These metabolites and their downstream products have a wide diversity of anticarcinogenic effects.
Cruciferous vegetables are rich in glucosinolates that can be metabolized by myrosinase-expressing gut bacteria to thiohydroxymate-O-sulfonate, which can be further converted to isothiocyanates, indole and nitrile.
Several mechanisms that may mediate the pro-carcinogenic effects of H 2S include: impaired fuel utilization of butyrate by colonocytes, increased cell proliferation, DNA damage, and inflammation. Gut sulfate-reducing bacteria can reduce inorganic sulfur in processed food and beverages to produce H 2S. Gut bacteria can ferment sulfur-containing amino acids to produce hydrogen sulfide (H 2S). Sulfur-containing amino acids and inorganic sulfur may have procarcinogenic properties, whereas glucosinolates and allyl sulfur compounds possess antineoplastic activities. Omega-3 fatty acids can inhibit inflammation and promote resolution through lipid mediators (i.e., lipoxin, resolvin and protectin) and directly via G protein-coupled receptor 120 (GPR120) signaling. Vitamin D exerts anti-inflammatory effects through bile acid catabolism, suppression of NFκB and COX2 signaling, and enhanced production of interleukin-10 (IL10).
Calcium may inhibit colorectal carcinogenesis through direct effects on cell proliferation, differentiation and apoptosis, and binding to free fatty acids and bile acids. B vitamins also counteract oxidative stress through lowering homocysteine. As reactive oxygen species scavengers, antioxidant nutrients can protect colonocytes from oxidative stress. Sulfur-containing amino acids and inorganic sulfur are also metabolized by gut microbes to produce hydrogen sulfide (H 2S), which can be toxic to the colorectal mucosa and induce oxidative stress. Bile acids are metabolized by gut microbes to generate secondary bile acids, which can promote colorectal carcinogenesis through increased pro-inflammatory effectors and oxidative stress mediated via engagement of nuclear factor-κB (NFκB) and cyclooxygenase-2 (COX2/prostaglandin synthase-2) pathways. All rights reserved.Ĭonsumption of saturated or trans-fats increases free fatty acids and bile acid levels. Dietary modification therefore has the promise of reducing colorectal cancer incidence.Ĭolorectal Cancer Diet Microbiota Prevention.Ĭopyright © 2015 AGA Institute. Emerging evidence also implicates the gut microbiota as an important effector in the relationship between diet and cancer. These include the direct effects on immune responsiveness and inflammation, and the indirect effects of overnutrition and obesity-risk factors for colorectal cancer. Diet likely influences colorectal carcinogenesis through several interacting mechanisms. Nutrients and foods also may interact, as a dietary pattern, to influence colorectal cancer risk. There is substantial evidence for the potential chemopreventive effects of vitamin D, folate, fruits, and vegetables.
Calcium, fiber, milk, and whole grains have been associated with a lower risk of colorectal cancer, and red meat and processed meat have been associated with an increased risk. In the past few decades, findings from extensive epidemiologic and experimental investigations have linked consumption of several foods and nutrients to the risk of colorectal neoplasia. Electronic address: has an important role in the development of colorectal cancer. 3 Department of Medicine, Harvard Medical School, Boston, Massachusetts Channing Division of Network Medicine, Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, Massachusetts Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.2 Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts Department of Genetics and Complex Diseases, Harvard School of Public Health, Boston, Massachusetts Department of Medicine, Harvard Medical School, Boston, Massachusetts Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts.1 Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts.