Prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) is a widespread environmental health concern, yet its impact on early childhood growth trajectories remains poorly understood. In a prospective birth cohort in China (PKUBC-T), we identified distinct growth trajectories from birth to age 3 years using K-means clustering for longitudinal data (N = 1467) and measured 16 plasma PAHs in first-trimester maternal samples (N = 333). Twenty maternal single nucleotide polymorphisms (SNPs) related to PAHs metabolism were genotyped. Modified Poisson and weighted quantile sum regression showed that higher prenatal PAHs exposure was associated with increased risk of rapid higher growth trajectory, with phenanthrene, pyrene, and fluoranthene contributing most. This trajectory is characterized by a marginally higher BMI Z-score at birth, followed by rapid growth during infancy and sustained high levels thereafter. Furthermore, the AHR rs2066853 variant significantly modified the association, with the positive association being observed only among mothers carrying GA/AA genotypes (RR, 2.44; 95% CI, 1.51-3.97) but not among those with GG homozygotes (P for interaction is 0.049). We provide evidence that prenatal PAHs exposure may alter early childhood growth patterns, with effects modified by maternal genetic susceptibility. If confirmed, these findings highlight the mechanistic importance of AHR signaling in environmental developmental toxicity and underscore the need for exposure reduction and targeted maternal monitoring.

In the context of climate change, extreme environmental events are becoming increasingly frequent and severe, profoundly affecting human health and creating a vicious cycle of mutual reinforcement. This review examines evolving trends in climate change–related extreme events and compound exposures, such as heatwaves, cold spells, heavy rainfall, floods, and hurricanes, and summarizes their impacts on major health outcomes, including respiratory, cardiovascular, cerebrovascular, infectious, and kidney diseases, as well as mental health and adverse birth outcomes. It further outlines interventions and future directions for adaptation, planning, and resilience across six levels: individual, interpersonal, community, institutional, environmental, and public policy. Despite growing research in this area, substantial knowledge gaps remain, including the scarcity of evidence from low- and middle-income countries, methodological inconsistencies, limited investigation of compound events, and insufficient attention to morbidity and adaptation effectiveness. Future research should employ harmonized, long-term, and multi-regional approaches to more accurately quantify health burdens and enhance global resilience to climate change.

Background:Lifestyle modification represents the cornerstone of the prevention and early management of obesity, hepatic fat content and stiffness in children. We aimed to evaluate the effectiveness of an mHealth-supported multifaceted lifestyle intervention on body-mass index (BMI), hepatic fat content and stiffness in children with overweight or obesity, and to estimate its potential long-term macroeconomic benefits. Methods:In this cluster randomised controlled trial, six primary schools in Ningbo, China, were randomly assigned (1:1) to an intervention or control group. Children aged 8-10 years with overweight or obesity were enrolled. The intervention integrated school-based health education and polices, physical activity promotion, dietary guidance delivered by clinical nutritionists, and supportive mHealth components. Primary outcomes were changes in BMI, controlled attenuation parameter (CAP), and liver stiffness measurement (LSM). Intention-to-treat analysis was performed using generalised linear mixed models accounting for school-level clustering and adjusting for baseline outcome values, age, and sex. A post-hoc macroeconomic simulation projected long-term economic effects. This trial is registered with ClinicalTrials.gov, NCT05482191. Findings:From 6 to 30 September, 2022, 331 children (mean age 8.5 years [SD 0.3]; 36.3% girls) were enrolled. Compared with controls, the intervention group showed significant reductions in BMI (mean difference -0.38 kg/m2, 95% CI -0.59 to -0.16; p < 0.0001), CAP (-15.73 dB/m, -22.39 to -9.07; p < 0.0001), and LSM (-0.69 kPa, -0.89 to -0.48; p < 0.0001). Changes in BMI mediated 11.9% and BMI Z score 9.1% of the intervention's effect on CAP (both p < 0.05). No adverse events were reported. Macroeconomic modelling suggested that national implementation could yield cumulative economic gains of approximately RMB 694.96 billion (US$ 97.47 billion) during 2026-2050. Interpretation:The mHealth-assisted lifestyle intervention significantly improved BMI, hepatic fat content and stiffness in children. The accompanying macroeconomic benefits support its integration into national public health and economic strategies. Funding:Major Science and Technology Projects for Health of Zhejiang Province; Cyrus Tang Foundation 2022.

