with an increased risk of incident dementia.

dementia risk scores↗

PubMed2022

Improving risk indexes for Alzheimer's disease and related dementias for use in midlife.

Knowledge of a person's risk for Alzheimer's disease and related dementias (ADRDs) is required to triage candidates for preventive interventions, surveillance, and treatment trials. ADRD risk indexes exist for this purpose, but each includes only a subset of known risk factors. Information missing from published indexes could improve risk prediction. In the Dunedin Study of a population-representative New Zealand-based birth cohort followed to midlife (N = 938, 49.5% female), we compared associations of four leading risk indexes with midlife antecedents of ADRD against a novel benchmark index comprised of nearly all known ADRD risk factors, the Dunedin ADRD Risk Benchmark (DunedinARB). Existing indexes included the Cardiovascular Risk Factors, Aging, and Dementia index (CAIDE), LIfestyle for BRAin health index (LIBRA), Australian National University Alzheimer's Disease Risk Index (ANU-ADRI), and risks selected by the Lancet Commission on Dementia. The Dunedin benchmark was comprised of 48 separate indicators of risk organized into 10 conceptually distinct risk domains. Midlife antecedents of ADRD treated as outcome measures included age-45 measures of brain structural integrity [magnetic resonance imaging-assessed: (i) machine-learning-algorithm-estimated brain age, (ii) log-transformed volume of white matter hyperintensities, and (iii) mean grey matter volume of the hippocampus] and measures of brain functional integrity [(i) objective cognitive function assessed via the Wechsler Adult Intelligence Scale-IV, (ii) subjective problems in everyday cognitive function, and (iii) objective cognitive decline measured as residualized change in cognitive scores from childhood to midlife on matched Weschler Intelligence scales]. All indexes were quantitatively distributed and proved informative about midlife antecedents of ADRD, including algorithm-estimated brain age (β's from 0.16 to 0.22), white matter hyperintensities volume (β's from 0.16 to 0.19), hippocampal volume (β's from -0.08 to -0.11), tested cognitive deficits (β's from -0.36 to -0.49), everyday cognitive problems (β's from 0.14 to 0.38), and longitudinal cognitive decline (β's from -0.18 to -0.26). Existing indexes compared favourably to the comprehensive benchmark in their association with the brain structural integrity measures but were outperformed in their association with the functional integrity measures, particularly subjective cognitive problems and tested cognitive decline. Results indicated that existing indexes could be improved with targeted additions, particularly of measures assessing socioeconomic status, physical and sensory function, epigenetic aging, and subjective overall health. Existing premorbid ADRD risk indexes perform well in identifying linear gradients of risk among members of the general population at midlife, even when they include only a small subset of potential risk factors. They could be improved, however, with targeted additions to more holistically capture the different facets of risk for this multiply determined, age-related disease.

Alzheimer’s disease↗

PubMed2026

Urban heat island and risk of rheumatoid arthritis: Insights from genetic predisposition and proteomics.

BACKGROUND: Urban heat island (UHI) exposure is an increasingly common consequence of urbanization and climate warming, but its association with rheumatoid arthritis (RA) risk remains unclear. OBJECTIVE: To investigate the association between UHI exposure and incident RA, and to further assess the roles of genetic susceptibility and plasma proteomic profiles in this association. METHODS: This study included 400,628 urban residents with UHI exposure data and free of RA at baseline. Cox proportional hazards models were used to evaluate the association between UHI exposure and incident RA. Polygenic risk scores were used to assess effect modification by genetic susceptibility. Proteomic analyses identified candidate proteins and enriched pathways underlying the association. Mendelian randomization, colocalization, and mediation analyses assessed causal relevance and mediation. RESULTS: Over a median follow-up of 14.05 years, 5397 incident RA cases were documented. Each standard-deviation increase in UHI exposure was associated with a 17% higher risk of RA. This association was more pronounced among older adults and individuals with lower socioeconomic status. An additive interaction was observed between UHI exposure and genetic risk for RA. Proteomic analyses suggested that this association may involve not only canonical immune-inflammatory pathways, but also hypoxia response and protein transport, with CD40, VCAM1, and SUGP1 emerging as potential molecular mediators. CONCLUSIONS: UHI exposure may be a modifiable environmental risk factor for RA and provide new insights into the biological mechanisms underlying this association.

