ULTRA-PROCESSED FOODS AND CANCER DEVELOPMENT: INFLAMMATORY AND METABOLIC PATHWAYS INVOLVED

Resumo

Introduction: The global increase in cancer incidence has been closely associated with changes in dietary patterns, particularly the rising consumption of ultra-processed foods (UPFs). These foods are typically rich in added sugars, unhealthy fats, additives, and low in fiber and bioactive compounds, contributing to metabolic dysfunction and chronic inflammation, that are key processes in carcinogenesis. Objective: The aim of this study is to investigate the role of ultra - processed food consumption in cancer development, focusing on the underlying inflammatory and metabolic pathways. Methods: This study consists of a narrative literature review based on searches conducted in PubMed, Scopus, and Web of Science using descriptors related to ultra -processed foods, cancer, inflammation, and metabolic pathways. Experimental, epidemiological, and clinical studies investigating the biological mechanisms linking UPFs to cancer were included. Results: High consumption of UPFs has been associated with increased risk of several cancers, including colorectal, breast, and pancreatic cancer. Mechanistically, UPFs promote metabolic disturban ces such as insulin resistance, hyperinsulinemia, and obesity, which activate proliferative pathways including insulin/IGF -1 signaling and PI3K/Akt/mTOR cascade. Additionally, these foods contribute to chronic low -grade inflammation through activation of n uclear factor-kappa B (NF- κB) and the NLRP3 inflammasome, leading to increased production of pro-inflammatory cytokines such as TNF -α, IL -6, and IL -1β. Additives and food contaminants, including emulsifiers and advanced glycation end products (AGEs), may d isrupt gut microbiota composition and increase intestinal permeability, promoting endotoxemia and activation of toll-like receptor 4 (TLR4). This process further amplifies inflammatory signaling and oxidative stress, characterized by increased reactive oxy gen species (ROS), DNA damage, and genomic instability. Furthermore, reduced intake of protective compounds such as fibers and polyphenols impairs antioxidant defenses and anti-inflammatory pathways. Conclusion: Ultra-processed food consumption contributes to cancer development through interconnected metabolic and inflammatory pathways involving insulin signaling, chronic inflammation, oxidative stress, and gut microbiota dysregulation. Reducing UPF intake and promoting dietary patterns rich in minimally pr ocessed foods may represent an important strategy for cancer prevention. Further longitudinal and mechanistic studies are needed to clarify causal relationships and support public health recommendations.