Medicine and Pharmacology

Abstract: Obesity affects over 890 million adults and remains a major driver of non-communicable disease burden. The gut microbiome is increasingly recognised to influence energy harvest, immune regulation and host metabolism through altered microbial metabolites. Obesity-related gut dysbiosis signatures include reduced microbial diversity, depletion of beneficial taxa including the barrier-supporting Akkermansia muciniphila and the short-chain fatty acid (SCFA)-producing Faecalibacterium prausnitzii, inconsistent findings for the Firmicutes/Bacteroidetes ratio and species-level shifts reported in several cohorts including depletion of Alistipes finegoldii. Proposed mechanisms include enhanced energy harvest, SCFA-mediated regulation of adiposity and inflammation, bile acid signalling, gut-brain appetite signalling, intestinal barrier dysfunction and immune dysregulation. Early-life microbial perturbations may further shape long-term obesity risk through developmental programming. Maternal obesity, caesarean delivery, formula feeding and antibiotic exposure may seed obesogenic profiles, whereas breastfeeding is associated with enrichment of Bifidobacterium and SCFA-producing bacteria. Interventions such as dietary modulation, prebiotics, next-generation probiotics and bariatric surgery show therapeutic potential, although causality remains unproven in most human studies.Future research should prioritise phenotype-stratified randomised controlled trials, Mendelian randomisation studies and longitudinal cohorts to establish mechanistic links between gut microbiota and obesity. Overall, this review reframes obesity as a disorder of disrupted metabolic and immune signalling and positions the gut microbiome as a promising target for precision strategies aimed at restoring metabolic and immune homeostasis.

Abstract: Background/Objectives: Although the exact etiology of Inflammatory Bowel Diseases (IBD) is not yet fully understood, recent evidence suggests that both genetic and dietary factors are involved in their pathogenesis. The aim of the present exploratory study was to investigate how first-degree relatives (FDRs) of individuals with IBD perceive genetic risk and the role of diet in IBD prevention. Methods: A mixed methods approach was followed. A total of 103 unaffected FDRs of individuals living with IBD in Greece participated in an online questionnaire examining demographic characteristics, disease-related knowledge, risk perception, and beliefs about the role of diet in IBD onset and prevention. Through 16 semi-structured interviews, the beliefs of unaffected FDRs, their dietary practices and the factors affecting those practices for IBD prevention were investigated using Framework analysis guided by the Health Belief Model. Results: Quantitative findings showed that perceived importance of diet was the strongest predictor of dietary change, while genetic beliefs were associated with reduced preventive behaviors despite professional consultation. Qualitative findings provided a deeper understanding of participants’ beliefs, highlighting that diet was mainly viewed as relevant to IBD management rather than prevention. Fear of disease onset and healthcare professional guidance were perceived as key facilitators of dietary changes. Conclusions: Our findings highlight the need for individualized dietary counselling and improved risk communication, to enhance implementation of preventive dietary practices and bridge the gap between knowledge and behavior in IBD prevention.

Abstract: Background/Objectives: Coeliac disease (CD) is a chronic immune-mediated disorder triggered by gluten ingestion in genetically predisposed individuals with a higher prevalence among first-degree relatives. Despite its established hereditary risk, little is known about how parents with at least one child with CD perceive this risk in their unaffected children. This study examined parental perceptions and dietary practices regarding CD prevention in unaffected children. Methods: A cross-sectional mixed-methods study was conducted. The quantitative component consisted of an online questionnaire survey in parents in Greece. Quantitative data were analyzed using descriptive statistics and multivariable logistic regression analysis. The qualitative component included semi-structured interviews with parents of children with CD and unaffected children in Greece. Data were analyzed using framework analysis. Results: Although parents demonstrated high awareness of genetic risk, this was not translated into preventive dietary modifications. Belief in the role of diet as preventive CD strategy emerged as the only significant predictor of dietary change. Diet was widely recognised as important for overall health or as a therapeutic regimen for children living with CD; however, it was not perceived as a preventive strategy for CD. Reported family barriers to adopting a healthy diet included financial constraints and limited guidance, whereas advice from healthcare professionals emerged as a key facilitator of dietary change. Conclusions: Although parents recognize the genetic risk to CD, they rarely implement dietary changes as CD preventive behavior for their unaffected children. These findings underscore the need for clearer dietary guidance and targeted professional support for families with children with CD and unaffected siblings.