Humans↗

PubMed2026

Is ophthalmology a pain-free career? A systematic review and meta-analysis of musculoskeletal pain among ophthalmologists.

OBJECTIVE: To estimate the pooled prevalence, anatomical distribution, and occupational impact of work-related musculoskeletal (MSK) pain among ophthalmologists, and to identify modifiable ergonomic risk factors. DESIGN: A systematic review and meta-analysis of published data. The protocol was preregistered (PROSPERO CRD42023422368) and reported in accordance with PRISMA. PARTICIPANTS: The participants were 6691 ophthalmologists from 21 studies. METHODS: Electronic databases (MEDLINE, Embase, Cochrane, and PubMed) were searched for peer-reviewed quantitative studies reporting MSK pain prevalence in ophthalmologists. Pooled estimates with 95% CI were calculated using random-effects models; heterogeneity was quantified using I². MAIN OUTCOME MEASURES: Prevalence of overall and site-specific MSK pain; effects on workload and productivity; prevalence of treatment or mitigation strategies. RESULTS: The pooled prevalence of any MSK pain was 70% (95% CI: 65%-75%; I² = 92%); neck (41%; 95% CI: 35%-47%; I² = 95%), lower back (36%; 95% CI: 32%-39%; I² = 87%), and shoulder pain (28%; 95% CI: 22%-35%; I² = 91%) were most common. Pain led to workload modification in up to 44% and contributed to reduced clinical volume, sick leave, or contemplation of early retirement. Forty-six percent (95% CI: 22%-71%) pursued no treatment; 39% (95% CI: 30%-49%) used medical therapy; and 29% (95% CI: 20%-41%) sought physiotherapy. Heterogeneity was high across studies, reflecting differing case definitions and self-reported measures. CONCLUSIONS: MSK pain affects most ophthalmologists, particularly in the cervical and lumbar regions and frequently alters practice patterns. These findings underscore the need for early ergonomic training, structured micro-breaks, and workspace redesign. Prospective intervention trials are required to establish causality and quantify benefit.

Humans↗

PubMed2026

A Novel Complete F8 Tandem Duplication Causing Elevated Factor VIII Activity and Associated with Venous Thromboembolism.

Background Coagulation factor VIII (FVIII) is a critical component of the intrinsic coagulation pathway. While elevated FVIII levels are an established risk factor for venous thromboembolism (VTE), genetic variants in the F8 gene directly causing such elevations remain scarce. Here, we report a novel complete F8 tandem duplication identified in a female patient with splanchnic venous thrombosis (SVT). Methods We performed genetic testing using a thrombophilia panel targeting 35 genes involved in thrombosis and haemostasis to detect both point variants and copy number variations (CNVs). Family co-segregation analysis and phenotypic assays for FVIII and von Willebrand factor (VWF) were conducted. The structural basis of the identified F8 copy number gain was elucidated using optical genome mapping (OGM). Full-length F8 mRNA amplification, quantitative PCR, plasma FVIII Western blotting, and X-chromosome inactivation analysis were performed to assess the functional consequences of the duplication. Thrombin generation test (TGT) was employed to assess the hypercoagulable state. Results Genetic testing identified three copies of all 26 exons of the F8 gene in the proband, which was also detected in her mother (CNVs = 3) and son (CNVs = 2). One-stage clotting and chromogenic assays confirmed persistently elevated FVIII activity in the proband and her mother, accompanied by increased FVIII antigen levels. The OGM analysis confirmed a 229 kb tandem duplication including the F8 gene on one of the proband's X chromosomes. The junction regions exhibited high sequence homology and were rich in repetitive sequences, which precluded precise breakpoint mapping. Full-length F8 mRNA amplification revealed no aberrant transcripts, whereas quantitative PCR showed increased F8 mRNA expression in all carriers. Plasma FVIII Western blotting indicated FVIII heavy and light chains of expected molecular weights with increased band intensity in carriers. X-chromosome inactivation analysis in female carriers showed no significant skewing. TGT in two available carriers showed increased thrombin generation compared with a normal control at both low (1 pM) and high (5 pM) tissue factor concentrations. Conclusion We identified a novel complete F8 tandem duplication associated with increased FVIII expression and a hypercoagulable phenotype in a female patient with SVT. These findings support F8 gene dosage gain as a rare gain-of-function mechanism contributing to elevated FVIII levels and thrombophilia, while variation in VWF levels and acquired risk factors may modify thrombotic penetrance.

coagulation factor VIII↗

PubMed2026

Comparison of Performance of Publicly Available Polygenic Risk Scores to Predict Clinically Actionable Coronary Artery Calcium Scores: The BioHEART-CT Cohort.

