Nutrients最新文献

Background/objectives: Depression is a common mental disorder that has a substantial impact on both society and health. The potential health benefits of tea consumption have been suggested; however, whether the type of tea and drinking patterns such as frequency and intake are related to the risk of depression remain unclear, especially in different populations. This study utilized data from 27,119 Taiwan Biobank enrollees to evaluate the relationship between the prevalence of self-reported lifetime history of depression and tea consumption, including the type, drinking frequency, and daily intake.

Methods: Tea consumption was categorized by type (fully fermented, semi-fermented, and non-fermented), frequency and daily intake. Self-reported questionnaires were used to record self-reported lifetime history of depression status. The association between tea consumption and self-reported lifetime history of depression was investigated using multivariable logistic regression.

Results: Overall, tea consumption was significantly associated with a low prevalence of self-reported lifetime history of depression (odds ratio [OR] 0.736). While this association was found for semi-fermented and non-fermented teas (OR, 0.674), it was not found for fully fermented tea. Although a daily consumption of one-two cups (350-700 mL) was significantly associated with a low prevalence of self-reported lifetime history of depression, drinking more than three cups per day showed no association. Furthermore, regarding the frequency of tea consumption, those who drank tea every day were significantly associated with a low prevalence of self-reported lifetime history of depression, while those who only drank tea weekly or monthly were not. Subgroup analysis showed that tea consumption was not associated with a lower prevalence of self-reported lifetime history of depression in older individuals (≥65 years), those with diabetes, smokers, and those who drank alcohol, suggesting that health status and lifestyle factors may influence the possible associations of tea consumption. However, the interaction analysis did not achieve significance. We acknowledge that the formal interaction tests were not statistically significant and that these findings should therefore be considered exploratory.

Conclusions: Consuming semi-fermented and non-fermented tea was associated with a low prevalence of self-reported lifetime history of depression; however, the association depended on the quantity and frequency of consumption. Further research is warranted to explore the biological mechanisms of different types of tea and develop intervention strategies for high-risk populations.

Background/Objectives: Periodontitis and low BMD often occur after menopause, but the role of nutritional status in the oral-skeletal link is unclear. This study examined whether nutritional biomarkers relate to periodontitis severity and modify the relationship between low BMD and periodontal destruction in postmenopausal women. Methods: This cross-sectional study included 120 postmenopausal women who underwent comprehensive periodontal measurements at six sites per tooth and were classified according to the 2017 World Workshop staging and grading framework. Areal BMD was measured using dual-energy X-ray absorptiometry (DXA). Objective biomarkers included serum 25(OH)D, plasma vitamin C, RBC omega-3 index, and serum ferritin. Mechanistic measures were serum CTX, P1NP, and urinary 8-OHdG/creatinine. The main periodontal outcome was the mean CAL. Results: Low BMD was associated with greater periodontal destruction (mean CAL 2.06 vs. 1.45 mm; adjusted β = 0.664 mm, 95% CI 0.465-0.863; p < 0.001). Higher 25(OH)D and omega-3 index were independently associated with lower mean CAL (β = -0.024 mm per 1 ng/mL and β = -0.107 mm per 1%, respectively), with false discovery rate control applied across nutritional biomarkers. Across the cohort, serum 25(OH)D showed a weak inverse correlation with CTX (r = -0.14; p = 0.141), and exploratory mediation analyses suggested only small indirect effects via CTX and 8-OHdG. Conclusions: In women after menopause, lower BMD is associated with greater periodontal tissue loss. Objective nutritional biomarkers, especially 25(OH)D and omega-3 levels, correlate with biologically plausible pathways involved in periodontal destruction and remodeling. This supports the idea that nutrition could be a key factor linking oral health and skeletal health.

