Nutrition Journal最新文献

Purpose: This study evaluated the predictive value of nutritional and molecular biomarkers for assessing therapeutic response to neoadjuvant chemoradiotherapy (NCRT) and long-term outcomes in older adult patients with locally advanced rectal carcinoma (LARC).

Methods: A retrospective cohort study analyzed 231 patients over 60 years old with LARC who underwent NCRT followed by radical resection between 2012 and 2018 at Fujian Medical University Union Hospital. The immunohistochemical (IHC) evaluation comprised 62 biopsy specimens from the same institution and 29 from the First Affiliated Hospital of Fujian Medical University.Transcriptomic data from GSE145037 (discovery cohort) and GSE35452 (validation cohort) were utilized to identify senescence-associated genes.

Results: from multivariate Cox regression identified pathological TNM stage (HR = 2.617, 95% CI 1.825-3.754, P < 0.001) and Geriatric Nutritional Risk Index (GNRI) (HR = 0.266, 95% CI 0.116-0.612, P = 0.002) as independent prognostic factors for disease-free survival (DFS), contributing to the development of a new DFS nomogram.Through random forest modeling, Epithelial Growth Factor Receptor (EGFR) overexpression and IQ Motif Containing GTPase Activating Protein 2 (IQGAP2) underexpression emerged as key aging-related biomarkers linked to GNRI. R2 platform analysis confirmed their prognostic significance, with elevated EGFR and low IQGAP2 correlating with reduced survival.Consistently, NCRT responders exhibited lower EGFR (P < 0.05) and higher IQGAP2 expression versus non-responders in both GSE145037 and GSE35452 datasets. External IHC validation reinforced these patterns in tumor microenvironment.

Conclusion: GNRI serves as a robust nutritional assessment tool for older adult LARC patients. The EGFR and IQGAP2 expression demonstrates dual utility in evaluating age-related malnutrition and predicting NCRT resistance, providing mechanistic insights for personalized therapeutic strategies.

Background: There is no prospective epidemiologic evidence to support whether tea consumption has protective effect on the relationship between meat intake and obesity.

Methods: This study utilized data from the UK Biobank, including 206,142 participants for primary analysis. Dietary tea and meat intake was calculated based on food consumption from 24-hour dietary recall, and subsequently categorized into three groups (low, medium, and high) using tertiles. Time-dependent Cox models were used to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) for the separate and joint associations of dietary tea and meat intake with risk of incident obesity. To assess the potential modified effect of tea in the association of meat intake with the risk of incident obesity, we examined the both multiplicative and additive interactions. Stratified analysis was performed by levels of tea intake. Subgroup analyses were performed by sex, polygenic risk score (PRS), the Townsend Deprivation Index (TDI), age and cholesterol.

Results: During a median follow-up of 11.51 years, 11,627 incident obesity cases were identified. A near-linear dose-response relationship was observed between higher consumption of total, processed, and white meat-though not red meat-and increased obesity risk, independent of tea intake. For instance, even when accompanied by high tea consumption, high intake of each meat type remained significantly associated with elevated obesity risk (total meat: HR = 1.425, 95% CI: 1.286 to 1.579; red meat: HR = 1.217, 95% CI: 1.086 to 1.365; processed meat: HR = 1.521, 95% CI: 1.326 to 1.745; white meat: HR = 1.508, 95% CI: 1.314 to 1.732). No significant statistical or additive interactions were detected between tea and meat consumption. Consistent with this, among high meat consumers, even the highest level of tea intake did not attenuate the risk (total meat: HR = 1.483, 95% CI: 1.347 to 1.632; red meat: HR = 1.210, 95% CI: 1.086 to 1.348; processed meat: HR = 1.403, 95% CI: 1.243 to 1.584; white meat: HR = 1.536, 95% CI: 1.350 to 1.747). Subgroup analyses yielded generally consistent results but suggested potential sex-specific differences.

Conclusions: There is no interactive effect between meat and tea consumption, implying that tea intake could not serve as a remedy for high meat consumption. Independent of the amount of tea consumed, there is still an elevated risk when consuming high level of meat.

Background: Human milk palmitic acid (PA) is mainly esterified at the sn-2 position of triacylglycerols, while infant formula contains palmitate predominantly in the sn-1/3 positions. Current evidence on long-term health effects of increasing sn-2 palmitate in formula remains insufficient. This study investigated the effects of high sn-2 PA formula (> 40%) on fecal saponified fatty acid, calcium, magnesium and stool characteristics in healthy full-term infants.