AIM: Coronary artery disease (CAD) remains the leading cause of morbidity and mortality globally. Polygenic Risk Scores (PRS) have been trained against major adverse cardiovascular outcomes (MACE) in large cohorts. Few studies have examined the effectiveness of these CAD MACE PRS tools in detecting individuals with subclinical coronary calcification. An association would provide an opportunity for clinical translation and targeting of CT imaging to new patients at risk for subclinical disease. METHODS: An analysis of 53 publicly available CAD PRS tools was completed in participants of the BioHEART-CT Discovery 1000 cohort presenting for clinically referred CT coronary angiography (CCTA). Associations between PRS and two binary CACS outcomes reflecting clinically significant coronary calcification were assessed: a) Absolute CACS (CACS ≥100 Agatston units [AU]; and b) Percentile CACS (CACS ≥75th age-/sex-adjusted percentile). Models were adjusted for genetic principal components, modifiable cardiovascular risk factors, and age/sex (in Absolute CACS). A subgroup analysis was performed using Framingham Risk Score (FRS) at baseline. RESULTS: Among 803 BioHEART-CT Discovery 1000 participants, 487 (60.6%) had any detectable coronary calcium. Most PRS tools demonstrated significant association with CACS outcomes, particularly evident when PRS was modelled as a continuous predictor. For Percentile CACS, 94.3% of PRS tools were significantly associated after full adjustment (median OR per PRS SD 1.41 (IQR 1.23-1.60). Quintile-based analysis revealed that individuals in the Top Quintile PRS had up to 7.99-fold increased odds of Percentile CACS ≥75th compared to those in the Bottom Quintile. Analysis by FRS group revealed positive performance, especially in individuals of Low FRS wherein incorporating a PRS increased pre-test probability from 14% to 26%. CONCLUSION: Whilst most CAD PRS tools have been developed against clinical events, we show their ability to predict clinically relevant coronary calcification. Utility appears strongest in individuals traditionally considered lower risk, presenting an opportunity for clinical translation for improved diagnosis in the primary prevention setting, with the potential to triage individuals into a CACS screening pathway.

coronary artery disease↗

PubMed2026

Lifestyle Combination Patterns as Key Modifiable Factors for Type 2 Diabetes Mellitus Risk among Middle-Aged Korean Men.

BACKGRUOUND: The increasing prevalence of type 2 diabetes mellitus (T2DM) worldwide highlights the need to understand risk factors and effective prevention strategies. Although individual lifestyle factors associated with diabetes risk have been identified, research on their collective interactions is limited. This study aimed to identify lifestyle combination patterns in middle-aged Korean men and evaluate their impact on T2DM risk. METHODS: A total of 2,332 middle-aged men without T2DM at baseline (2001-2002) from the Korean Genome and Epidemiology Study (KoGES) cohort were included. T2DM incidence was tracked through the 8th follow-up survey (2017-2018). Lifestyle combination patterns were identified using factor analysis based on sociodemographic, lifestyle, and dietary data. Cox regression was used to assess T2DM incidence across patterns. RESULTS: Four lifestyle combination patterns were identified: 'Healthy Lifestyle,' 'Low Carb & High Protein,' 'High SES & Irregular Lifestyle,' and 'Bad Eating Habits.' The risk of developing T2DM varied across patterns. The 'Healthy Lifestyle' and 'Low Carb & High Protein' patterns showed a slight decrease in risk in T3, but the differences were not significant. The 'High SES & Irregular Lifestyle' pattern was associated with a higher T2DM risk in T3 than in T1 (hazard ratio [HR], 1.25; 95% confidence interval [CI], 1.05 to 1.55), but the association was attenuated after adjustment for family history. The 'Bad Eating Habits' pattern showed a 1.21-fold higher risk in T3 (HR, 1.21; 95% CI, 1.01 to 1.47). CONCLUSION: This study underscores the existence of distinct lifestyle combination patterns and their differential implications for T2DM risk. These findings support the need for tailored preventive strategies based on lifestyle patterns.

Humans↗

PubMed2025

Genome-wide association study of adolescent-onset depression.