Abstract: Background/Objectives: Coeliac disease (CD) is a highly heritable autoimmune disease. Given the high risk among first-degree relatives, early screening and prevention are essential, yet clinical guidelines vary. This review analyzed clinical practice guidelines issued by leading European, British, and North American organisations over a 12-year period (2014–2026) regarding genetic screening and lifestyle/dietary prevention strategies. Methods: A systematic search was conducted across official databases of prominent societies (ESSCD, UEG, ESPEN, NASPGHAN, AGA, ESPGHAN, WGO, BSG, ACG) for English-language guidelines and position papers. Extracted statements addressing genetic testing (HLA-DQ2/DQ8) and early-life risk-modifying strategies were coded into three thematic domains: 1) genetic predisposition, 2) lifestyle prevention or 3) both. Results: Eleven manuscripts yielded 399 statements, categorized into genetic predisposition (n=23, 5.8%), lifestyle prevention (n=30, 7.5%) and integrated approaches (n=2, 0.5%), with the remainder (n=344, 86.2%) addressing unrelated clinical topics. Universal consensus confirmed the high negative predictive value of HLA-DQ2/DQ8 testing to rule out CD, whereas dietary strategies (breastfeeding duration and timing of gluten introduction) showed no protective effect. ESPGHAN exclusively provided evidence regarding early-life high-risk genotypes and concluded that risk-stratified dietary guidance based on specific HLA profiles remains currently unsupported. Conclusions: Current CD guidelines demonstrate substantial international consensus regarding the role of genetic testing in disease exclusion and risk stratification. However, recommendations integrating genetic susceptibility with preventive lifestyle interventions remain scarce. Future research should focus on generating robust evidence to support precision prevention approaches and facilitate the harmonization of international guidelines.

Abstract: Background: Given the rising global prevalence of dementia and its complex etiology, involving genetic and environmental risk factors, the aim of the present exploratory study was to investigate how offspring of individuals with dementia perceive genetic risk and the role of diet in dementia prevention. Methods: A mixed-methods study was conducted in Greece. Overall, 118 offspring completed an online questionnaire as-sessing demographics, risk perceptions, and dietary beliefs and practices in dementia prevention. Additionally, 22 semi-structured interviews explored dietary beliefs, prac-tices, and influencing factors using framework analysis. Results: Most participants (76.3%), widely recognized diet's role in dementia prevention, while 52.5% perceived offspring as having increased genetic risk. 40.7% reported making dietary changes to reduce disease risk, with healthcare professional consultation being the strongest pre-dictor of dietary modifications (OR = 26.612, p < 0.001). Qualitative findings showed that while dementia was viewed as severe, personal susceptibility was often perceived as uncertain or distant. Key barriers, facilitators, and the role of self-efficacy in adopt-ing healthier dietary practices were also explored. Conclusions: Our findings highlight the importance of personalized dietary counselling and risk communication in demen-tia, to support the implementation of dietary modifications and reduce the gap be-tween knowledge and behavior in dementia prevention.