Methods: In this cluster-randomized controlled trial, healthy infants < 14 d were assigned to breastfeeding (BF group, n = 66), high sn-2 palmitate formula (sn-2 group, n = 66, 46.3% sn-2 PA) or low sn-2 palmitate formula (control group, n = 67, 10.3% sn-2 PA). Infant demographics, feeding status, stool characteristics, physical exams, and stool samples were collected at 6, 16, and 24 weeks. Per-protocol analysis was used.

Results: The sn-2 group exhibited a significant time-dependent decline in fecal saponified PA and calcium over time (P_{h for Trend} < 0.001). The BF group declined faster than the sn-2 group (P_{adjusted for Group*Time} < 0.001). Fecal saponified PA proportion in sn-2 group was significantly lower than controls at all timepoints. At week 24, fecal calcium was lower in the sn-2 group vs. control (0.9 vs. 1.3 mg/g, P = 0.010). No significant difference was found in stool frequency, consistency or size between sn-2 and control groups at any point.

Conclusion: Infant formula enriched with > 40% sn-2 palmitate reduces fecal fatty acid and calcium excretion, supports efficient lipid and calcium absorption, shows a fecal magnesium pattern similar to breastfed infants, but does not alter stool characteristics relative to the control formula.

Trial registration: The trial is registered at Chinese Clinical Trial Registry: ChiCTR1800014479; 30/Jan./2018.

Background: Emerging evidence suggests gut microbiota modulation may influence neurocognitive function through the gut-brain axis. Although preliminary studies indicate probiotics' potential benefits for mild cognitive impairment (MCI), well-designed randomized controlled trials remain limited. This protocol paper describes a rigorously designed, registered clinical trial investigating the effects of targeted probiotic supplementation on cognitive and physiological outcomes in MCI participants.

Methods: A total of 110 middle-aged and older participants aged 55-80 years with MCI were scheduled to be included in the study, and randomized in a 1:1 ratio to either a probiotic group receiving supplementation consisting of Lactiplantibacillus plantarum ST-III, Lacticaseibacillus rhamnosus KF7, and Lacticaseibacillus paracasei BD5115, or a placebo group with maltodextrin for 12 months. All the participants, researchers, and analysts will remain blinded to the information regarding group allocation in the study. The primary outcome will be the effect of probiotic supplementation on cognitive function, measured by Montreal Cognitive Assessment (the Chinese Beijing Version). The secondary outcomes will include the impact of probiotic supplementation on digestive health, sleep health, facial aging, fundus conditions, olfactory and auditory function, body composition, bone density, and muscle function. Brain magnetic resonance imaging and wearable device including continuous glucose monitor and smart band will also be employed.

Discussion: This study will provide some new insights on how probiotic supplementation could impact cognitive function and other aging-related physiological functions in MCI adults and explore the potential underlying mechanisms. The findings may inform the development of strategies to delay cognitive decline by modulating the gut-brain axis in this high-risk population.

Trial registration: ChiCTR2400084594.

Background: Population aging is becoming increasingly prominent. Although various dietary factors have been associated with aging in older people, no dietary score specifically related to phenotypic aging has yet been developed.

Methods: We used data from the Guangzhou Biobank Cohort Study (GBCS) and National Health and Nutrition Examination Survey (NHANES). Interpretable machine learning framework including adaptive elastic-net (AENET), eXtreme Gradient Boosting (XGBoost), and Random Survival Forests (RSF) analysis combined with Shapley additive explanations (SHAP) were used to construct and validate a dietary index related to aging. Accelerated age is defined as the residual from a linear regression of phenotypic age on chronological age, with values greater than 0 indicating the presence of accelerating age.

Findings: In GBCS, of 9512 participants, the mean phenotypic age was 58.8 (standard deviation = 9.2) years. A dietary aging risk index (DARI) was constructed using nutrients and phenotypic age, with median (interquartile range) being 0.03 (0.01, 0.06). During an average follow-up of 16.1 years, after adjusting for twelve potential confounders, higher DARI were associated with older phenotypic age (β = 0.08 years, 95% confidence interval (CI) = 0.06-0.10), higher risks of accelerating age (odds ratio = 1.63, 95% CI = 1.38-1.93) and all-cause mortality (hazards ratio (HR) = 1.10, 95% CI = 1.04-1.17). The association with all-cause mortality was more pronounced in current smoker (HR = 1.29, 95% CI = 1.12-1.50). In NHANES, higher DARI were associated with lower α-Klotho levels (β=-0.020 pg/ml, 95% CI=-0.036 to -0.004).

Conclusions: This study developed and validated a DARI using machine learning methods, offering a comprehensive measure of the impact of multiple nutrients on phenotypic aging. An online tool was created to facilitate its application in population studies.