Obesity, diabetes, and hypertension are major global health burdens influenced not only by lifestyle factors but also by genetic predisposition, sleep quality, chrononutrition, and circadian rhythms. This review examined how these factors interact in metabolic and cardiovascular diseases, with emphasis on sex-specific differences. A narrative review was conducted using PubMed, Scopus, and Web of Science databases for studies published between 2006 and 2026. A total of 112 studies were synthesized, including randomized trials, observational studies, systematic reviews, meta-analyses, Mendelian randomization, and mechanistic investigations. Evidence indicates that genetic susceptibility and circadian disruption contribute significantly to obesity, diabetes, and hypertension. Sleep deprivation, obstructive sleep apnea, and circadian misalignment were consistently associated with insulin resistance, appetite dysregulation, elevated blood pressure, and increased cardiometabolic risk, particularly among shift workers. Hormonal and metabolic pathways involving leptin, ghrelin, cortisol, and melatonin appear to mediate these effects. Important sex differences were observed, with women showing greater vulnerability to sleep-related appetite disturbances and men presenting a higher prevalence of visceral adiposity, sleep apnea, and hypertension. Chrononutrition strategies, including time-restricted eating and Mediterranean dietary patterns, showed beneficial effects on sleep quality, glycemic control, inflammation, and metabolic health. Emerging evidence also suggests bidirectional interactions between gut microbiota rhythmicity and circadian regulation. Genetic predisposition, sleep disturbances, and circadian disruption interact to influence metabolic and cardiovascular disease risk. Integrative approaches combining chrononutrition, sleep hygiene, circadian alignment, and personalized nutritional strategies may improve the prevention and management of cardiometabolic diseases.

The role of dietary protein quality, as defined by the Digestible Indispensable Amino Acid Score (DIAAS) and amino acid composition, in protein kinetics, muscle anabolism, and cardiometabolic health was reviewed, with emphasis on younger and older adults. Protein quality was formerly assessed by the Protein Digestibility-Corrected Amino Acid Score (PDCAAS); however, the DIAAS is more accurate because it accounts for the true ileal digestibility of indispensable amino acids (IAAs). On a gram-for-gram basis, excellent-quality proteins stimulate muscle mass and health outcomes, particularly in the context of age-related anabolic resistance and sarcopenia, but effects on cardiometabolic disease progression are less clear. Exploring the links between DIAAS, whole-body protein net balance (NB), muscle protein synthesis (MPS), and cardiometabolic outcomes could refine dietary strategies to mitigate muscle loss and disease risk. Literature databases were searched for studies on the DIAAS, protein metabolism, and cardiometabolic health. Excellent-quality proteins, compared with lower-quality proteins, improve digestibility and IAA bioavailability, and enhance NB, MPS, and muscle preservation in young and older adults. Some evidence suggests specific amino acid enrichments (eg, cysteine, glycine, arginine, glutamine, glutamate) may improve cardiometabolic health outcomes, whereas enrichments common in higher-quality proteins (eg, leucine, isoleucine, valine, lysine, methionine) may increase cardiometabolic disease risk. Strategically combining protein sources with specific amino acids to improve the DIAAS may also mitigate metabolic and cardiovascular disease risk. Future studies may evaluate DIAAS-driven anabolic and metabolic responses in splanchnic tissues. The DIAAS, as a direct and additive metric of IAA availability, may offer the most accurate assessment of protein-quality effects on anabolism. Considering food protein quality, combinations, and constituent amino acid influences on anabolic and cardiometabolic outcomes could enhance dietary guidelines and interventions.