Abstract: Background/Objectives: Enteral nutrition (EN), delivered either exclusively (EEN) or partially (PEN) in combination with the Crohn’s Disease Exclusion Diet (CDED), represents an evidence-based dietary therapy for active Crohn’s Disease (CD), recommended in clinical guidelines. However, adherence to this therapy remains suboptimal among adult patients. This study aimed to explore the intention to repeat CDED & PEN alongside perceived factors affecting adherence to CDED & PEN in CD adult patients. Methods: A cross-sectional qualitative study was conducted. Semi-structured interviews were undertaken and analysed using thematic analysis. Results: Out of the 88 patients screened, 15 adults with CD participated in semi-structured interviews. Four overarching themes emerged: (1) intention to repeat PEN & CDED, with all participants reporting willingness to repeat CDED & PEN in the event of future relapse; (2) barriers to CDED & PEN adherence, including challenges in social situations involving food; (3) facilitators of CDED & PEN adherence, such as improved symptom control and increased sense of security; and (4) dual factors affecting CDED & PEN adherence, whereby meal preparation demands, taste and variety, and social and environmental support acted as either facilitators or barriers against adherence depending on individual circumstances. Conclusions: Greek adults with CD showed strong willingness to reinitiate CDED and PEN during relapse. Addressing modifiable barriers, particularly dietary monotony and financial burden, alongside strengthening structured dietitian support and personalized dietary guidance, may help optimize adherence in clinical practice.

Abstract: Background: Repeated endurance exercise induces transient inflammatory, oxidative and metabolic responses that drive skeletal muscle adaptation. This study investigated whether the consumption of San Carlo 1931® water, a mineral water with a human-like electrolyte profile, modulates these responses in a murine model of repeated swimming exercise. Methods: Male C57BL/6 mice underwent swimming exercise (10 min/day) for 2, 3 or 4 weeks while receiving either San Carlo 1931® water or control water. Grip strength, inflammatory cytokines (IL-6 and TNF), oxidative stress markers (MDA, GPx, and CAT), lactate metabolism (lactate, LDH, and monocarboxylate transporters), citrate synthase activity and the expression of PGC-1α, FNDC5, MuRF1 and myostatin were evaluated. Results: San Carlo 1931® water prevented the early decline in grip strength, attenuated the early exercise-induced inflammatory response, reduced circulating lactate and hepatic LDH activity, enhanced citrate synthase activity and progressively decreased MCT4 expression, indicating improved oxidative metabolism. No significant changes were observed in MCT1 protein expression. These adaptations were accompanied with unchanged PGC-1α expression, early FNDC5 induction and a time-dependent regulation of muscle remodeling markers, with transient progressive MuRF1 upregulation and myostatin induction. Conclusions: The consumption of San Carlo 1931® water modulate inflammatory and metabolic responses to repeated endurance exercise, suggesting a potential role in supporting physiological adaptation to exercise-induced stress.

Abstract: Background: Acute brain injury, including traumatic brain injury (TBI), stroke and subarachnoid hemorrhage, and secondary neurological injury such as sepsis-associated encephalopathy (SAE) and delirium, is a major cause of morbidity in the intensive care unit (ICU), and few treatments alter its course once it is established. Critical illness, and brain injury in particular, rapidly disrupts the gut microbiota (GM) and the production of its metabolites. This dysbiosis matters most in neurologically injured patients, because microbial metabolites and a leaky intestinal barrier feed neuroinflammation through the gut-brain axis. Feeding timing and fasting affect circadian biology, the daily rhythm of the GM, and host metabolic pathways such as ketogenesis, insulin signaling and autophagy, which is why time-restricted or fasting-mimicking strategies might preserve these functions and reduce neuroimmune dysregulation after brain injury. Methods: We searched the literature for randomized trials, crossover pilot studies, mechanistic human research, and guideline statements comparing continuous, cyclic, and intermittent enteral strategies, and evaluated translational pathways for GM‑targeted feeding interventions. Results: Available studies showed no consistent difference in mortality between continuous and intermittent gastric feeding in ICU adults on mechanical ventilation. While intermittent/cyclic regimens were not associated with an improvement of patient-centred outcomes, pilot studies demonstrated that short macronutrient interruptions (e.g., 12 hours) reliably induced a metabolic fasting response in prolonged ICU length of stay. One RCT had GM end-points and reported feasible modulation of gut taxa and 58 differentially abundant serum metabolites with sequential feeding. Notably, none of these trials were performed specifically in brain-injured patients, and GM and neuroinflammatory outcomes remain largely unmeasured. Conclusions: Time-restricted, microbiome-protecting approaches are biologically plausible and deserve a phased translational program to test them in clinical trials. Future trials should focus on brain-injured and other neurologically relevant ICU patients, in whom the gut-brain axis is most engaged, and should pair mechanistic endpoints with clinical safety and proper control for confounders.