Adolescent depression is a heritable psychiatric condition with rising global prevalence and severe long-term outcomes, yet its biological underpinnings remain poorly understood. We conducted the first genome-wide association study of adolescent-onset depression, comprising 102,428 cases (diagnosis or clinical symptom thresholds) and 286,911 controls, including diverse ancestries. Cross-ancestry meta-analysis identified 52 independent variants across 17 loci; European-only analysis found 61 variants at 29 loci, with a SNP-based heritability of 9.8%. Comparative analyses revealed two genes unique to adolescent-onset versus lifetime depression, enriched in neuronal subtypes, and two genes as potential drug repurposing targets. Polygenic scores were associated with adolescent-onset depression across ancestries, persistent depression trajectories, more severe outcomes, as well as reduced cortical volume, surface area and white matter integrity. Genetic correlation and Mendelian randomisation analyses support shared genetic liability and causal links with early puberty and modifiable health and behavioural risk factors. These findings uncover novel genetic loci and refine biological pathways underlying adolescent-onset depression, revealing age-specific mechanisms and early intervention opportunities.

Journal Article↗

PubMed2026

Genetic architecture of endometriosis: risk factors, comorbidities and clinical implications.

BACKGROUND: In 1999, Dr Susan Treloar and colleagues conducted a landmark twin study in Australia and reported their estimate of 51% for the heritability of endometriosis. This important result led several groups to begin mapping genetic factors contributing to increased endometriosis risk. Despite early challenges, advances in genome-wide association studies (GWAS) have identified multiple genetic risk factors and some target genes implicated in follow-up studies on genetic regulation of transcription. Access to large publicly available genetic datasets and analysis with endometriosis GWAS results is also providing new opportunities to answer important questions about comorbid conditions associated with endometriosis and their implications for clinical practice. OBJECTIVE AND RATIONALE: The objective of the review is to summarize the last 25 years of genetic studies in endometriosis, outline contributions to our understanding of the disease, and suggest future directions to accelerate biological insights from genetic studies to improve clinical outcomes. SEARCH METHODS: A comprehensive review of scientific literature on the genetics of endometriosis was conducted through searches in PubMed and Google Scholar up to June 2026. Search terms included "endometriosis AND (genetics OR GWAS OR genetic risk factors)", For studies addressing the functional characterization of genetic risk loci, additional searches employed the terms "endometriosis AND (genotype-phenotype associations OR colocalization OR eQTL OR mQTL OR multi omics methods)". To identify studies examining shared genetic risk between endometriosis and comorbid conditions, the search strategy included "endometriosis AND (genetic correlation OR colocalization OR Mendelian randomisation)". Publications reporting discoveries related to genetic risk factors for endometriosis and studies interpreting their biological and clinical significance were critically evaluated, and 144 publications were discussed in the review. OUTCOMES: Discovery of genetic risk factors started slowly and has accelerated in recent years with developments in technology and international collaborations to combine data and increase statistical power. GWAS have mapped 80 genetic risk factors that implicate gene regulation of hormonal targets, development of the reproductive tract, regulation of cell proliferation, and regulation of epithelial cell differentiation. In common with most other complex diseases, effects of individual common genetic risk factors are small. However, several examples demonstrate that small effect sizes are not a good predictor for the impact of drugs developed against genetically validated targets. Genetic risk factors implicate five genes regulating gonadotrophin release and oestrogen action, the major target pathway of current drugs for treatment of endometriosis demonstrating proof-of-principal for biologically meaningful results. Genetic correlation and Mendelian Randomization studies highlight important causal relationships between endometriosis and comorbid conditions including a possible role for testosterone during development and shared genetic risk factors for gynaecological, gastrointestinal, pain, psychiatric, and inflammatory conditions. Understanding causal relationships between endometriosis and related conditions will aid clinical management and more personalized treatments. WIDER IMPLICATIONS: Genetic studies provide novel insights into endometriosis pathogenesis and associations with related comorbid conditions. Genetic factors modifying gene regulation and disease risk likely act in specific cell types, and access to datasets from genetically informed cell-based models, single-cell and spatial omics data are needed to accelerate progress. Future studies should address critical questions of heterogeneity and disease subtypes, expand the search for genetic risk factors to non-European populations, evaluate the role of rare and structural variants, and better integrate data from functional, genomics, genetics, and clinical studies to reduce diagnostic delay, develop novel treatment strategies, and translate discoveries into personalized management strategies for affected individuals. REGISTRATION NUMBER: N/A.

comorbid conditions↗

PubMed2026

Prevalence and risk factors of nutritional anaemia among adolescents in India: a systematic review with meta-analysis of prevalence.

BACKGROUND: Nutritional anaemia is a major public health concern among adolescents in India, threatening physical growth, cognitive development, and future maternal health. This systematic review with meta-analysis of prevalence aimed to estimate the pooled prevalence of nutritional anaemia among Indian adolescents aged 10-19 years and identify key associated risk factors. METHODS: A systematic search was conducted across PubMed, Embase, Web of Science, and Scopus up to February 2025. Data were extracted on study design, setting, diagnostic methods, prevalence, and risk factors. Quality was assessed with a modified Newcastle-Ottawa Scale. A random-effects meta-analysis estimated pooled prevalence, with subgroup analyses by state and gender, and pooled odds ratios for risk factors. RESULTS: Forty-five studies encompassing diverse Indian regions and 159,979 adolescents were included. The pooled prevalence of nutritional anaemia was 56% (95% CI: 49%-63%), with higher rates among girls (62%) than boys (39%). Iron deficiency (OR 2.38-4.68), other micronutrient deficiencies, low socioeconomic status, poor dietary diversity, female gender, and inadequate supplementation were consistently associated with higher anaemia risk. CONCLUSION: Nutritional anaemia impacts more than half of Indian adolescents, with notable regional and gender differences. Its complex nutritional, socioeconomic, and behavioural causes demand targeted, context-specific interventions to enhance adolescent health nationwide.

Humans↗

PubMed2026

Toxoplasma gondii IgG seroprevalence in Mauritanian dromedary camels: First multi-regional survey.

Toxoplasma gondii is a globally distributed zoonotic parasite, and dromedary camels are important intermediate hosts in arid and semi-arid regions. However, information on T. gondii exposure in camels is lacking in Mauritania, which harbors one of the largest camel populations in West Africa. This study reports the first multi-regional seroepidemiological survey to estimate T. gondii seroprevalence and identify associated risk factors in Mauritanian dromedaries. Between 2023 and 2024, serum samples were collected from 953 camels across eight climatically distinct regions. Anti-T. gondii IgG antibodies were detected using the Modified Agglutination Test (MAT; cutoff≥1:20). Risk factors investigated included geographical region, sex, age group, and season of sampling, using multivariable logistic regression and a mixed-effects linear probability model accounting for regional clustering. The overall seroprevalence was 15.0% (143/953). Exposure varied markedly across regions, ranging from 0% in the hyper-arid northern regions of Adrar and Tagant to 41.7% in the southern Sahelian region of Guidimakha. This pronounced spatial gradient is consistent with contrasting climatic and ecological conditions, as higher rainfall and humidity in the south are hypothesized to favor environmental oocyst survival compared to the extreme aridity of the north. Geographical region and age were independent predictors of seropositivity. Compared with camels from Nouakchott, those from Guidimakha had higher odds of exposure (aOR = 2.63), whereas camels from Trarza had a markedly lower risk (aOR = 0.09). Camels older than 6 years were more than twice as likely to be seropositive as those aged 3-5 years, whereas sex and season were not associated with seropositivity. These findings indicate that T. gondii exposure is widespread in Mauritanian dromedaries and that ecological conditions may influence exposure patterns. The marked spatial heterogeneity supports targeted surveillance and One Health interventions to reduce the potential zoonotic risk associated with camel-derived food products.

Animals↗

PubMed2026

Relationship between menopausal hormone therapy and incidence risk of breast cancer: systematic review and meta-analysis.

