Journal of Nutrition Health & Aging最新文献

Background: Sarcopenia and altered body composition are established prognostic markers in several malignancies, but their relevance in non-muscle-invasive bladder cancer (NMIBC) remains unclear. This study evaluated associations between body composition indices-body mass index (BMI), skeletal muscle index (SMI), and psoas muscle index (PMI)-and recurrence risk in high-risk NMIBC patients treated with intravesical Bacillus Calmette-Guérin (BCG).

Methods: Body composition was assessed on computed tomography at primary diagnosis. Sarcopenia was defined using published sex-specific cut-offs. Recurrence-free survival (RFS) was analyzed using Kaplan-Meier estimates, Cox regression with linear and spline terms, and a gradient boosted machine (GBM) model.

Results: A total of 118 patients (median age 71 years; 78% male) were included. Tumor stages were pTa (40%), pT1 (54%), and primary carcinoma in situ (CIS) in 6%. During a mean follow-up of 32 months, 30 patients (25.4%) developed recurrence. Median BMI was 26 kg/m². SMI and PMI were higher in men and declined with age, whereas BMI remained stable. Sarcopenia prevalence varied widely across definitions (6-66%) with low-to-moderate concordance (Cohen's κ: 0-0.58). No sarcopenia definition independently predicted recurrence. In the GBM model, BCG maintenance, tumor stage, CIS, age, BMI, SMI, and PMI were important predictors. Spline Cox models demonstrated nonlinear U-shaped associations between BMI, SMI, PMI, and recurrence risk, with increased risk at both low and high values.

Conclusions: Body composition shows nonlinear associations with recurrence in high-risk NMIBC. Both low and excessive body and muscle mass may adversely affect disease control. The heterogeneity and limited prognostic value of current sarcopenia definitions highlight the need for standardized, multiparametric, and nonlinear risk modeling approaches.

Objectives: Muscle strength is a fundamental determinant of functional capacity across adulthood. While dietary protein has been widely studied, prospective evidence considering overall dietary patterns remains inconsistent. We examined the association between macronutrient-based dietary patterns and incident decreased muscle strength among adults aged 40 years and older.

Methods: We analyzed 31,968 adults aged ≥40 years without decreased muscle strength at baseline from the Korean Genome and Epidemiology Study. The participants were categorized into four groups according to macronutrient energy proportions: high-carbohydrate, high-fat, high-protein, and normal diets. The incidence of decreased muscle strength was defined as <28 kg in men and <18 kg in women at follow-up. Cox proportional hazards models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) of decreased muscle strength between groups, and linear mixed-effects models were used to evaluate longitudinal changes in handgrip strength, including time, group, and the group-by-time interaction.

Results: During a median follow-up of 4.0 years, 2,194 participants developed incident decreased muscle strength (incidence rate 1.65 per 100 person-years). The high-protein dietary pattern was associated with a higher risk of incident decreased muscle strength compared with the normal diet (Adjusted HR 1.45, 95% CI 1.06-1.99), whereas no significant associations were observed for high-carbohydrate or high-fat dietary patterns. Changes in dietary patterns from baseline to follow-up were not significantly associated with the risk of decreased muscle strength, and the magnitude of change in handgrip strength over time did not differ across dietary pattern groups.

Conclusions: In middle-aged and older Korean adults, the high-protein dietary pattern was associated with an increased risk of incident muscle strength decline compared to the normal dietary pattern, whereas high-carbohydrate and high-fat patterns were not. These findings suggest that a balanced macronutrient composition, rather than protein intake alone, may be relevant to muscle strength.

Objective: To investigate the relationship of body composition with coronary plaque components and vascular inflammation.

Materials and methods: This retrospective study included 412 individuals who underwent computed tomography angiography scan between August 2024 and July 2025. Body composition including both muscle and adipose components was analyzed. Plaque characteristics and pericoronary fat attenuation index (FAI) were quantified. The associations between body composition, plaque burden, and FAI were examined using correlation and multivariable linear regression analyses. Furthermore, we explored the mediating roles of specific body composition metrics in the relationship between body mass index (BMI) and plaque burden, as well as the potential mediation by FAI in the association linking body composition to plaque burden.

Results: Of all-subjects, 269 (65.29%) were male. The average age was 62.85 ± 13.81 years old. Correlation analyses revealed significant moderate to strong positive associations of BMI, visceral adipose tissue (VAT), intermuscular adipose tissue (IMAT), and fatty muscle fraction (FMF) with lipid plaque burden. Additionally, BMI was moderately positively correlated with calcified plaque burden, while skeletal muscle (SM) was weakly negatively correlated with it. Specifically, in a multivariable-adjusted model, higher BMI (β= 0.053) were independently associated with greater lipid plaque burden. Higher BMI (β = 0.909) and lower SM (β = -0.004) were associated with an increased calcified plaque burden. Moreover, higher BMI (β = -0.547), subcutaneous adipose tissue (SAT) (β = -0.004), and SM (β = -0.001), as well as lower VAT (β = 0.005), epicardial adipose tissue (EAT) (β = 0.041), IMAT (β = 0.061), and FMF (β = 0.075) remained independently associated with decreased FAI. Mediation analysis revealed that SM and VAT mediated -29.555% and 56.489% of the association between BMI and calcified plaque burden and lipid plaque burden, respectively. Furthermore, FAI mediated 40.426% of the effect of VAT and 30.909% of the effect of IMAT on lipid plaque burden.