Abstract: Background: Type 2 diabetes mellitus (T2D) is one of the fastest-growing chronic diseases worldwide, affecting an estimated 589 million adults in 2024, with projections rising to 853 million by 2050. Dietary modification is a cornerstone of both T2D prevention and management. Among the various dietary approaches, plant-based dietary patterns have gained increasing attention; however, uncertainty remains regarding the optimal dietary composition and the contribution of specific food groups. Methods: This narrative review summarizes the current evidence on plant-based dietary patterns and their association with T2D prevention and metabolic control, with a particular focus on legumes, dietary fiber, and red and processed meat. Evidence from prospective cohort studies, randomized controlled trials, and meta-analyses were evaluated. Results: Higher adherence to healthy plant-based dietary patterns was consistently associated with a 23-33% lower risk of developing T2D, improved insulin sensitivity, and approximately a 0.30- 0.47% reduction in glycated hemoglobin (HbA_1c). Greater consumption of legumes and dietary fiber was linked to improved glycemic control, enhanced gut microbiota composition, reduced low-grade inflammation, and beneficial effects on body weight and lipid metabolism. In contrast, higher intake of processed meat and unprocessed red meat was consistently associated with an increased risk of T2D. Importantly, unhealthy plant-based diets characterized by refined grains, sugar-sweetened beverages, and highly processed foods provided little metabolic benefit and may even increase diabetes risk by up to 10%. The interpretation of the available evidence is limited by the predominance of observational studies, heterogeneous definitions of plant-based dietary patterns, self-reported dietary assessments, and the limited availability of long-term randomized controlled trials. Conclusions: Current evidence supports healthy plant-based dietary patterns as an effective strategy for the prevention and management of T2D. Dietary patterns emphasizing whole plant foods, including legumes, whole grains, fruits, vegetables, nuts, and seeds, while limiting processed and excessive red meat intake, are associated with improved metabolic health. Future high-quality randomized controlled trials with standardized dietary definitions are needed to further define the optimal composition of plant-based diets for diabetes prevention and treatment.

Abstract: Integrating botanical extracts rich in bioactive compounds, such as bilberry (Vaccinium myrtillus L.) and blackcurrant (Ribes nigrum), may represent an adjunctive nutritional strategy to support the management of chronic low-grade inflammation and, more cautiously, oncology supportive care. Both species contain high levels of anthocyanins and other flavonoids, which are associated with anti-inflammatory effects through modulation of redox-sensitive and inflammatory signaling pathways, reduction of selected pro-inflammatory mediators, and potential contributions to intestinal eubiosis. A growing body of evidence also suggests that anthocyanins can influence host physiology indirectly via gut microbiota-mediated biotransformation and the generation of phenolic metabolites and short-chain fatty acids (SCFAs), which may impact barrier integrity, immune regulation and systemic inflammatory tone. Preclinical studies report antineoplastic mechanisms—such as modulation of proliferation, apoptosis and angiogenesis—however, these findings are largely derived from in vitro and animal models and should be considered hypothesis-generating. Importantly, the use of standardized anthocyanin-rich dry extracts should not be interpreted as an alternative to standard antineoplastic therapies. When clinically used, standardized dry fruit extracts should be framed as nutraceutical/food-based interventions within an overall nutritional plan, with attention to product standardization, dosing, and potential interaction pathways. Overall, bilberry and blackcurrant represent promising candidates in the context of nutritional modulation of inflammation, oxidative stress and gut microbiota. Robust, long-term trials are still needed to clarify efficacy on patient-relevant clinical endpoints and safety during concomitant anticancer therapies.

