Obesity and Cancer: Excess Body Fat as a Risk Factor in Carcinogenesis; Consequences Across Human Body Systems and Significance for Associated Medical Specialties

Obesity is a known risk factor for various cancers, influencing carcinogenesis through metabolic, hormonal, and inflammatory pathways. Excess adiposity leads to insulin resistance, chronic inflammation, and hormonal imbalances, all of which contribute to tumor development. Obesity increases the risk of cancers in the endocrine system (e.g., thyroid, pancreatic, adrenal) due to insulin resistance and altered hormone levels. In the reproductive system, it raises the risk of breast, ovarian, endometrial, and prostate cancers through hormone dysregulation and inflammation. Obesity is also linked to digestive system cancers, including esophageal, liver, and colorectal cancers, due to metabolic dysfunction and chronic inflammation. The role of obesity in lung cancer remains debated, but metabolic changes may influence tumor progression. Obesity contributes to hematologic cancers, such as leukemia, by altering immune function and promoting inflammation. Other systems show varying associations with obesity and cancer risk. Key mechanisms include metabolic dysregulation, chronic inflammation, epigenetic changes, and elevated insulin/IGF-1, which promote tumor growth. Early detection through imaging and biomarkers, along with lifestyle changes (e.g., diet, exercise) and pharmacologic treatments (e.g., metformin, GLP-1 agonists), can reduce cancer risk and improve outcomes. Personalized treatment for obese cancer patients requires adjustments in surgery, chemotherapy, radiotherapy, and immunotherapy. This review explores obesity’s association with cancers across body systems, overviews the mechanisms of obesity contributing to carcinogenesis, and summarizes clinical and public health implications, including screening, prevention, treatment, and policy interventions.