Xiangwei Li

Objectives: We assessed how socioeconomic status (SES) and diet quality, separately and jointly, related to depressive and anxiety symptoms in older Chinese adults. Methods: Data came from 9278 participants aged 65 years or older in the 2018 Chinese Longitudinal Healthy Longevity Survey. Education, main occupation before age 60, and annual household income were integrated into latent SES classes. Diet quality was represented by the Chinese-modified Mediterranean-DASH Intervention for Neurodegenerative Delay score (cMIND), Healthy Eating Index (HEI), Dietary Diversity Score (DDS), and Anti-Inflammatory Dietary Diversity Score (AIDDS). Depression and anxiety symptom status was determined from the 10-item Center for Epidemiologic Studies Depression Scale (CES-D-10) and 7-item Generalized Anxiety Disorder Scale (GAD-7). We used multivariable logistic models, joint-exposure models, restricted cubic splines, exploratory SES-by-diet interaction models, and multiple imputation for missing covariates. Results: Relative to high SES, low SES was associated with greater odds of depressive symptoms (OR = 1.50, 95% CI: 1.32–1.71) and anxiety symptoms (OR = 1.76, 95% CI: 1.43–2.16). All four dietary indices showed inverse associations with both outcomes. The largest joint estimates occurred for low SES plus low AIDDS (depressive symptoms: OR = 2.26, 95% CI: 1.94–2.64; anxiety symptoms: OR = 2.69, 95% CI: 2.12–3.40). No overall multiplicative interaction was found for dichotomized diet scores. For standardized continuous scores, nominal SES-by-diet interactions were observed for HEI, DDS, and AIDDS for depressive symptoms, but after Benjamini-Hochberg false-discovery-rate (FDR) correction only DDS and AIDDS remained below q < 0.05; no anxiety interaction survived correction. Conclusions: Socioeconomic disadvantage and poorer diet quality were each associated with greater symptom burden, while their co-occurrence identified the least favorable joint profile. Longitudinal and intervention studies are needed before dietary improvement can be interpreted as reducing SES-related mental-health inequalities.

Background: Metabolic syndrome (MetS) is a cluster of risk factors that increases cardiometabolic disease and mortality. A continuous MetS Score has been developed to quantify MetS severity, but its association with all-cause mortality in older Chinese adults remains unclear. Methods: We analyzed 2,443 participants from the Chinese Longitudinal Healthy Longevity Survey (CLHLS, 2008–2018 and 2011–2018). MetS Score was derived by confirmatory factor analysis using triglycerides, HDL-C, fasting glucose, systolic blood pressure, and BMI. Participants were categorized into quartiles (Q1-Q4). Cox proportional hazards models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause mortality. Subgroup analyses examined heterogeneity by age, sex, residence, and other covariates, and restricted cubic splines explored dose–response relationships. Results: During 10,356 person-years of follow-up, 1,412 deaths occurred (136.3/1,000 person-years). Each 1-unit increase in MetS Score was associated with a 13.9% lower mortality risk (HR = 0.861, 95% CI: 0.787–0.942). The protective effect was concentrated in Q4 vs. Q1 (HR = 0.792, 95% CI: 0.669–0.938). Subgroup analyses showed stronger associations in those aged ≥80 years (HR = 0.785, 95% CI: 0.660–0.935), women (HR = 0.758, 95% CI: 0.617–0.931) and rural residents (HR = 0.817, 95% CI: 0.618–0.980). Restricted cubic splines confirmed a linear inverse association overall and among the ≥80 years group. Conclusion: MetS Score, reflecting MetS severity, was inversely associated with all-cause mortality in older Chinese adults, particularly among those aged ≥80 years. These findings suggest that higher MetS Score may paradoxically confer survival benefits in the older adults, warranting further mechanistic studies.

As global aging intensifies, elucidating reproductive health’s epigenetic aging associations is crucial. However, the impact of reproductive history on multi-generational DNA methylation (DNAm) clocks remains insufficiently characterized, representing a significant gap in understanding biological vs. chronological aging divergence. This study analyzed 1117 U.S. women aged 50 or older from NHANES 1999–2002 to examine associations between reproductive history and 12 DNA methylation (DNAm) algorithms. Multivariable linear/logistic regression models assessed associations between reproductive indicators and DNAm age acceleration, adjusting for sociodemographic/biological confounders. The β coefficients represent the change in DNAm age acceleration in years. Pregnancy frequency (per additional pregnancy) showed positive associations with PhenoAgeacc ( β = 0.14, 95%CI:0.01–0.27) and GrimAge2Mortacc ( β = 0.10, 0.03–0.18). Categorical analyses revealed that high pregnancy parity (≥5) significantly increased the odds of GrimAge2Mortacc (OR = 2.34, 95% CI: 1.15–4.71), while high live birth parity (≥5) was associated with increased odds of HannumAgeacc (OR = 2.57, 95% CI: 1.01–6.92). Most primary associations involving second-generation clocks remained robust after false discovery rate correction. While menarche timing showed no significant associations, later menopause and a longer reproductive lifespan were significantly associated with decelerated biological aging after multiple testing correction. These findings suggest that parity and reproductive timing are associated with biological aging trajectories through methylation mechanisms, advancing our understanding of sex-specific aging drivers.

While individual associations between social determinants of health (SDoH), behavioral factors, and incident dementia have been established, the cumulative

Although obesity is a well-established risk factor for metabolic dysfunction-associated steatotic liver disease (MASLD), the impact of long-term weight trajectories on MASLD risk remains unclear. We aimed to examine the association between weight change trajectories across adulthood and the risk of ultrasound-defined MASLD. We analysed data from 4999 participants from the Healthy Happy Aging Community Cohort. Weight trajectories were assessed using body mass index (BMI) at age 25 years, ten years before baseline, one year before baseline, and at baseline. MASLD was defined as a median (MD) controlled attenuation parameter (CAP) of ≥274 dB/m and severe steatosis as a MD CAP of ≥302 dB/m via vibration-controlled transient elastography. There were 2247 (44.9%) patients with MASLD, of whom 1468 (29.4%) had severe steatosis. Compared with stable normal weight, sustained obesity (BMI ≥ 30 kg/m² at all time points) demonstrated a strong association with MASLD risk (adjusted odds ratio (aOR) = 2.17; 95% confidence interval (CI) = 1.64-2.86), particularly for severe steatosis (aOR = 2.52; 95% CI = 1.74-3.66). The transition from non-obese to obese status was associated with a 2.5-fold increase in risk (aOR = 2.51; 95% CI = 1.81-3.48), with a more pronounced effect observed in men (P-interaction 2) remained the strongest independent predictor (aOR = 4.12; 95% CI = 2.70-6.29). Long-term obesity and weight gain, especially in early adulthood, significantly increase MASLD risk. Sustained obesity and progression to obesity were key risk factors, with severe obesity showing the strongest association. Early weight management is crucial for MASLD prevention.

Emerging perfluoroalkyl substances (PFAS), such as perfluorononanoic acid (PFNA) and perfluorosulfonic acid (PFSA), are pervasive environmental contaminants that may influence human health. Their effects on aging, particularly through recently developed robust DNA methylation (DNAm) aging algorithms, remain largely unexplored. Using data from 326 U.S. adults aged ≥50 years (NHANES 1999–2000), we quantified serum PFAS via isotope-dilution tandem mass spectrometry and computed 12 DNAm aging algorithms. Weighted multivariable linear regression models assessed PFAS-DNAm aging associations, stratified by sex and age. PFNA exposure was significantly associated with DNAm algorithms via GrimAgeMortacc (β = 2.74, 95% CI: 1.04–4.44) and GrimAge2Mortacc (β = 2.45, 0.60–4.31), with stronger magnitudes in males ( P -interaction = 0.0050) and adults aged 50–64 ( P -interaction = 0.0270). PFSA was associated with LinAgeacc (β = 4.17, 0.60–7.74). Sex-stratified analyses revealed male-specific PFNA-HorvathAgeacc associations (β = 4.11, 0.71–7.52). These findings suggest that PFNA and PFSA may drive epigenetic aging disparities in aging populations, with males and middle-aged individuals at heightened risk. These findings underscore the need to regulate emerging PFAS and integrate epigenetic biomarkers into environmental health risk assessments.