Abstract: Fibromyalgia and chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) are chronic, multisystem disorders characterized by persistent fatigue, musculoskeletal pain, cognitive dysfunction, sleep disturbances, and markedly reduced quality of life. Fatigue is one of the most disabling symptoms and remains insufficiently addressed by current therapeutic approaches. Increasing evidence implicates mitochondrial dysfunction, oxi-dative and nitrosative stress, immune dysregulation, and impaired nicotinamide adenine dinucleotide (NAD⁺) metabolism as central mechanisms underlying fatigue in these conditions. Micronutrients constitute essential cofactors of mitochondrial bioenergetics, redox homeostasis, and immune metabolism. This narrative review synthesizes current evidence on mitochondrial dysfunction in fibromyalgia and CFS/ME and examines the mechanistic and clinical rationale for targeted micronutritional interventions aimed at restoring redox balance, mitochondrial efficiency, and Adenosine triphosphate (ATP) production. Particular attention is given to strategies targeting glutathione repletion, NAD⁺ metabolism, and electron transport chain function. Finally, we present a proposal for a randomized placebo-controlled clinical trial in fibromyalgia patients with severe fatigue (PROMIS Fatigue T-score > 60), designed to evaluate a mitochondrial-oriented micronutritional formulation as an adjunctive therapeutic approach.

Abstract: Background/Objectives: Meal sequence (MS) has been proven to suppress the postprandial blood glucose variability, potentially preventing the onset of diabetes and its complications. However, existing evidence in healthy individuals has not been conclusive because it solely focuses on single-meal postprandial glucose, overlooking the potential influence of preceding meals. Methods: A 24-day randomized, single-blinded crossover study investigated the MS effect in real-life settings. Among 12 participants, 8 (66.7%) were female, with 158/342 (46.2%) observations available for analysis. Results: In per-protocol (PP) analysis, the effect of MS on incremental glucose peak (IGP) was -11.47 (95% confidence interval [CI] -38.04 to 15.09, p-value = 0.395) mg/dL. After adjusting for confounders in model 2 and model 3, the effect of MS on IGP was -12.24 (95% CI -37.09 to 12.61) and -11.25 (95% CI -40.63 to 20.13), respectively. In intention-to-treat analysis (ITT), the effect of MS on IGP was -12.09 (95% CI -38.82 to 14.65, p-value = 0.373) mg/dL. After adjusting for confounders in model 2 and model 3, the effect of MS on IGP was -12.75 (95% CI -37.62 to 12.12) and -14.31 (95% CI -47.14 to 18.53), respectively. Conclusions: This result contradicts previous studies conducted in diabetes patients under free-living conditions and in both healthy individuals and diabetes participants in experimental settings. Discrepancies may be due to different instruction designs, low MS adherence, and irregular meal timing in healthy participants under the free-living conditions of our study. This study reported no evidence of MS effect on the IGP in young, healthy individuals in a real-life time setting. The improved meal quality was seen while following MS by increasing fiber intake and prolonging meal duration. Further studies should aim to stabilize meal timing and strictly instruct the MS implementation.

