Why Does Obesity as an Inflammatory Condition Predispose to Colorectal Cancer?

Abstract

Obesity is a complex and multifactorial problem of global importance. Additionally, obesity causes chronic inflammation, upregulates cell growth, disturbs the immune system, and causes genomic instability, increasing the risk of carcinogenesis. Colorectal cancer is one of the most common cancers, and it has become a global problem. In 2018, there were around 1.8 million new cases and around 881,000 deaths worldwide. Another risk factor of colorectal cancer associated with obesity is poor diet. A Western diet, including a high intake of red and processed meat and a low consumption of whole grains, fruits, vegetables, and fiber, may increase the risk of both colorectal cancer and obesity. Moreover, the Western diet is associated with a proinflammatory profile diet, which may also affect chronic low-grade inflammation. In fact, people with obesity often present gut dysbiosis, increased inflammation, and risk of colorectal cancer. In this article, the association between obesity and colorectal cancer is discussed, including the most important mechanisms, such as low-grade chronic inflammation, gut dysbiosis, and poor diet.

Gustave Roussy Immune Score (GRIm-Score) as a Prognostic and Predictive Score in Metastatic Colorectal Cancer

“…Inflammation within the tumor microenvironment has been recognized as a hallmark of cancer, contributing to tumor proliferation, angiogenesis, and immune evasion [20]. In CRC, chronic inflammation associated with conditions, such as inflammatory bowel disease (IBD) [21] or obesity [22], has been implicated in promoting tumorigenesis and influencing disease behavior. Moreover, inflammatory markers, such as C-reactive protein (CRP) [23], interleukin-6 (IL-6) [24], and tumor necrosis factor-alpha (TNF-α) [25], are elevated in CRC patients and correlated with tumor aggressiveness and poor prognosis.…”

Microbiome Dysbiosis, Dietary Intake and Lifestyle-Associated Factors Involve in Epigenetic Modulations in Colorectal Cancer: A Narrative Review

“…Furthermore, inflammatory signaling pathways in colonic epithelial cells and immune cells, such as signal transducer and activator of transcription 3 (STAT3) and nuclear factor-kappa B (NF-kB), are triggered by high-fat diets. 156 , 157 These pathways may facilitate the growth of tumor cells in the colon and the synthesis of cytokines that encourage inflammation. 154 …”

The Gum–Gut Axis: Periodontitis and the Risk of Gastrointestinal Cancers

“…Beyond individual pathogens, intestinal dysbiosis, defined as an imbalance in the whole taxonomy and function of the gut microbiota, has been implicated in the pathogenesis of several types of cancer, including those of the digestive tract [ 60 ]. Indeed, dysbiosis promotes tumorigenesis through several mechanisms, including the production of pro-inflammatory metabolites such as trimethylamine N-oxide (TMAO) and LPS, the impairment of the immune response, and the induction of genotoxic stress and nitosative DNA damage [ 20 ].…”