Nutrients

Background: Few studies have examined changes in diet quality into old age, and related these changes to musculoskeletal outcomes. We examined this among Hertfordshire Cohort Study participants. Methods: In total, 178 individuals provided diet quality scores derived in 1998–2004, 2011 and 2017 (median age 64.0, 74.7 and 80.7) using principal component analysis of food frequency questionnaires; higher scores indicated healthier diets (more fruit and vegetables, oily fish and wholemeal bread, and less white bread, added sugar, full-fat dairy products, chips and processed meat). Pearson correlations between diet quality scores at each time-point were computed. Group-based trajectory modelling of diet quality scores was implemented; trajectory groups as predictors of musculoskeletal outcomes (history of hip/knee replacement, osteoporosis, fall in previous year, low grip strength, low gait speed) in 2017 were examined using logistic regression with age and sex included as covariates. Results: Diet quality showed moderate stability over time (0.64 < r < 0.74). Three trajectory groups were identified: low (29%), medium (51%), and high diet quality (20%). A higher diet quality group was related to greater odds (95% CI) of hip/knee replacement (1.85 (1.05, 3.26) per higher category); associations with other musculoskeletal outcomes were weak (p > 0.17). Conclusions: Weak associations were observed between diet quality trajectories and musculoskeletal outcomes. However, higher diet quality was related to increased likelihood of hip/knee joint replacement, potentially due to confounding by socioeconomic position. The stability of diet quality suggests individuals with poorer diets around age 65 are likely to maintain these patterns into old age and may benefit from targeted interventions.

Background/Objectives: During oral and gut microbiota dysbiosis, lipopolysaccharides (LPSs) of major bacteria, such as Porphyromonas gingivalis and Escherichia coli, translocate into the bloodstream and lead to endotoxemia. Cerebral endothelial cells are targets of LPSs that may aggravate inflammation and cerebrovascular disorders. This study aimed to evaluate the protective role of the characterized polyphenol-rich extract of the Dodonaea viscosa medicinal plant and a predominant component, epicatechin, on murine bEnd.3 cerebral endothelial cells exposed to P. gingivalis or E. coli LPSs. Methods: The effects of LPSs and polyphenols were assessed on cell viability (MTT, trypan blue exclusion assays) and inflammatory, redox, vasoactive and permeability markers (RT-qPCR, Western blot, ELISA, FITC-Dextran test). Results: The data show that LPSs activated the TLR2-4/NFĸB signaling pathway and promoted IL-1β, IL-6, TNF-α, MCP-1, COX-2, iNOS, ICAM-1, VCAM-1 and E-selectin production without affecting cell viability. LPSs induced oxidative stress by elevating intracellular ROS levels and altering the expression of genes encoding NOX2-4, SOD, catalase, GPx, HO-1 and Nrf2. LPSs imbalanced NO vasodilator and ET-1 vasoconstrictor levels and reduced the production of occludin and ZO-1 tight junction proteins. Meanwhile, LPSs raised the permeability to FITC-Dextran, suggesting cell integrity loss. The extent of endothelial dysfunction caused by LPSs depended on their bacterial origin. Importantly, plant polyphenols and epicatechin exerted anti-inflammatory and antioxidant effects, and attenuated LPSs’ deleterious action on vasoactive and permeability markers. Conclusions: This study shows that polyphenols limit cerebral endothelial cell dysfunction under inflammatory conditions mediated by LPSs, highlighting their therapeutic potential in protecting brain homeostasis during oral and gut microbiota dysbiosis.

Background: Structured lipids, composed of re-esterified triacylglycerols containing eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and medium-chain fatty acids, may influence metabolism and endurance performance. This trial aimed to evaluate the effects of eight weeks of structured lipid supplementation on substrate utilization, erythrocyte fatty acid content, and endurance performance in healthy untrained men. Methods: In a double-blind, placebo-controlled, randomized design, 36 participants (18 per group) received either structured lipids or placebo supplementation for eight weeks. Pre- and post-supplementation assessments included maximal oxygen uptake, time to exhaustion, substrate oxidation during exercise at 65% VO_2max, and erythrocyte membrane fatty acid content. Non-parametric statistical methods were used to analyze within- and between-group differences. Results: After supplementation, the structured lipids group showed statistically significant within-group changes in substrate utilization, including lower respiratory exchange ratio and higher percentage fat oxidation, total fat oxidation, and mean fat oxidation rate. Statistically significant increases were also observed in erythrocyte EPA + DHA content and time to exhaustion. Compared with the placebo group, the structured lipids group showed statistically significant post-intervention differences in substrate oxidation, erythrocyte EPA + DHA levels, and time to exhaustion. Conclusions: Eight weeks of structured lipid supplementation increased erythrocyte membrane EPA and DHA and enhanced fat oxidation during moderate-intensity exercise in untrained men. Although endurance performance improved, the change was within natural variability and showed substantial interindividual differences. Further rigorously controlled studies are needed to determine whether these metabolic adaptations yield meaningful functional benefits.