Background/Objectives: Fetal growth restriction (FGR) represents a model of adverse intrauterine programming associated with an increased risk of cardiometabolic disorders later in life. We examined the relationships between birth weight, catch-up growth, adipokine signaling, and early cardiometabolic risk in adolescents. Methods: This cross-sectional study included 80 term-born adolescents (40 FGR, 40 controls) matched for age and sex. Anthropometry, blood pressure, lipid profile, fasting glucose, adipokines (leptin, adiponectin), and ghrelin levels were assessed. Associations between birth weight, growth rate, adipokines, and cardiometabolic outcomes were analyzed. Results: Birth weight was not associated with adiposity, lipid profile, blood pressure, or glycemic status (p > 0.05). In contrast, catch-up growth in the FGR group was correlated with increased BMI (ρ = 0.680, p < 0.001), central adiposity (ρ = 0.714, p < 0.001), systolic blood pressure (ρ = 0.448, p = 0.0037) and diastolic blood pressure (ρ = 0.325, p = 0.0409). Mediation analyses showed that the current BMI largely explains the associations between catch-up growth and cardiometabolic risk, systolic blood pressure, and waist circumference (β = 2.832 kg/m² per 1-unit increase in ΔZ; p < 0.001). The hypertensive effect of catch-up growth was amplified in overweight/obese adolescents (β = 8.13 mmHg; p = 0.006). Catch-up growth was independently associated with higher leptin (β = 220 ng/L; p = 0.022) and a higher leptin/ghrelin ratio (β = 2.330; p = 0.034). Conclusions: Postnatal growth acceleration, rather than fetal size alone, drives early cardiometabolic susceptibility following FGR through adiposity-mediated and endocrine pathways.

Background/Objectives: Cancer and their treatments could impact physical, nutritional, and psychological health, negatively influencing overall well-being. Accordingly, Health-Related Quality of Life (HRQoL) could be influenced by lifestyle habits, such as physical activity. This study aimed to assess physical activity levels in patients with a primary cancer diagnosis and their association with HRQoL at the first nutritional assessment. Methods: Data from the NUTRISCREEN project, part of the ONCOCAMP study (ClinicalTrials.gov ID: NCT06270602), were analyzed. Nutritional and sarcopenia risk, anthropometry and body composition parameters were collected. HRQoL and physical activity (as MET levels) were assessed through validated questionnaires. Descriptive statistics summarized categorical and continuous variables, and multivariable ordinal logistic regression models were performed. Results: Nutritional and sarcopenia risk decreased progressively with higher MET levels (p = 0.005 and p < 0.001, respectively). Adjusted multivariable models showed that HRQoL functional scores improved with increasing MET levels, with significant positive trends for physical (p < 0.001), role (p < 0.001), emotional (p = 0.003), and social functioning (p = 0.001), and global health status (p < 0.001). Conversely, symptom burden, including fatigue, nausea and vomiting, pain, dyspnea, insomnia, appetite loss, and constipation, decreased across MET quartiles (all p < 0.05). Conclusions: Overall, our findings suggest that physical activity may positively influence HRQoL among cancer patients. Early assessment helps to identify patients at risk of inactivity and support tailored rehabilitation programs to promote active lifestyles, preserve muscle mass, improve outcomes and overall health status.

Vitamin D (VD), a fat-soluble prohormone, exerts diverse effects on cellular proliferation, differentiation, and immune modulation, with accumulating evidence supporting its role in pancreatic ductal adenocarcinoma (PDAC) biology. Experimental studies demonstrate that VD and its analogs can inhibit PDAC cell growth and remodel the tumor microenvironment, potentially contributing to tumor suppression. Epidemiological data indicate that VD deficiency is prevalent among PDAC patients and is associated with increased inflammatory biomarkers and reduced overall survival, particularly in early-stage disease. However, meta-analyses reveal inconsistent associations between circulating 25-hydroxyvitamin D levels and PDAC incidence, while higher levels may be linked to improved survival but not reduced risk of disease onset. The clinical utility of VD supplementation for PDAC prevention or treatment remains uncertain, with ongoing debate regarding optimal dosing, timing, and patient selection. This narrative review synthesizes current evidence on the mechanistic, epidemiological, and clinical relevance of VD in PDAC. Particular emphasis is placed on existing knowledge gaps and the need for well-designed clinical trials to clarify the potential therapeutic and prognostic role of VD in pancreatic cancer.