The rapid clinical uptake of incretin-based antiobesity pharmacotherapies has reinforced appetite regulation as a core therapeutic target. However, real-world implementation is often constrained by cost, access, tolerability, and patient preferences, sustaining demand for complementary, lower-cost strategies that may support appetite control and adherence to lifestyle interventions. This review synthesizes mechanistic and clinical evidence on natural strategies intended to suppress appetite as adjuncts to obesity management, integrating homeostatic and hedonic appetite regulation with gut-brain signaling. A structured search of major biomedical databases from inception to June 2025 was conducted, and evidence was synthesized qualitatively by intervention type. Mechanistic and preclinical findings were used to contextualize human data. Across natural strategies, biologic plausibility is common, but the human evidence base remains fragmented and heterogeneous in intervention definition, outcome measurement, and follow-up duration. Reported effects are generally small to modest and short term, with inconsistent links to objective intake measures and durable clinical outcomes. Safety and tolerability profiles vary across approaches, and product or formulation variability, limited long-term data, and inconsistent quality reporting frequently constrain interpretation and generalizability. Overall, natural strategies for appetite suppression may be considered biologically plausible adjuncts, but current evidence supports cautious integration rather than stand-alone use. Future studies should prioritize standardized appetite measurement, objective intake assessments, longer follow-up, and rigorous reporting of safety, tolerability, and product quality to enable clinically actionable guidance.

Globally, there are differences in the way oats are regulated-particularly regarding the food labeling when oats are called gluten-free, with the potential to impact people who have celiac disease or related conditions. The potential cross-contact of oats with wheat, rye, and barley during processing is a concern for people with gluten-related disorders. This study examined selected international regulations governing gluten-free foods, the regulatory treatment of oats, and the requirements for declaring oats as an ingredient on gluten-free food labels. A comparative review of key regulatory frameworks was undertaken, including the World Health Organization and Food and Agriculture Organization-Codex Alimentarius Standard, and regulations from the United Kingdom (UK), the European Union (EU), the United States, Canada, and Australia and New Zealand (ANZ). All of the listed jurisdictions, with the exception of ANZ, define gluten-free foods as foods containing less than 20 mg gluten/kg food (20 ppm) (in the United States), or less than or equal to 20 ppm. In ANZ, a gluten-free food must not contain detectable gluten or oats, which prohibits oats from being labeled as gluten-free. The United States alone classifies oats as not containing gluten. The regulations of many countries are based on the premise that oats processed with minimizing of gluten cross-contact are safe for most individuals with celiac disease, but stipulate that oats are only permitted to be labeled gluten-free if they contain <20 ppm (in the United States) or ≤20 ppm gluten (in the remaining listed jurisdictions with the exception of ANZ). The current ANZ labeling regulations are not aligned with other international regulations, and emerging clinical evidence suggests it may be timely and impactful to re-evaluate the regulatory definitions of oats, such that individuals can safely identify products suitable for their medical requirements.

Ultra-processed foods (UPFs) now contribute a substantial share of total energy intake. A growing body of evidence has linked UPF consumption to adverse health outcomes, but existing umbrella reviews are mainly restricted to studies published before mid-2023 and have seldom rigorously examined the shape of dose-response relationships, evaluating both linearity and nonlinearity. The aim of this study was to synthesize updated meta-analytic evidence on associations between UPF consumption and major health outcomes in children and adults. A narrative umbrella review synthesized meta-analyses of studies published through December 9, 2025. Outcomes included obesity, type 2 diabetes (T2D), cardio-cerebrovascular diseases (CCVDs), nonalcoholic fatty liver disease (NAFLD), cognition, mental health (anxiety and depression), dental health, cancer, and all-cause mortality. For each outcome, a lead meta-analysis was selected by comprehensiveness, recency, and methodological quality (separately for children and adults when feasible). Methodological quality was assessed using a ROBIS (Risk of Bias Assessment Tool for Systematic Reviews)-adapted tool. Certainty of evidence was rated with GRADE (Grading of Recommendations, Assessment, Development and Evaluation). Twelve lead meta-analyses (mainly from observational studies) covering 13 outcomes were identified (4/13 in children). Across all but 1 outcome, higher (vs lower) UPF consumption was associated with increased risk (see graphical abstract). Dose-response evidence indicated a 10% higher risk per 10% increase in UPF intake for T2D, a curvilinear risk increase for CCVDs, and no significant association for NAFLD; for other outcomes, rigorous dose-response analyses were lacking. Certainty of evidence was high for 1 outcome, moderate for 6, and low for 6 other outcomes. This updated umbrella review confirmed harmful associations of UPFs with multiple health outcomes, and added insights on children's health, cognition, dental health, CCVDs, and dose-response. Despite remaining methodological gaps (including observational-based and nonrigorous dose-response analyses), current evidence supports population-wide strategies to reduce UPF intake. Systematic Review Registration: PROSPERO registration no. CRD420251230427.