Obstructive sleep apnea (OSA), obesity, and cancer constitute an interconnected pathophysiological triad withi mportant implications for morbidity and mortality. Obesity is a major upstream driver of both OSA and tumorigenesis, while OSA contributes independently through intermittent hypoxia, sleep fragmentation, systemici nflammation, oxidative stress, immune dysregulation, and sympathetic activation. Emerging evidence links OSA-associated hypoxemia to cancer initiation, progression, and treatment response, with hypoxic burden and nocturnal oxygen desaturation metrics outperforming the apnea-hypopnea index in predicting cancer-related outcomes. Mechanistic advances implicate immune checkpoint signaling, extracellular matrix remodeling, and metabolic-hepatic pathways as key mediators of OSA-related oncogenesis. Epidemiological studies support associations between OSA and several malignancies independent of obesity, although residual confounding remains a challenge. Therapeutically, continuous positive airway pressure may mitigate hypoxemia-related pathways, whereas bariatric surgery and GLP-1/GIP receptor agonists off er the potential to simultaneously reduce obesity, OSA severity, and cancer risk. Precision medicine approaches integrating hypoxemia phenotyping, immune profi ling, and targeted interventions are needed to optimize prevention and treatment strategies.

Obesity has become a global public health crisis in recent years, with its continuous rise posing significant health risks. It is associated with a range of chronic diseases, including cardiovascular disease, type 2 diabetes, and certain types of cancer. Additionally, obesity leads to poor health outcomes and reduces life expectancy. The lymphatic system, a critical part of the circulatory system, has traditionally been recognized for its primary functions in immune surveillance and maintaining tissue fluid balance. Lymphatics also play a more complex role in lipid metabolism, immune regulation, and inflammation control, which significantly influences metabolic health. Despite these insights, the specific mechanisms of interaction between lymphatic dysfunction and obesity, as well as the directionality of causality, are not yet fully understood. This review aims to systematically synthesize and evaluate existing evidence regarding the interrelationship between lymphatic dysfunction and obesity. Its goal is to provide novel perspectives for developing innovative preventative and therapeutic strategies targeting lymphatic function in obesity.

The rising prevalence of childhood obesity is closely linked to the early onset of comorbid conditions, notably metabolic dysfunction-associated steatotic liver disease (MASLD), a hepatic manifestation of metabolic syndrome characterized by hepatic steatosis in the absence of significant alcohol intake. The pathophysiology of MASLD includes complex interactions among various factors such as hormonal, genetic, lifestyle and nutritional, and environmental dynamics. Emerging evidence indicates that MASLD is independently associated with a higher risk of cardiovascular disease (CVD), irrespective of traditional CV-risk factors such as hypertension, dyslipidemia, and diabetes mellitus. A comprehensive, multipronged approach is central to the detection, monitoring, and management of MASLD and associated adverse cardiovascular outcomes in children. Currently, there are no approved medications or other specific therapies for pediatric MASLD. While early stages of the disease are potentially reversible through lifestyle modifications, including diet/nutrition and physical activity, these strategies are often difficult to implement and sustain over time. Early detection of progression of MASLD to more severe conditions is hampered by the lack of reliable noninvasive methods of risk assessment tools. The objective of this review is to (1) succinctly summarize the relationship between MASLD and CVD risk in children and (2) discuss advances in MASLD management and treatment in children. We believe that this article will stimulate new avenues for research into MASLD and its broader cardiometabolic implications in pediatric populations.