Obesity and metabolic disorders remain major global health concerns, traditionally attributed to excessive caloric intake and poor diet quality. Recent studies emphasize that the timing of meals plays a crucial role in determining metabolic health. This review explores chrononutrition, a growing field that examines how food intake patterns interact with endogenous circadian rhythms to influence energy balance, glucose and lipid metabolism, and cardiometabolic risk. The circadian system, which includes a central clock in the suprachiasmatic nucleus and peripheral clocks in metabolic tissues, regulates physiological functions on a 24 h cycle. While light entrains the central clock, feeding schedules act as key synchronizers for peripheral clocks. Disrupting this alignment—common in modern lifestyles involving shift work or late-night eating—can impair hormonal rhythms, reduce insulin sensitivity, and promote adiposity. Evidence from clinical and preclinical studies suggests that early time-restricted eating, where food intake is confined to the morning or early afternoon, offers significant benefits for weight control, glycemic regulation, lipid profiles, and mitochondrial efficiency, even in the absence of caloric restriction. These effects are particularly relevant for populations vulnerable to circadian disruption, such as adolescents, older adults, and night-shift workers. In conclusion, aligning food intake with circadian biology represents a promising, low-cost, and modifiable strategy to improve metabolic outcomes. Integrating chrononutrition into clinical and public health strategies may enhance dietary adherence and treatment efficacy. Future large-scale studies are needed to define optimal eating windows, assess long-term sustainability, and establish population-specific chrononutritional guidelines.

Nutrition plays a central role in the biological mechanisms that shape aging, health span, and longevity. Micronutrients—including vitamins, trace el

Background: Obesity impairs renal function through direct mechanisms, such as proinflammatory adipocytokine production, and indirect mechanisms, including obesity-related comorbidities. Despite the increasing prevalence of obesity and chronic kidney disease (CKD), clinical guidelines for their combined management remain lacking. Very Low Energy Ketogenic Therapy (VLEKT) has demonstrated efficacy in weight loss, but evidence on its safety and efficacy in individuals with obesity and mild renal impairment is limited. This study aimed to assess the efficacy and safety of Phase 1 of VLEKT in individuals with obesity and mild renal impairment. Methods: This cross-sectional study included 73 individuals with overweight or obesity (mean age 53.7 ± 8.8 years; BMI 35.3 ± 4.2 kg/m²) and an estimated glomerular filtration rate (eGFR) of at least 60 mL/min/1.73 m² (evaluated using the CKD-EPI equation). Anthropometric (weight, BMI, and waist circumference) and biochemical parameters (fasting plasma glucose, insulin, cholesterol profile, triglycerides, AST, ALT, and urea) were collected at baseline and after 45 (±2) days of Phase 1 of VLEKT. Results: At baseline, 54.8% of participants had an eGFR <90 mL/min/1.73 m², while 45.2% had an eGFR ≥ 90 mL/min/1.73 m², with no significant differences in sex distribution. After 45 (±2) days of Phase 1 of VLEKT, both groups showed significant reductions in BMI (p < 0.001), waist circumference (p < 0.001), fasting plasma glucose (p ≤ 0.004), insulin (p < 0.001), HOMA-IR (p < 0.001), total cholesterol (p < 0.001), LDL cholesterol (p < 0.001), LDL/HDL ratio (p ≤ 0.002), triglycerides (p ≤ 0.009), AST (p ≤ 0.034), and ALT (p ≤ 0.009). Notably, the eGFR significantly increased in participants with an eGFR < 90 mL/min/1.73 m² (p < 0.001), while no changes were observed in those with an eGFR ≥ 90 mL/min/1.73 m². Conclusions: Phase 1 of VLEKT could effectively promote weight loss and metabolic improvements without compromising renal function, even in individuals with obesity and mild renal impairment. Further research is warranted to confirm the efficacy and safety of VLEKT and to assess outcomes across all protocol phases.

Several antioxidants play an important role in improving athletic performance. Increased inflammation and oxidative stress during physical performance result in the production of free radicals, including reactive oxygen species (ROS), which leads to fatigue, muscle damage, and impaired performance. However, moderate and transient increases in ROS are physiologically essential, acting as signaling mediators that trigger adaptive cellular responses. Despite their harmful effects on athletic performance, ROS may also enhance physical protection by acting as signaling molecules against increased physical stress. Healthy dietary patterns such as the Mediterranean diet (MD) may contribute to decrease oxidative stress thanks to its content in fruits, vegetables, olive oil, legumes, and herbs/spices. Indeed, the beneficial effects of the MD can be attributed not only to its antioxidant properties but also to its well-documented anti-inflammatory effects, lipid-modulating actions, immune-supportive functions, and modulation of gut microbiota composition, which collectively influence metabolic and physiological resilience. The MD also plays a key role in competitive sport and training. In addition, several researchers have reported that the MD is essential for reducing risk of injury and illness, recovering and adapting between bouts of activity, and enhancing performance. In this context, following the key principles of an MD could also represent a useful framework for good dietary in competitive athletes. In this narrative review, we discuss the potential effects of antioxidants in sport and the impact of individual foods or compounds of the MD on oxidative stress and exercise performance in competitive athletes and physically active individuals. The potential modifications which could be made to the MD will be highlighted to maximize health and performance effects, in accordance with contemporary sports nutrition practices.

This review explores the complex interplay between menopause, estrogen decline, lipid metabolism, and gut microbiota alterations. It highlights the physiological and metabolic changes that predispose postmenopausal women to dyslipidemia and increased cardiovascular disease risk, with particular emphasis on the emerging role of the gut microbiota in modulating lipid homeostasis and inflammatory pathways. In addition, it examines the therapeutic potential of microbiota-targeted nutritional strategies to restore metabolic balance and improve cardiometabolic outcomes in postmenopausal women. Recent clinical and experimental evidence indicates that menopause-related hormonal changes and aging are associated with gut microbiota dysbiosis, which may contribute to adverse lipid profiles through mechanisms involving bile acid metabolism, short-chain fatty acid production, and low-grade systemic inflammation. Associations between specific microbial taxa and lipid metabolic patterns have been reported; however, findings remain heterogeneous and causal relationships are difficult to establish due to confounding factors such as diet, lifestyle, and medication use. Nutritional interventions aimed at modulating the gut microbiota—including Mediterranean, plant-based, and DASH dietary patterns, increased dietary fiber intake, and supplementation with prebiotics, probiotics, polyphenols, phytoestrogens, and omega-3 fatty acids—have shown potential to improve lipid profiles and cardiometabolic risk markers. The gut microbiota emerges as a relevant contributor to menopause-associated dyslipidemia and cardiovascular risk. While microbiota-targeted nutritional strategies are promising, further longitudinal and interventional studies are needed to clarify causal pathways and identify clinically actionable microbial signatures. Integrating microbiome-informed nutritional approaches into clinical practice may represent a future strategy to improve cardiometabolic health in postmenopausal women.