Background/Objectives: Low vitamin D status was found to attenuate the impact of metformin on circulating levels of anterior pituitary hormones, but this inhibitory effect was absent in vitamin D-repleted subjects. No previous study investigated the interaction between metformin and exogenous vitamin D at the pituitary levels in individuals with normal vitamin D status. Methods: Our pilot, single-center, prospective, matched-cohort study enrolled 59 postmenopausal women with subclinical hypothyroidism and 25-hydroxyvitamin D levels in the range between 75 and 150 nmol/L. For the following six months, all the participants were treated with either metformin/vitamin D combination therapy (group 1, n = 27) or metformin alone (group 2, n = 32). The outcomes of interest included 25-hydroxyvitamin D, fasting glucose, HOMA-IR, HbA_1c, TSH, FSH, LH, prolactin, ACTH, free thyroid hormones, estradiol and IGF-1. A parallel study investigated the impact of vitamin D monotherapy on the outcome measures in insulin-resistant women meeting the remaining inclusion criteria. Results: No differences in baseline biomarker values were observed between groups 1 and 2. Ninety-three percent of the patients completed the study. The increase in 25-hydroxyvitamin D levels was observed exclusively in group 1. Although glucose homeostasis markers and post-treatment levels of TSH and FSH were lower at the end of the study than at baseline in both groups, the effect of treatment was more pronounced in group 1 than in group 2. Metformin/vitamin D combination therapy, but not metformin alone, reduced LH and prolactin levels. In both groups, the TSH- and gonadotropin-lowering effects of metformin correlated with baseline levels of these pituitary hormones. Levels of ACTH, free thyroxine, free triiodothyronine, estradiol and IGF-1 remained stable throughout the study. The effects of vitamin D monotherapy were confined to an increase in plasma 25-hydroxyvitamin D concentrations and a modest enhancement in insulin sensitivity. Conclusions: Exogenous vitamin D potentiates the pituitary effects of metformin in postmenopausal women with subclinical hypothyroidism.

Background/Objectives: Human milk composition is shaped by gestational age at delivery and stage of lactation; however, proteomic differences between milk from mothers of preterm and term infants and their temporal patterns remain incompletely characterised. Methods: This prospective study enrolled 40 lactating mothers: 20 who delivered preterm infants (<32 weeks' gestation) and 20 who delivered at term (37-42 weeks). Each provided milk samples during early lactation (first 10 days postpartum) and during later lactation (week five postpartum). Milk serum was analysed using quantitative data-independent acquisition mass spectrometry. Differential protein abundance was assessed separately at each time point; functional annotation was performed using Gene Ontology biological process analysis. Results: Eighty samples were analysed. On average, a total of 662 proteins were identified per sample, of which 169 were consistently quantified across all samples (1% FDR). During early lactation, 10 proteins differed significantly, with bidirectional changes and moderate effect sizes. At week five, 19 proteins were differentially abundant, predominantly higher in preterm samples. Immune-related proteins constituted the largest functional category at both stages. Immunoglobulin heavy constant gamma 4 remained consistently downregulated in preterm milk (1.6-fold lower abundance). Ferritin heavy chain (1.5) and HLA class II histocompatibility antigen gamma chain (1.8) were elevated only early, whereas calprotectin subunits S100A8 (5.6) and S100A9 (5.2) were markedly upregulated later. Conclusions: Proteomic differences vary across lactation stages, highlighting lactation stage as an essential contextual variable in comparative milk proteomics.

Objectives: Dendrobine (DDB) is one of the active ingredients in Dendrobium and has been reported to have significant neuroprotective properties. Nevertheless, the precise mechanisms underlying its action have not been fully clarified. The microglial imbalance of polarization is regarded as one of the key determinants in the etiology of neurodegenerative conditions, in the contribution of neuroinflammation. The recovery of M1/M2 balance and the inhibition of over-production of the pro-inflammatory effects have become major topics in modern studies of preventing and treating neurodegenerative diseases. Methods: Therefore, the present study aimed to explore the effects of DDB on the Lipopolysaccharide (LPS)-induced neuroinflammatory model in BV2 microglial cells and the potential molecular mechanisms of microglial M1/M2 polarization. Result: The results showed that DDB significantly suppressed Nitric Oxide (NO) release and ROS levels in LPS-induced BV2 cells. ELISA, qPCR, Western blot, and immunofluorescence results indicated that DDB reduced pro-inflammatory mediators Tumor Necrosis Factor-alpha (TNF-α), Interleukin-6 (IL-6), and nterleukin-1 beta (IL-1β) and increased anti-inflammatory mediators Interleukin-10 (IL-10) and Arginase-1 (Arg-1). Consistently, it decreased M1-like markers Inducible Nitric Oxide Synthase (iNOS) and Cluster of Differentiation 16/32 (CD16/32) while increasing M2-like/repair-associated markers (CD206 and Arg-1), suggesting a shift toward a more anti-inflammatory microglial activation profile based on the assessed marker pane. Conclusions: These results suggested that DDB can suppress the production of inflammatory cytokines and modulate microglial polarization, which indicated that DDB can be used as an effective compound in the prevention of neuroinflammation-related disorders.

