Background: The visceral adiposity index (VAI) is a marker of abdominal fat distribution and adipose tissue function. However, the association between VAI and femur bone mineral density (BMD) and osteoporosis is unclear among the U.S. older adults.Methods: Cross-sectional data for adults aged 60 years and older from the 2007–2020 National Health and Nutrition Examination Survey (NHANES) were included. Multivariable linear and logistic regression were used to evaluate the association between VAI and femur BMD and osteoporosis. We used the smooth curve fitting to address nonlinearity. Moreover, a two-piecewise linear regression model was used to explain the nonlinearity further.Results: The findings of the multivariable logistic regression models showed that as the VAI value increased by one unit, the prevalence of osteoporosis decreased by 1.2% after adjusting for covariates associated with osteoporosis. The multivariable linear regression models demonstrated that VAI was positively correlated with femur BMD. Further analysis revealed an inverted L-shaped and inverted U-shaped relationship between VAI and femur BMD at different sites.Conclusions: Our findings indicated that an increased VAI is independently linked to a higher prevalence of osteoporosis among the U.S. older adults. Further analysis reveals that once VAI reaches a certain threshold, femur BMD no longer increases and may even decrease. This suggests that a moderate accumulation of visceral fat may be beneficial for bone health, while excessive visceral fat could potentially have detrimental effects.

Background: Mental health issues among middle-aged and older adults are gaining increasing attention. Recent studies have shown that relative grip strength is associated with cardiovascular diseases and various cancers, but its relationship with depression remains unclear.Methods: This cross-sectional study included data from adults aged 50 years and older from the 2011–2014 National Health and Nutrition Examination Survey. Relative grip strength is calculated by dividing the maximum absolute grip strength of both hands by BMI. The Patient Health Questionnaire (PHQ-9) was used to evaluate the depressive outcome. Multivariate logistic regression was performed to assess the association between relative grip strength and depression.Results: In this study, a total of 3,639 participants (≥50 years) with a mean age of 64.3 ± 9.3 years were enrolled, of whom 48.9% were male. Compared with individuals with lower relative handgrip strength in Q1 (≤1.64 kg/BMI), the adjusted OR values for relative handgrip strength and depression in Q2 (1.64–2.17 kg/BMI), Q3 (2.17–2.84 kg/BMI), and Q4 (≥2.84 kg/BMI) were 0.69 (95% CI: 0.51, 0.93, p = 0.016), 0.36 (95% CI: 0.24, 0.55, p < 0.001), and 0.32 (95% CI: 0.20, 0.51, p < 0.001), respectively. The relationship between relative grip strength and depression presented an L-shaped curve (nonlinear, p = 0.006), with an inflection point of roughly 2.98 kg/BMI. Among participants with relative grip strength < 2.98 kg/BMI, the OR of incident depression was 0.41 (95% CI: 0.30–0.55, p < 0.001).Conclusion: Our findings indicated that relative grip strength was inversely associated with incident depression and demonstrated an L-shaped relationship among U.S. middle-aged and older adults. Relative grip strength could be the indicator for future screening of mental health.

Objective: To explore the causal relationships between 91 circulating inflammatory cytokines and sarcopenia-related traits (low hand grip strength, appendicular lean mass, and usual walking pace) by Mendelian randomized analysis.Methods: Independent genetic variations of inflammatory cytokines and sarcopenia-related traits were selected as instrumental variables from publicly available genome-wide association studies (GWAS). The MR analysis was primarily conducted using the inverse variance-weighted (IVW) method. Sensitivity analyses included Steiger filtering and MR PRESSO, with additional assessments for heterogeneity and pleiotropy.Results: The IVW method indicated a causal relationship between Vascular Endothelial Growth Factor A (VEGF-A) and low hand grip strength (OR = 1.05654, 95% CI: 1.02453 to 1.08956, P = 0.00046). Additionally, Tumor Necrosis Factor-beta (TNF-β) was found to have a causal relationship with appendicular lean mass (ALM) (β = 0.04255, 95% CI: 0.02838 to 0.05672, P = 3.96E-09). There was no evidence suggesting a significant causal relationship between inflammatory cytokines and usual walking pace.Conclusion: Our research substantiated the causal association between inflammatory cytokines, such as VEGF-A and TNF-β, and sarcopenia. This finding may provide new avenues for future clinical treatments.

Aberrant hypermethylation and hypomethylation both play important roles in myelodysplastic syndrome (MDS). Hypomethylating agents targeting hypermethylation have been employed for the MDS treatment, but the treatment effect is limited. Novel drugs for DNA hypomethylation‐targeted therapy may be needed to improve clinic efficacy for the treatment of MDS. Chinese medicine (CM) herbs have been used to treat MDS for many years in our hospital. However, the long‐term treatment effect and mechanism remain unclear. In this study, all 135 patients received CM treatment for at least 36 months. The response rates for CM treatment were 81.53% (106/130) for hematological improvement in 130 MDS‐RCMD patients and 80% (4/5) for bone marrow CR in 5 MDS‐RAEB patients, respectively. The Human Methylation 850K BeadChip showed that 115 genes (50.88%) were aberrantly hypomethylated in 5 MDS patients compared with 3 healthy individuals. GO‐analysis showed that these hypomethylated genes participated in many cancer‐related biological functions and pathways. Furthermore, 60 genes were hypermethylated and the protein expression level of DNMT1 was significantly increased in the 5 MDS patients after 6 months of CM treatment. Our study suggests that CM can improve aberrant hypomethylation by increasing DNMT1 expression in MDS. The data support the clinical application of CM herbs containing arsenic as an innovative hypermethylation‐inducing regimen for the treatment of MDS.

Cellular senescence is increasingly recognized as a key mechanism linking aging to chronic disease. Diabetic atherosclerosis (DAS), a major macrovascular complication of type 2 diabetes, often progresses despite standard metabolic and lipid-lowering therapies, highlighting the involvement of aging-related processes beyond classical metabolic and inflammatory pathways. This review synthesizes evidence to propose a conceptual framework in which stress-induced senescence is a key disease-oriented aging mechanism contributing to DAS initiation and progression. Hyperglycemia and lipotoxicity induce premature senescence in endothelial cells, vascular smooth muscle cells, and macrophages through oxidative stress, mitochondrial dysfunction, and activation of the NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome. Senescent cells secrete a senescence-associated secretory phenotype (SASP), which amplifies chronic vascular inflammation, promotes plaque instability, and facilitates systemic propagation of senescence, thereby contributing to multi-organ dysfunction in the heart, brain, and kidneys. Together, these features position DAS as a representative model of stress-accelerated vascular aging. From a therapeutic perspective, we discuss emerging senescence-targeted strategies, including senolytics, senomorphics, and multi-target interventions derived from integrative medicine, with emphasis on their potential to modulate the aging tissue microenvironment and delay disease progression. By framing diabetic atherosclerosis within the context of aging biology, this review provides a disease-focused perspective on mechanisms and therapeutic opportunities underlying age-associated vascular disorders.