Abstract: Moringa stenopetala is a nutritionally rich medicinal plant widely used in traditional medicine for managing metabolic, infectious, inflammatory, and chronic diseases. Despite its extensive ethnomedicinal use, its pharmacological effects and safety profile are reported variably across experimental and regulatory studies. To summarize the pharmacological activities, safety profile, and experimental evidence of Moringa stenopetala based on in vitro and in vivo studies. A narrative synthesis of published experimental studies, including in vitro assays, in vivo animal models, toxicity studies, and chemical analyses, was performed. Studies evaluating metabolic, antimicrobial, cardiovascular, neurological, anticancer, reproductive, and toxicological outcomes were included. The findings were synthesized qualitatively. This review demonstrated that Moringa stenopetala possesses broad pharmacological activities in both in vitro and in vivo models. Leaf extracts at 250–500 mg/kg for 14–28 days significantly reduced blood glucose, improved lipid profiles, and restored pancreatic β-cells in diabetic animals. Antioxidant studies showed strong radical-scavenging activity and increased levels of endogenous antioxidant enzymes. Antimicrobial investigations demonstrated potent antibacterial and antifungal effects, with MIC values as low as 0.31 mg/mL. Antiparasitic studies using 400 mg/kg for 7 days reduced parasitemia and improved survival in infected mice. Cardiovascular studies using 10–1000 mg/kg extracts showed antihypertensive, vasorelaxant, diuretic, and natriuretic effects. Additional studies reported analgesic, anti-inflammatory, anticonvulsant, neuroprotective, antidiarrheal, and anticancer activities. Toxicological evaluations showed favorable safety profiles, with LD50 values >5000 mg/kg and minimal organ toxicity. Moringa stenopetala possesses broad pharmacological potential supported mainly by preclinical evidence. However, toxicity studies indicate possible dose-dependent safety concerns, particularly at high exposure levels. The absence of human clinical confirmation highlights the need for further translational and clinical research.

Abstract: Epidemiological and clinical evidence indicates that obesity-associated metabolic dysfunction increases the risk of depression, which is often resistant to conventional antidepressant therapies. Elucidating targeted mechanisms underlying obesity-induced depression is therefore essential for developing effective interventions. Accumulating evidence identifies neuroinflammation as a central link between obesity and depressive disorders. Obesity-driven inflammatory signaling disrupts multiple neurobiological processes implicated in depression, thereby contributing to the onset and progression of inflammatory depression. Polyphenols, a diverse class of plant-derived secondary metabolites, have demonstrated neuroprotective properties, largely attributed to their anti-neuroinflammatory effects. By modulating inflammatory pathways and restoring neurobiological homeostasis, polyphenols may represent a promising therapeutic strategy for obesity-related depression. This review summarizes the pathophysiological mechanisms through which obesity induces neuroinflammation and subsequently promotes depressive symptoms. It further evaluates current evidence regarding the efficacy and effective dosing of polyphenols in attenuating inflammatory signaling and alleviating obesity-associated inflammatory depression. Given their anti-neuroinflammatory potential, polyphenols may serve as a valuable adjunctive approach for the management of obesity-induced depression.

Abstract: Creatine monohydrate is among the most evidence-supported ergogenic aids in adults, but its use by adolescent athletes remains controversial because age-specific trials are sparse. This critical narrative review evaluated performance effects, safety, and conditions for responsible use in adolescent athletes. PubMed/MEDLINE, Google Scholar, Semantic Scholar, the Cochrane Library, and ClinicalTrials.gov were searched from 1992 through 19 June 2026, with reference-list screening. Direct sport-specific evidence remains limited, heterogeneous, short term, and predominantly male. Trials in soccer, swimming, basketball, weightlifting, and rehabilitation suggest possible improvements in power, repeated-sprint performance, jumping, selected technical outcomes, and recovery-related measures; however, small samples and narrow endpoints preclude conclusions about overall competitive performance. A 32-week uncontrolled cohort in female football players found no clinically meaningful biochemical safety signal, whereas a single high-dose loading case reported acute kidney injury; neither design can estimate causal risk. Controlled studies have not shown consistent clinically important adverse effects at studied doses, yet long-term safety, sex- and maturation-specific responses, and uncommon events remain insufficiently characterized. Creatine should therefore be neither routinely recommended nor categorically prohibited. Consideration should be restricted to mature, trained adolescents after dietary, medical, psychosocial, and product-quality assessment, family involvement, qualified supervision, conservative dosing, and planned follow-up.