Conclusion: Different body composition metrics exert divergent effects on various components of coronary plaque. Our study suggests that VAT and IMAT may contribute to lipid plaque formation, potentially mediated by a state of increased vascular inflammation as captured by FAI, while a higher muscle mass may protect against the progression of calcified plaque. These findings highlights the necessity of precise body composition analysis in cardiovascular risk assessment.

Objectives: The determinants of functional limitation trajectories after stroke remain scarce. This study aimed to investigate the association of early body mass index (BMI) changes with trajectories of activities of daily living (ADLs) and instrumental activities of daily living (IADLs) following stroke.

Design: Three cohorts from Europe and the United States.

Setting: Community.

Participants: Stroke survivors.

Measurements: BMI changes were assessed 1-4 years after self-reported stroke and categorized as decreased (≤-5% initial BMI), increased (≥5% initial BMI), and stable. An alternate cut-point of 2% was also used. Functional limitations were measured as the number of ADL and IADL limitations, which were repeatedly measured for up to 24 years after stroke. Associations were evaluated using segmented linear mixed-effects models after adjusting for demographic, behavioral, and medical factors.

Results: The study population comprised 2544 adults with stroke (mean [standard deviation] age 70.0 [10.9] years; 52.0% women). Based on a 5% cutoff, the number of ADL and IADL limitations was higher in the groups of decreased (ADL: 0.56 [95% CI = 0.28, 0.85]; IADL: 0.66 [95% CI = 0.38, 0.94]) and increased BMI (ADL: 0.55 [95% CI = 0.28, 0.81]; IADL: 0.59 [95% CI = 0.33, 0.85]) compared to stable BMI, respectively. Similar findings were obtained for a 2% cutoff. These differences frequently persisted for 24 years for decreased BMI and 6-12 years for increased BMI.

Conclusion: Early decreased BMI, and to a lesser extent increased BMI, following stroke could be a marker of long-term adverse trajectories of physical functioning, underlying the importance of nutritional and physical activity management after a stroke.

Background: Biological aging and dietary fatty acid balance may influence the bidirectional progression between atrial fibrillation (AF) and heart failure (HF); however, most studies focus on single endpoints, overlooking intermediate states.

Objective: To evaluate the independent and joint associations of phenotypic age acceleration (PhenoAgeAccel) and the plasma omega-6/omega-3 (ω-6/ω-3) polyunsaturated fatty acid (PFUA) ratio with AF-HF transitions, and to examine mediation by lipids and C-reactive protein.

Methods: In a retrospective cohort of 191,091 UK Biobank participants free of baseline cardiovascular disease, PhenoAgeAccel was calculated as the residual from regressing phenotypic age on chronological age. The ω-6/ω-3 ratio was quantified by nuclear magnetic resonance. Incident AF and HF were modeled using clock-forward multistate Markov models for four transitions: baseline to AF, baseline to HF, AF to HF, and HF to AF. These transitions represent sequential disease progression, where either AF or HF may occur first and later progress to AF-HF comorbidity. Hazard ratios (HRs) were estimated per 1-SD increment. Joint exposure and mediation analyses were performed.

Results: Over a median 15.4 years, 10,084 developed AF and 3,117 H F; 1,335 transitioned from AF to HF and 426 from HF to AF. Per 1-SD higher PhenoAgeAccel, risks increased for baseline-to-AF (HR 1.12 [95% CI 1.10-1.15]), baseline-to-HF (1.24 [1.21-1.26]), AF-to-HF (1.12 [1.09-1.15]), and HF-to-AF (1.06 [1.01-1.12]). Per 1-SD higher ω-6/ω-3 ratio, risks rose for baseline-to-AF (1.04 [1.02-1.06]), baseline-to-HF (1.07 [1.05-1.10]), AF-to-HF (1.12 [1.07-1.18]), and HF-to-AF (1.10 [1.01-1.20]). Mediation occurred via triglycerides (up to 38.5% of ω-6/ω-3-AF association) and CRP (up to 10.7% of PhenoAgeAccel-HF association).

Conclusion: Higher PhenoAgeAccel and ω-6/ω-3 PFUA ratios were independently associated with higher risks of AF-HF transitions, with these associations partly explained by lipid and inflammatory pathways.