Early-life growth from in utero to early childhood plays a critical role in shaping long-term health, yet the impact of prenatal PM2.5 constituent exposure on weight growth trajectories remains unclear. We included 16,372 mother-child pairs from a Chinese birth cohort. Prenatal PM2.5 and its constituents [organic carbon (OC), elemental carbon (EC), ammonium (NH4+), nitrate (NO3-), and sulfate (SO42-)] exposures were estimated using a modified Community Multiscale Air Quality model. A latent class growth model was employed to explore weight growth trajectories from 20 gestational weeks in utero, birth, 6 months, 1, 2, and 3 years. Associations were analyzed using multinomial logistic regression and quantile-based g-computation (QGC). Three distinct weight Zscore growth trajectories were identified: normal (26.6% in boys, 17.7% in girls), approaching-risk-of-overweight (63.0%, 66.7%), and risk-of-overweight (10.4%, 15.6%). An interquartile range increase in prenatal exposure to PM2.5 was associated with a 13.5% higher risk of the approaching-risk-of-overweight trajectory (risk ratio [RR]=1.135, 95% CI: 1.050, 1.228) and a 23.2% higher risk of the risk-of-overweight trajectory (RR=1.232, 95%CI: 1.103, 1.376). Similar associations were observed for OC, EC, NH4+, and SO42-,with stronger effects for the risk-of-overweight trajectory. In QGC models, each quintile increase in prenatal mixture exposures of PM2.5 constituents had RRs of 1.354 (95%CI: 1.104, 1.662) for approaching-risk-of-overweight and 1.606 (95%CI: 1.192, 2.161) for risk-of-overweight, respectively. These findings highlight the adverse impact of prenatal PM2.5 and constituent exposures on early-life growth, and underscore the need to reduce prenatal PM2.5 exposure to promote healthy growth trajectories in early childhood.

Early-life growth trajectories, especially during the first two years, are important for future health. However, in the context of rapidly rising childhood obesity, it is essential to characterize BMI-for-age Z-score (BAZ) trajectories in early childhood, compare optimal modeling approaches, and identify associated risk factors. This prospective birth cohort study enrolled participants in Jinan, Shandong from 2019 to 2022. World Health Organization (WHO)-standardized BAZ scores were calculated for children at eight timepoints (0–24 months). Sex-specific BAZ trajectories were derived using growth mixture modeling (GMM) and k-means for longitudinal data (KML). The possible risk of being overweight (BAZ > 1) at age three years was predicted using logistic regression with five folds cross-validation, comparing model performance via the area under the curve (AUC). Associations between trajectory classification and antenatal and postnatal factors were examined. A total of 4629 mother-infant dyads were enrolled in this study. The KML-derived four-class trajectory model demonstrated optimal predictive performance for possible risk of being overweight at age three years, achieving an AUC of 0.749 and significantly outperforming the GMM model (AUC = 0.571). Male sex [odds ratio (OR) = 1.314; 95

Introduction Early childhood obesity has become a major public health concern globally. The preschool period (ages 4-6 years) represents a critical window for obesity prevention due to its long-term implications on growth trajectories and behaviour formation. However, existing evidence for effective interventions targeting this age group remains limited and inconsistent, particularly in low- and middle-income countries.Methods and analysis The Peking University-Smart Monitoring and Responsive Technology for Early Childhood Health is a cluster-randomised controlled trial designed to evaluate the effectiveness and sustainability of a multi-component, digital health-assisted obesity prevention intervention. The trial involves approximately 980 children aged 4-6 years (middle and senior kindergarten classes) from 14 kindergartens, randomly allocated to either the intervention (n=7) or control (n=7) groups. The intervention spans 9 months, followed by a 12-month post-intervention follow-up. Interventions are delivered across kindergartens, families and healthcare systems. A digital Smart Health Platform is integrated into the intervention to provide health education, real-time feedback and interactive support, enabling personalised health management and promoting parental engagement. Data are collected at baseline, 4, 9 and 21 months. The primary outcome is the between-group difference in changes in body mass index Z-score at 9 months. Secondary outcomes include other anthropometric indicators, dietary intake, physical activity levels and other measurements. In addition, a process evaluation will be conducted to assess fidelity and participant engagement, and a health economic evaluation will estimate cost-effectiveness and cost-benefit outcomes.Ethics and dissemination Ethical approval for this study was obtained from the Ethics Committee of the Shandong Maternal and Child Health Hospital (no. 2025-042). Findings from the trial will be disseminated through peer-reviewed publications and conference presentations to inform future childhood obesity prevention policies and practices.Trial registration number NCT07117149.

Despite growing concern, the developmental effects of prenatal exposure to indoor and ambient particulate pollution remain poorly characterized. This study examined their individual and joint associations with infant growth. Embedded in the PKUBC-T birth cohort (initiated in June 2018, China), this study included 1068 mother-infant pairs. The PM1 and PM2.5 concentrations from the last menstrual period to delivery were predicted via a validated machine learning model, whereas PM2.5 constituents' concentrations were derived via a modified Community Multiscale Air Quality Model. Indoor air pollution was assessed via questionnaires covering four dimensions. Infant growth was evaluated using body mass index (BMI) Z-scores and weight-for-length (WFL) Z-scores at one year, with overweight/obesity (OWOB) defined by World Health Organization standards. Generalized linear regression indicated that increased exposure to indoor air pollution was associated with elevated BMI Z-scores (β = 0.089, 95 % CI: 0.007, 0.171) and WFL Z-scores (β = 0.094, 95 % CI: 0.013, 0.176) in offspring. PM1 and PM2.5 also exhibited positive associations with these growth indicators. Infants whose mothers were exposed to higher levels of organic carbon (OC), elementary carbon (EC), NH4+ and SO42- had an elevated risk of overweight/obesity (OWOB). Stratified analyses revealed that joint exposure to PM₁ above the median and indoor air pollution was related to increased infant growth, despite nonsignificant multiplicative interaction effects. Similar joint effects were observed for indoor air pollution and PM2.5, along with its constituents. This study highlights synergistic harms of combined indoor-outdoor air pollution on infant growth, reinforcing the need for integrated policies targeting indoor combustion and ambient PM reduction to safeguard early-life development.

Climate change has increasingly been recognized as a critical public health challenge. Although exposure to high temperatures has been linked to pregnancy complications and adverse fetal outcomes, the key underlying physiological mechanisms remain unclear. In this prospective birth cohort study, we examined the association between heat stress exposure, assessed using the Universal Thermal Climate Index (UTCI), and fetal umbilical artery blood flow measured by umbilical artery Doppler indices. Our findings showed that heat exposure was associated with elevated umbilical artery blood flow indices, indicated by a 44.7 % increase in the systolic/ diastolic ratio (S/D ratio) (0.96, 95 % CI: 0.91-1.01), a 34.6 % increase in the pulsatility index (PI) (0.28, 95 % CI: 0.26-0.29), and a 23.3 % increase in the resistive index (RI) (0.12, 95 % CI: 0.12-0.13). Analysis of acute heat stress exposure during the week preceding ultrasound examination revealed significant increases in umbilical artery blood flow indices. When defined as UTCI exceeding the 90th percentile of the maximum daily UTCI during the study period for >= 2 consecutive days, heat stress was associated with increases of 0.054 (95 % CI: 0.039, 0.068) in PI and 0.016 (95 % CI: 0.011, 0.020) in RI. Longer heat stress exposure lasting >= 4 days resulted in increases of 0.058 (95 % CI: 0.034, 0.081) in PI and 0.018 (95 % CI: 0.009, 0.025) in RI. This study advances our understanding of the physiological mechanisms through which elevated temperatures impact maternal and fetal health. The findings will help inform future prevention strategies, targeted interventions, and evidence-based health policies.

OBJECTIVE:To systematically investigate the associations between umbilical cord blood protein expression profiles and early infant neurodevelopment using a prospective birth cohort, to identify potential early biomarkers through high-throughput proteomics, and to explore underlying biological mechanisms, thereby providing scientific evidence for early identification of neurodevelopmental risks and understanding the molecular basis of neurodevelopmental deviations in general populations. METHODS:Based on the Peking University Birth Cohort in Tongzhou, this study enrolled 96 children who completed ages and stages questionnaires, third edition (ASQ-3) assessments at 1 and 3 years of age. Participants were classified into an abnormal group (n=42) and a control group (n=54) according to ASQ-3 screening results. Non-targeted quantitative proteomics was performed on cryopreserved umbilical cord blood plasma samples collected at birth. Differential expression analysis, principal component analysis (PCA), orthogonal partial least squares discriminant analysis (OPLS-DA), and weighted gene co-expression network analysis (WGCNA) were conducted to identify differentially expressed proteins, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analyses. The fold change (FC) was calculated. Independent samples t-test was used for statistical comparison, with Benjamini-Hochberg method applied to calculate false discovery rate (FDR) for multiple testing correction. RESULTS:Proteomic analysis identified 8 214 common proteins, among which 385 proteins were differentially expressed (P < 0.05, |log2FC| >0.585), including 189 proteins upregulated and 196 proteins downregulated in the abnormal group. PCA and OPLS-DA revealed systematic differences in protein expression patterns between the two groups. WGCN A identified 10 co-expression modules, with the yellow module showing significant negative correlation with ASQ-3 abnormal grouping (r=-0.233, P=0.024) and the pink module positively correlating with communication domain scores (r=0.342, P=0.003). Enrichment analyses demonstrated that differential proteins and key modules were primarily enriched in two functional categories: (1) genetic information processing pathways, including ribosome, spliceosome, and mRNA processing; and (2) cytoskeleton organization and Wnt signaling pathways. These pathways held significant biological relevance in the pathogenesis of neurodevelopmental disorders. CONCLUSION:Perturbations in proteins associated with genetic information processing and cytoskeleton/Wnt signaling pathways in umbilical cord blood may represent important molecular characteristics of early neurodevelopmental screening abnormalities in infants. This study provides potential peripheral blood biomarker combinations for early identification of neurodevelopmental risks in general populations and offers novel insights into the biological mechanisms underlying neurodevelopmental deviations. Future research should validate these findings in larger-scale cohorts and elucidate specific functional mechanisms of key proteins through experimental studies.

In women of reproductive age, metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with increased risks of gestational complications and adverse pregnancy outcomes. In addition, gestational MASLD may affect the lifelong health trajectory of the offspring. The live-streamed exercise intervention in pregnant women with metabolic dysfunction-associated steatotic liver disease (Live-MASLD) trial aims to investigate the efficacy of a live-streamed exercise intervention in ameliorating MASLD progression and improving maternal-infant health outcomes. A two-arm randomized controlled trial will be conducted across two centers. Pregnant individuals with MASLD in their first trimester will be recruited and randomly allocated to a control group or an intervention group. The control group will receive routine prenatal healthcare, while the intervention group will undergo a supervised, live-streamed exercise program during the second and third trimesters. Assessments will occur at baseline, second trimester, third trimester, delivery, and 42 days postpartum. Process evaluation will be conducted to allow for a health economic evaluation of the intervention. The primary outcome will describe between-group differences in changes to the hepatic steatosis index (LiSA) as quantitatively measured by visual transient elastography (ViTE). The findings from the Live-MASLD study will provide scientific evidence and implementation guidance for the clinical management of pregnant women with MASLD.

Behavioral interventions have been shown to be effective in improving dietary behavior and reducing childhood obesity. There is limited evidence on how concurrent changes in dietary behavior from intervention studies affect childhood obesity. The present study aimed to evaluate the mediating effect of concurrent changes in dietary behaviors between the intervention and changes in adiposity indicators. This study included 1180 children from the DECIDE-Children study, which was conducted across three areas in China, aiming to promote children’s healthy diet and physical activity, while also engaging schools and families to support children’s behavioral changes. Dietary behaviors were collected by a revised version of the Food Frequency Questionnaire and a self-designed questionnaire. Adiposity outcomes were objectively measured by trained personnel. Generalized linear mixed models were used to estimate the association between scores of dietary behavioral changes and adiposity indicator changes. Mediation analyses were used to evaluate how scores of dietary behavioral changes mediated the effect of intervention on adiposity indicator changes. Six hundred children in the intervention group and five hundred and eight in the control group with both baseline and follow-up data were included. Each increase in dietary behavioral change score was associated with a 0.06 (p = 0.016) decrease in changes in BMI and other adiposity indicators. Scores of dietary behavioral changes mediated 13.87% (p < 0.001), 11.81% (p < 0.001), 17.60% (p = 0.024), and 16.78% (p = 0.032) of the association between intervention and changes in body mass index (BMI), BMI z-score, body fat percentage, and waist circumference, respectively. Scores of dietary behavioral changes mediated the intervention effect on adiposity indicator changes. Future interventions targeting childhood obesity should incorporate promoting multiple dietary behaviors simultaneously.

Accumulating evidence indicates that maternal exposure to carbon black nanoparticles (CBNPs) during gestation can induce multiple system abnormalities in offspring, whereas its potential mechanism in respiratory disease is still largely unknown. In order to explore the effect of maternal exposure to CBNPs on offspring’s lung and latent pathogenesis, we respectively established in vivo model of pregnant rats exposed to CBNPs and ex vivo model of lung epithelial cells treated with pups’ serum of pregnant rats exposed to CBNPs. After maternal exposure to CBNPs, epithelial-mesenchymal transition (EMT) and fibrosis levels increased as a result of DDRGK1-mediated reticulophagy upregulated in offspring’s lung. DDRGK1 as FAM134B’s cargo bound with FAM134B to mediate reticulophagy. Transcription factor “SP1” positively regulated DDRGK1 gene expression by binding to its promoter. Furthermore, the upregulation of NSUN2 elevated m5C methylation of SP1 mRNA and the protein level of SP1 subsequently increased through Ybx1 recognizing and stabilizing m5C-methylated SP1 mRNA, followed by the increased levels of reticulophagy and fibrosis in lung epithelial cells treated with offspring’s serum of matrix exposed to CBNPs during gestation. In conclusion, NSUN2/Ybx1/m5C-SP1 axis promoted DDRGK1-mediated reticulophagy, which played an important role in EMT-induced fibrosis in offspring’s lung tissue after maternal exposure to CBNPs during gestation.

Environmental noise pollution is increasing, while risks of cardiovascular diseases (CVD) associated with environmental noise in low- and middle-income countries (LMICs) still remain under-recognized. In this study, we utilized land-use regression (LUR) models at high spatial resolution to assess environmental noise and linked the exposure to digital healthcare data from the Yinzhou Regional Health Information Platform (YRHIP) in China to assess the associations of environmental noise with risks of CVD. Among 533,512 participants, mean (SD) age was 53.66 (15.52) years with females constituting 52.8 %. The mean environmental noise level was 59.34 dB[A]. A total of 177,111 (33.20 %), 18,030 (3.38 %), 15,912 (2.98 %), 9,601 (1.80 %), and 161,889 (30.34 %) participants were diagnosed with CVD, cerebrovascular diseases, ischemic heart diseases (IHD), stroke, and hypertension, respectively. Multivariable modified Poisson regression models incorporating community as a random-effect term were used to evaluate associations of environmental noise with the prevalent risk of CVD and its major subtypes. Individual covariates (age, sex, marital status, education, lifestyles), area-level covariates (urbanicity, population density, GDP), and PM2.5 were adjusted. We observed positive associations between residential environmental noise exposure and CVD (prevalence ratio (PR) 1.06, 95 % CI: 1.02-1.09 per 5 dB[A]), IHD (PR 1.14, 95 % CI: 1.07-1.21 per 5 dB[A]), and hypertension (PR 1.06, 95 % CI: 1.03-1.09 per 5 dB[A]), while no association was found for cerebrovascular diseases (PR 1.01, 95 % CI: 0.96-1.07 per 5 dB[A]) and stroke (PR 0.97, 95 % CI: 0.92-1.03 per 5 dB[A]). The risks of CVD and hypertension associated with environmental noise were higher among males and in the 50-60 years age group (P for interaction < 0.001). The associations between environmental noise and IHD were stronger in the ≥ 70 age group and among the participants with lower education levels (P for interaction < 0.05). The study fills the gap of knowledge about the associations between environmental noise, estimated using high spatial resolution LUR models, and CVD prevalent risk in LMICs. The evidence would provide significant implications for policy-making in terms of alleviating the surging disease burden of CVD related to environmental noise in LMICs.

Gestational diabetes mellitus (GDM) remains a major pregnancy metabolic issue. Although evidence suggested that essential trace elements (ETEs) may alter glycemic regulation during pregnancy, their associations with GDM remained uncertain. From the Peking University Birth Cohort in Tongzhou (PKUBC-T) with a total of 5426 participants, we randomly selected 200 cases with GDM and 200 matched controls without GDM to conduct a nested case-control study. The matching was on maternal age ( ± 2 years) and gestational week at which the oral glucose tolerance test was performed. We evaluated the levels of six ETEs (Cu, Zn, Se, Mo, Co, Cr) in serum samples collected at the first trimester (10.3 ± 1.6 gestational weeks). Associations were assessed with unconditional logistic regressions and Bayesian kernel machine regression. Serum Co concentrations in pregnant women with GDM (Median: 0.920 ug/L) were observed to be lower than in controls (Median: 0.973 ug/L). Compared to those with the lowest tertile, the pregnant women with the highest tertile of Co concentrations had decreased risk of GDM (OR = 0.56, 95

BACKGROUND:Children's respiratory health demonstrates particular sensitivity to air pollution. Existing evidence investigating the association between short-term ozone (O3) exposure and childhood pneumonia remains insufficient and inconsistent, especially in low- and middle-income countries (LMICs). METHOD:To provide more reliable and persuasive evidence, we implemented a multi-city, time-stratified case-crossover design with a large sample size, using data from seven representative children's hospitals across major geographical regions in China. To avoid the impact of the COVID-19 pandemic, individual-level medical records of inpatient children under 6 years of age diagnosed with pneumonia during 2016-2019 were collected. Conditional logistic regression models were fitted for each city, and city-specific estimates were pooled through a meta-analysis using a random-effects model. RESULTS:In total, the study included 137,470 pediatric pneumonia hospital admissions. The highest pooled estimate for O3 occurred at lag0-1, with a 10 µg/m3 increase in O3 associated with a 1.57% (95% CI: 0.67%-2.48%) higher risk of pediatric pneumonia hospital admissions. Stratified analyses indicated that the effects of O3 were robust across different sexes, age groups, and admission seasons. We also observed a statistically significant increase in risk associated with O3 concentrations exceeding the World Health Organization Air Quality Guidelines (WHO-AQGs). CONCLUSIONS:This study revealed a significant positive association between O3 and pediatric pneumonia hospital admissions. Our findings substantially strengthen the evidence base for the adverse health impacts of O3, underscoring the importance of O3 pollution control and management in reducing the public health burden of pediatric pneumonia.

BACKGROUND:Childhood obesity is a pressing global public health challenge requiring scalable prevention strategies. This study evaluated a tiered school-family-clinic intervention for obesity prevention among primary schoolchildren in China. METHODS:This cluster randomized controlled trial enrolled 1,627 third-grade students (intervention: n = 838; control: n = 789) from six primary schools in Ningbo, China. Intervention intensity was tailored to baseline weight status. In intervention schools, children without overweight or obesity received OptiChild, comprising health education and school weight-management policies. Children with overweight or obesity received SCIENT, adding teacher-led structured physical activity and individualized family dietary guidance from clinical nutritionists, supported by mobile health tools. Control schools maintained standard curricula. The primary outcome was change in body mass index (BMI). Secondary outcomes included BMI Z score, body fat distribution, blood pressure, and health behaviors. FINDINGS:After one academic year, BMI gain was attenuated in the intervention vs. control group (+0.02 vs. +0.24 kg/m2; mean difference [MD] -0.25; p = 0.006). Overweight/obesity prevalence declined from 24.8% to 18.9% in intervention schools vs. 23.6%-21.0% in controls (p = 0.015). OptiChild slowed BMI increase (+0.08 vs. +0.25 kg/m2; MD -0.19; p = 0.048) in children without baseline overweight and reduced incident overweight/obesity by 68% (1.1% vs. 3.5%; p = 0.007). SCIENT reduced BMI (-0.19 vs. +0.21 kg/m2; MD -0.38; p < 0.001). Both interventions improved health behaviors, with no adverse events reported. CONCLUSIONS:A tiered school-family-clinic intervention effectively mitigated BMI gain and reduced obesity prevalence, with promising implications for broader public health adoption. FUNDING:Major Science and Technology Projects for Health of Zhejiang Province.

Background and objectives: The objective of this study was to test the effects of objectively measured screen time using wearable cameras, along with dietary intake and physical activity level (and their interaction), on obesity among Chinese school-aged children. Methods: This study was conducted among 52 fourth-grade children (age: 9.76 ± 0.44; 50% boy) in Beijing, including children with obesity and age- and sex-matched normal-weight controls. Screen time (min/day) was coded from wearable camera images collected over one week using image recognition, physical activity measured using accelerometers, and dietary intake via camera-assisted 3-day 24 h dietary recalls. Logistic regression and generalized additive models assessed associations with obesity indicators, including general (obesity; percentage of body fat, BF%) and central (waist circumference; weight-to-height ratio). The combined effects of screen time with dietary and physical activity factors were also analyzed. Results: Children with obesity had longer daily screen time (94.91 ± 35.44 vs. 83.15 ± 36.86 min). Longer screen time was associated with higher energy and carbohydrate intake, more average duration per meal, a higher proportion of meals with screen, increased sedentary time, and a lower proportion of time spent in moderate-to-vigorous physical activity (MVPA). After adjusting for dietary intake and demographic covariates, longer screen time (≥1.3 h/day) was linked to higher odds of obesity (OR = 4.25, 95% CI = 1.09, 16.53) and BF% (OR = 6.14, 95% CI = 1.29, 29.10). Less protein intake (OR = 9.57, 95% CI = 1.31, 70.14), more proportion of meals with screen (OR = 6.40, 95% CI: 1.22, 33.61), less proportion of meals with social interaction (OR = 5.90, 95% CI: 1.01, 34.59), and less MVPA (OR = 5.21, 95% CI = 1.11, 24.43) with more screen time increased obesity risk. Conclusions: Objectively measured screen time was positively associated with the risk of childhood obesity. Longer screen time combined with lower protein intake, a higher proportion of meals consumed while watching screens, less meals with social interaction, and lower MVPA may collectively increase obesity risk. These findings call for efforts to reduce screen exposure, promote MVPA, and increase dietary protein intake. Additionally, encouraging children to avoid screen use during meals and promoting parent or peer companionship during eating may help reduce the risk of childhood obesity.

