Insulin resistance (IR) is traditionally viewed within the context of type 2 diabetes. However, it increasingly appears to represent a broader systemic metabolic risk state with potential relevance for carcinogenesis. Chronic hyperinsulinemia can activate insulin-like growth factor-1-dependent pathways, including phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin and mitogen-activated protein kinase signaling, promoting cellular proliferation while limiting apoptosis. At the same time, IR is closely linked to oxidative stress, chronic low-grade inflammation, and epigenetic alterations, together shaping a tumor-promoting microenvironment. Epidemiological studies report consistent associations between IR and increased cancer risk, particularly for endometrial, liver, and colorectal cancers. Yet causality remains uncertain and likely varies by tumor type. Notably, metabolic dysfunction may also occur in individuals with normal body mass index (BMI), underscoring the limitations of BMI-based risk assessment. Unlike previous reviews that primarily focused on individual mechanisms or epidemiological associations, this review examines IR as a systemic metabolic risk state by integrating molecular, epidemiological, biomarker-based, and prevention-oriented perspectives. Particular emphasis is placed on strategies for earlier risk identification using integrated biomarker approaches, including fasting glucose, homeostatic model assessment of insulin resistance, triglyceride-to-high-density lipoprotein ratio, high-sensitivity C-reactive protein, and insulin-like growth factor-1. Emerging tools such as continuous glucose monitoring and hepatokine profiling may further refine risk detection. Sustained lifestyle modification—diet, physical activity, sleep, and stress regulation—remains central to prevention. Pharmacological therapies, including glucagon-like peptide-1 receptor agonists and dual incretin agents, offer additional metabolic benefits, although their long-term impact on cancer risk is still unclear. Therefore, IR is best understood not as an isolated risk factor, but as a systemic metabolic risk state that may influence cancer development, with implications for prevention and early risk stratification.

Glucagon-like peptide-1 (GLP-1) receptor agonists and dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 receptor agonists have transformed obesity management by producing substantial, sustained weight loss and improving metabolic health. Alongside these benefits, their effects on appetite, food intake, and gastrointestinal function have raised increasing interest in the nutritional consequences of pharmacologically induced weight loss. Although reductions in energy intake contribute to therapeutic efficacy, they may also influence protein intake, dietary quality, micronutrient adequacy, and skeletal muscle health, particularly in individuals with pre-existing nutritional vulnerability. This narrative review summarizes current evidence regarding nutritional considerations during GLP-1-based therapy, including changes in dietary intake, protein and micronutrient adequacy, body composition, muscle health, and nutritional assessment. Particular attention is given to populations at increased nutritional risk, practical approaches to nutritional monitoring, and strategies to support adequate nutrition during treatment. Current evidence suggests that nutritional responses to GLP-1-based therapy are heterogeneous and cannot be adequately evaluated using body weight alone. Assessment of dietary intake, body composition, muscle function, physical performance, and individual clinical characteristics provides a more comprehensive understanding of nutritional status than anthropometric measures alone. While routine supplementation or intensive monitoring is not supported for all patients, a risk-based and individualized approach appears appropriate, particularly for older adults and individuals with sarcopenic obesity, previous bariatric surgery, chronic gastrointestinal disease, or persistent treatment-related gastrointestinal symptoms. Future research should establish clinically meaningful nutritional outcomes and determine which nutritional interventions improve patient-centered outcomes during long-term obesity management.

Sleep and nutrition are closely interconnected through behavioral, metabolic, and circadian pathways, yet the strength of evidence varies considerably across dietary exposures. This narrative review synthesizes current evidence on nutrients, foods, dietary patterns, chrononutrition, caffeine and alcohol in relation to sleep, while also considering the effects of insufficient sleep on dietary intake and metabolic health. The relevant literature was identified through searches of PubMed/MEDLINE, Scopus, and Web of Science, supplemented by examination of reference lists and targeted searches. Higher-quality dietary patterns, particularly Mediterranean-style diets, are generally associated with more favorable sleep characteristics, although predominantly observational evidence limits causal interpretation. Intervention studies of individual foods and supplements have reported benefits for selected sleep outcomes, but findings remain heterogeneous and are often based on small samples. Evidence for meal timing and time-restricted eating is similarly inconsistent and does not support a single eating schedule for improving sleep. In contrast, caffeine and alcohol have relatively well-established sleep-disrupting effects. Insufficient sleep can also alter dietary intake, energy balance, glucose regulation, and adiposity, highlighting the bidirectional nature of these relationships. Nutritional approaches may complement broader strategies for sleep and health, but current evidence does not support specific foods, supplements, or eating schedules as stand-alone treatments for sleep problems.