BACKGROUND: Menopausal hormone therapy (MHT) is widely prescribed for alleviating menopausal symptoms. Prior studies have mainly focused on individual hormone therapy formulations. This meta-analysis comprehensively synthesized evidence across various regimens to systematically evaluate the association between MHT and breast cancer risk. MATERIALS AND METHODS: We systematically searched CNKI, Wanfang, PubMed, and Web of Science from inception through August 2024. Eligible studies examining breast cancer risk following MHT were independently screened and assessed by two reviewers. The review and meta-analysis followed PRISMA guidelines. RESULTS: Thirty-four studies were included. The random-effects model showed a significant but heterogeneous overall association (OR = 1.15, 95% CI: 1.09-1.22; I² = 92.4%). Subgroup analysis identified hormone type, use status, and region as key determinants (P for interaction < 0.001). Stratification by hormone type resolved much of the heterogeneity, revealing risk confined to estrogen-progestin therapy (EPT; OR = 1.44, 95% CI: 1.26-1.64), while estrogen-only therapy (ET) showed no overall association (OR = 1.00, 95% CI: 0.91-1.10). Study type, region, and sample size were significant effect modifiers. For ET, randomized controlled trials demonstrated a protective effect (OR = 0.78, 95% CI: 0.70-0.87), contrasting with neutral findings from observational studies. CONCLUSIONS: MHT is associated with a modest but significant increase in breast cancer risk, primarily driven by EPT. This risk was not observed with ET in observational studies, though trials suggested a protective effect. Crucially, the association shows marked geographical heterogeneity, indicating risk is modified by regimen and regional factors.

Humans↗

PubMed2025

Entertainment activities and the risk of multiple sclerosis: A Mendelian randomization analysis.

Modifying environmental and lifestyle factors may have the potential to prevent and ameliorate multiple sclerosis. Further elucidating the etiology of multiple sclerosis and proposing actionable prevention measures are of significant importance, but establishing causality in epidemiological data can be challenging. This study employed a two-sample Mendelian randomization analysis to evaluate the causal effect of entertainment activity factors on the risk of multiple sclerosis. Publicly accessible summary statistics derived from genome-wide association studies were utilized to assess 14 modifiable forms of entertainment activities. The inverse variance weighted random effects method was used as the primary analytical approach to estimate causal effects. Additionally, MR-Egger, weighted median, and weighted mode methods were applied to assess robustness. Systematic sensitivity analyses and heterogeneity tests were conducted to verify the reliability of our findings. We found that spending time outdoors in the summer may prevent the development of multiple sclerosis (odds ratio = 0.995; 95% confidence interval 0.991-0.999; P = .010). In contrast, the other entertainment activities studied showed no significant causal relationship with multiple sclerosis. Our results suggest that spending time outdoors in the summer may protect against the development of multiple sclerosis, providing implications for preventive measures against the disease.

Humans↗

PubMed2026

Endovascular treatment after stroke beyond 24 h vs 6-24 h: a propensity score-matched cohort study.

BACKGROUND: Endovascular thrombectomy (EVT) is the standard treatment for acute ischemic stroke due to anterior circulation large vessel occlusion (LVO) within 6-24 h. However, the safety and feasibility of EVT for anterior circulation strokes beyond 24 h remain uncertain. METHODS: We conducted a retrospective cohort study of consecutive patients with anterior circulation LVO who underwent EVT at Changhai Hospital from 2018 to 2023. Patients were stratified into late (6-24 h) and very late (>24 h) windows. Propensity score matching (PSM) was performed to adjust for baseline imbalances, including age, sex, NIHSS, ASPECTS, occlusion location, perfusion parameters, and vascular risk factors. The primary outcome was functional independence (modified Rankin Scale [mRS] ≤ 2) at 3 months. Secondary outcomes included successful reperfusion (TICI 2b-3) and symptomatic intracranial hemorrhage (sICH). RESULTS: Among 1043 screened patients, 429 patients with anterior circulation LVO were included after exclusions, comprising 373 in the late window and 56 in the very late window. PSM yielded 42 matched pairs. Compared with the late window group, the very late window group showed no statistically significant differences in functional independence (54.8% vs. 57.1%; OR = 0.908, 95% CI 0.382-2.153, p = 0.830), successful reperfusion (88.1% vs. 92.9%; OR = 1.800, 95% CI 0.481-7.096, p = 0.460), sICH (2.4% vs. 9.5%; OR = 0.232, 95% CI 0.012-1.652, p = 0.200), intraprocedural complications (26.2% vs. 19.0%; OR = 1.508, 95% CI 0.540-4.362, p = 0.440), or postoperative complications (33.3% vs. 35.7%; OR = 0.900, 95% CI 0.363-2.219, p = 0.820). CONCLUSIONS: In this selected, single-center cohort of anterior circulation LVO patients undergoing EVT, treatment initiated beyond 24 h appeared to have comparable effectiveness and safety to treatment initiated within 6-24 h. Definitive evidence requires confirmation from adequately powered randomized controlled trials.

Humans↗