Introduction: Muscle function is influenced by hydroelectrolytic mechanisms that regulate cellular volume beyond isolated plasma electrolyte concentrations. However, the role of integrated hydration and electrolyte regulation profiles in muscle function among older adults remains insufficiently understood. Objective: To identify which physiological domains of hydroelectrolytic regulation are most strongly associated with muscle strength and functional performance in community-dwelling older adults. Methods: A cross-sectional study was conducted in 96 community-dwelling individuals aged ≥ 70 years. Markers of cellular hydration and membrane integrity were assessed using bioelectrical impedance analysis, together with first-morning fasting plasma and urinary sodium and chloride concentrations. Principal component analysis (PCA) was applied as a data-driven approach to identify latent domains of coordinated hydroelectrolytic regulation. Associations between component scores and handgrip strength and Timed Up and Go (TUG) were examined using two sequential multivariable regression models: Model 1 adjusted for sex and fat-free mass index (FFMI); Model 2 additionally adjusted for age, hypertension, and diuretic use. Results: Three principal components were retained, explaining 77.5% of total variance: PC1 (renal-cellular domain), PC2 (plasma electrolyte domain), and PC3 (cellular volume domain). For handgrip strength, Model 1 showed significant associations for PC3 (β = 0.152; p = 0.025) and PC1 (β = 0.180; p = 0.050). In Model 2, only PC3 remained independently associated (β = 0.146; p = 0.036). For TUG, Model 1 showed associations for PC1 (β = -0.262; p = 0.049) and PC3 (β = -0.238; p = 0.015). In Model 2, PC1 (β = -0.308; p = 0.019) and PC2 (β = -0.190; p = 0.046) remained independently associated, whereas PC3 was not. Conclusions: Maximal force production appears primarily associated with cellular volume regulation, whereas functional performance reflects broader multi-compartmental hydroelectrolytic integration involving renal and plasma domains. These findings suggest that multidimensional hydration profiling may complement isolated biochemical markers in the functional assessment of older adults, warranting validation in longitudinal studies.

Background and Purpose: The effects of B-vitamin combinations on the prevention of cardiovascular diseases, such as myocardial infarction (MI) and stroke, remain controversial. We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) over three decades to evaluate the association between B-vitamin combinations and mortality and arterial thrombotic outcomes. Methods: PubMed, Embase, Web of Science, and the Cochrane Library were systematically searched for RCTs with minimal duration over 24 months published between January 1996 and November 2025. Two reviewers independently screened studies, extracted data, and assessed risk of bias using the Cochrane Risk of Bias 2.0 tool. Random-effects models were used in this meta-analysis to calculate pooled risk ratios (RRs) and 95% confidence intervals (CIs). Results: Thirteen randomized trials enrolling 68,363 participants across both primary and secondary prevention populations were included. B-vitamin combinations were associated with a nonsignificant reduction in stroke and 3-point major adverse cardiovascular events (MACE) (stroke: RR 0.91, 95% CI 0.81-1.04; MACE: RR 0.93, 95% CI 0.86-1.01). No significant effects were observed for all-cause mortality (RR 1.01, 95% CI 0.96-1.06), cardiovascular mortality (RR 0.97, 95% CI 0.88-1.07), or MI (RR 0.97, 95% CI 0.91-1.03). In primary prevention populations, B-vitamin combinations were associated with significant reductions in stroke (RR 0.79, 95% CI 0.68-0.93) and MACE (RR 0.80, 95% CI 0.69-0.92). A modest reduction in MACE was also observed in secondary prevention populations (RR 0.91, 95% CI 0.83-0.99). Between-study heterogeneity was minimal to low for ischemic outcomes, supporting the robustness of these estimates, whereas substantial heterogeneity was observed for mortality outcomes in secondary prevention populations. Conclusions: The evidence is limited by heterogeneity in trial populations, vitamin formulations and doses, and outcome definitions, with substantial between-study inconsistency for mortality outcomes and imprecision in subgroup estimates derived from a small number of contributing trials. Overall, B-vitamin combinations do not confer consistent benefit for major cardiovascular outcomes but may reduce stroke and MACE in selected primary prevention populations, suggesting that baseline cardiovascular risk and regional folic acid fortification modify treatment effects and should guide future trial design and clinical use.