As the key organelle governed lipid homeostasis, lipid droplets (LDs) in skeletal muscle plays a critical role in regulating systemic insulin sensitivity. In type 2 diabetes mellitus (T2DM) patients intramyocellular lipid (IMCL) content negatively associates with insulin sensitivity, while endurance athletes exhibit IMCL levels were positively correlated to insulin sensitivity, which is known as the athlete’s paradox. To solve this paradox, LDs were isolated from skeletal muscle samples of seven athletes and nine T2DM patients, and the first proteome dataset of human skeletal muscle LD was established. Comparative proteomic analysis revealed 733 upregulated proteins in athlete LDs, primarily enriched in mitochondria, and 755 downregulated proteins, mainly associated with cytoskeletal components, relative to T2DM patients. Integrated analysis with tissue proteomics further indicated enhanced energy metabolism activity of LD-anchored mitochondria (LDAM) in athletes. Notably, adipose triglyceride lipase (ATGL) was specifically upregulated by 2.97-fold on LDs in athletes, while its overall tissue expression remained unchanged. Moreover, deletion of ATGL in myoblasts significantly reduced insulin-stimulated AKT phosphorylation. Additionally, skeletal muscle LDs from db/db and ob/ob mice exhibited reduced levels of mitochondrial proteins and ATGL. Together, our findings reveal a LD-based solution for the athlete’s paradox, and identify ATGL as a key regulator of skeletal muscle insulin sensitivity. The results also suggest that the “bad LDs” in the skeletal muscle of T2DM patients are characterized by higher levels of cytoskeletal proteins, reduced LDAM, and lower ATGL compared to the “good LDs” observed in athletes. ### Competing Interest Statement The authors have declared no competing interest.

Background/Objectives: This study investigates the impact of maternal glycemic levels during early and late pregnancy on offspring neurodevelopment in China. Methods: Fasting plasma glucose (FPG) and triglyceride (TG) levels were measured in maternal blood during pregnancy, and the TyG index was calculated to assess insulin resistance. Hyperglycemia was defined as FPG > 5.1 mmol/L. Neurodevelopmental outcomes in offspring aged 6–36 months were evaluated using the China Developmental Scale for Children, focusing on developmental delay (DD) and developmental quotient (DQ). Mothers were categorized into four glycemic groups: healthy glycemia group (HGG), early pregnancy hyperglycemia group (EHG), late pregnancy hyperglycemia group (LHG), and full-term hyperglycemia group (FHG). Linear and logistic regression models were applied. Results: Among 1888 mother–child pairs, hyperglycemia and FPG were associated with an increased risk of overall DD (aOR = 1.68; 95% CI 1.07–2.64) and lower DQ (aBeta = −1.53; 95% CI −2.70 to −0.36). Elevated FPG was linked to DD in fine motor and social behaviors. Compared to HGG, LHG and FHG significantly increased the risk of overall DD (aOR = 2.18; 95% CI 1.26–3.77; aOR = 2.64; 95% CI 1.38–5.05), whereas EHG did not. Male offspring were particularly vulnerable to early pregnancy hyperglycemia (aBeta = −2.80; 95% CI −4.36 to −1.34; aOR = 2.05; 95% CI 1.10–3.80). Conclusions: Maternal glycemic levels during pregnancy influence offspring neurodevelopment, with persistent hyperglycemia significantly increasing DD risk. Early pregnancy hyperglycemia particularly affects male offspring, underscoring the need for glycemic management during pregnancy.