Abstract: Post-exertional malaise (PEM) and cognitive dysfunction (“brain fog”) are among the most disabling features of Long COVID, yet approved disease-modifying treatments remain lacking. Emerging evidence implicates interacting disturbances in mitochondrial bioenergetics, redox regulation and neurovascular inflammation, although much of the supporting data derive from acute COVID-19, myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), mitochondrial disease and mechanistic pharmacology rather than from direct Long COVID studies. This narrative review develops a mechanism-based translational hypothesis: that a pathway-targeted nutraceutical combination may modulate these three axes more effectively than single-agent antioxidant approaches. Candidate modules comprise coenzyme Q10 and alpha-lipoic acid for bioenergetic support; selenium, sulforaphane and resveratrol for Nrf2–thioredoxin redox regulation; and Boswellia serrata, luteolin and eicosapentaenoic acid for prostaglandin and resolution-pathway modulation. The mitochondrial redox modulator sonlicromanol provides pharmacological precedent for combined antioxidant and prostaglandin-directed mechanisms, although the proposed nutraceutical strategy remains clinically untested. We summarise the mechanistic rationale, critically appraise direct versus indirect clinical evidence with explicit certainty grading, outline safety and interaction considerations, and propose a stratified randomised trial framework. This model reframes nutraceuticals as pathway-specific candidate interventions and provides a falsifiable basis for future Long COVID trials.

Abstract: Vascular aging is driven by a self-sustaining interplay between oxidative stress and chronic low-grade inflammation, collectively referred to as inflammaging. Diosmin, a cit-rus-derived flavonoid with antioxidant and anti-inflammatory properties, has not previ-ously been investigated in this context. Young (10-week-old) and aged (40-week-old) male Sprague–Dawley rats received diosmin (50 mg/kg/day) or vehicle for 3 months. Vascular function was assessed in mesenteric resistance arteries using pressure myography, while oxidative stress was evaluated by dihydroethidium and mitoSOX staining. Circulating malondialdehyde (MDA), tumor necrosis factor (TNF) and lipopolysaccharide-binding protein (LBP) were measured and vascular expression of Enos, Gpx, Sod2 and Xdh was an-alyzed. Aging was associated with impaired endothelium-dependent vasorelaxation, increased vascular ROS production and elevated circulating MDA and LBP levels. Chronic diosmin supplementation partially restored endothelial function and significantly reduced both NADPH oxidase–derived and mitochondrial ROS in aged vessels. These effects were ac-companied by decreased plasma MDA and LBP levels, while TNF remained unchanged. Diosmin did not significantly affect Enos, Gpx, or Sod2 gene’s expression, but attenuated the age-related upregulation of Xdh. Overall, diosmin mitigates vascular inflammaging by reducing ROS burden and improving nitric oxide bioavailability, highlighting its potential to counteract age-related vascular dysfunction through modulation of redox–inflammatory crosstalk.

Abstract: Background/Objectives: This study examined whether adding 10 g of protein to a high glycaemic index (GI) breakfast could attenuate postprandial glycaemic responses in children and young people (CYP) with type 1 diabetes (T1D). Postprandial glucose responses following this modified breakfast were compared with those after a high GI breakfast alone, a low GI breakfast, and participants’ usual breakfast. Methods: A pragmatic randomised crossover study was conducted in n=25 CYP aged 5–17 years. Participants consumed three standardised test breakfasts on two study occasions and their usual breakfast as a control. Test meals varied by GI, glycaemic load (GL), and protein content: high GI/high GL (HGL), high GI/high GL with an additional 10 g protein (HGLP), and low GI/medium GL (MGL). Continuous glucose monitoring data were collected for three hours following each meal. Linear mixed model analyses were used, and a subgroup analysis included participants using hybrid closed-loop (HCL) systems. Results: Participants (mean age 12.1 ± 3.6 years) mean postprandial glucose over three hour follow-up was significantly lower following the HGLP meal compared with the HGL meal (8.0 ± 2.2 vs 9.5 ± 2.5 mmol/L; p < 0.01). Time in Range (TIR) over 180 minutes was significantly shorter after the HGL meal compared with the control, HGLP, and MGL meals (p ≤ 0.03). Glucose excursions at 30 and 60 minutes were significantly higher following the HGL meal compared with all other meals, with differences persisting up to 120 minutes when compared with the HGLP meal. Results were not different for participants using HCL systems. Conclusions: Adding 10 g of protein to a high GI breakfast or choosing a lower GI option improves postprandial glycaemic control in CYP with type 1 diabetes.

Abstract: The development of functional staple foods with improved metabolic properties represents a practical dietary strategy for the prevention of type 2 diabetes. This study investigated the effects of incorporating sprouted fenugreek (Trigonella foenum-graecum L.) into wheat-based flatbread (chapatti) on postprandial glycemic and insulinemic responses in healthy adults. Wheat (cv. Galaxy 2013) and fenugreek seeds were germinated for up to 96 h and analyzed for nutritional composition and antioxidant activity. Composite flours containing 0%, 2.5%, 5%, and 7.5% sprouted fenugreek were formulated and evaluated for sensory acceptability. Eighteen healthy participants (18–25 years; BMI 21–22.5 kg/m²) consumed chapattis containing 7.5% sprouted fenugreek or control white flour in a ran-domized crossover design. Blood glucose and serum insulin were measured at 0, 30, 60, and 120 min postprandially. Sprouting significantly increased protein, dietary fiber, and antioxidant capacity in both wheat and fenugreek (p < 0.001). Total phenolic content in wheat increased from 55.82 to 110.17 mg GAE/100 g after 96 h of germination, accompa-nied by a significant rise in DPPH radical scavenging activity. The formulation containing 7.5% sprouted fenugreek showed the highest sensory acceptability (7.52/9). Fenu-greek-supplemented chapattis significantly reduced postprandial glucose and insulin re-sponses (p < 0.05) compared with control. Incorporation of 7.5% sprouted fenugreek into wheat flatbread improves nutritional quality while attenuating glycemic and insulinemic responses, suggesting a practical dietary strategy for metabolic health and diabetes pre-vention.

Abstract: Background: Marathon running triggers a robust systemic inflammatory response. Whether habitual dietary fat composition modulates pre-race cytokine concentrations or the magnitude and recovery of the exercise-induced inflammatory response remains unknown. Methods: Thirty-one recreational marathon runners (58.1% female; mean age 38.4 ± 10.2 years) completed the Diet History Questionnaire III to assess habitual dietary fat intake— including chain-length-specific SFA, MFA, PFA, trans fatty acids, and CLA — over the preceding three months. Circulating IFN-γ, IL-1β, IL-4, IL-6, IL-10, and TNF-α were measured pre-race, immediately post-race, and 48 hours post-race. Repeated-measures ANOVA examined cytokine changes; multivariable regression models estimated fat–cytokine associations adjusted for 11 pre-specified covariates, with Benjamini-Hochberg FDR correction applied across all models. Results: IL-6 rose markedly post-race (p < 0.001, generalized η² = 0.615) before returning to pre-race levels by 48 hours. IL-10 followed a similar trajectory (p < 0.001, generalized η² = 0.346). TNF-α showed a borderline non-significant trend (p = 0.056); IFN-γ, IL-1β, and IL-4 did not change significantly. MFA 20:1 was positively associated with IFN-γ concentrations at 48-hour post-race (β = 13.66; 95% CI: 8.94, 18.38, p<0.01, q=0.04) and TNF- α (β = 9.14; 95% CI: 6.43, 11.86, p<0.01, q=0.02). Conclusion: Habitual intake of the long-chain monounsaturated fatty acid 20:1 appear to be positively associated with IFN-γ and TNF-α at 48-hour post-race, suggesting it may slow resolution of exercise-induced inflammation. This pattern, emerging specifically during the recovery phase, suggests habitual fat quality may warrant consideration in future endurance-recovery nutrition research. This exploratory finding calls for replication in larger cohorts.