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Review
. 2015 May;148(6):1244-60.e16.
doi: 10.1053/j.gastro.2014.12.035. Epub 2015 Jan 6.

Nutrients, foods, and colorectal cancer prevention

Mingyang Song  1 , Wendy S Garrett  2 , Andrew T Chan  3
Affiliations
Review

Nutrients, foods, and colorectal cancer prevention

Mingyang Song et al. Gastroenterology. 2015 May.

Abstract

Diet has an important role in the development of colorectal cancer. 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. 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. There is substantial evidence for the potential chemopreventive effects of vitamin D, folate, fruits, and vegetables. Nutrients and foods also may interact, as a dietary pattern, to influence colorectal cancer risk VSports手机版. Diet likely influences colorectal carcinogenesis through several interacting mechanisms. These include the direct effects on immune responsiveness and inflammation, and the indirect effects of overnutrition and obesity-risk factors for colorectal cancer. Emerging evidence also implicates the gut microbiota as an important effector in the relationship between diet and cancer. Dietary modification therefore has the promise of reducing colorectal cancer incidence. .

Keywords: Colorectal Cancer; Diet; Microbiota; Prevention. V体育安卓版.

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Conflict of interest statement

No conflicts of interest to disclose for the authors.

Figures

Figure 1
Figure 1. Proposed canonical and non-canonical inflammatory mechanisms relating nutrients to colorectal cancer
Consumption of saturated or trans-fats increases free fatty acids and bile acid levels. 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. Sulfur-containing amino acids and inorganic sulfur are also metabolized by gut microbes to produce hydrogen sulfide (H2S), which can be toxic to the colorectal mucosa and induce oxidative stress. As reactive oxygen species scavengers, antioxidant nutrients can protect colonocytes from oxidative stress. B vitamins also counteract oxidative stress through lowering homocysteine. Calcium may inhibit colorectal carcinogenesis through direct effects on cell proliferation, differentiation and apoptosis, and binding to free fatty acids and bile acids. Vitamin D exerts anti-inflammatory effects through bile acid catabolism, suppression of NFκB and COX2 signaling, and enhanced production of interleukin-10 (IL10). 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.
Figure 2
Figure 2. Metabolism and antineoplastic pathways of calcium and vitamin D
Vitamin D signaling via vitamin D receptor (VDR) and retinoid X receptor (RXR) regulates the transcription of numerous genes involved in carcinogenesis through effects on inflammation, cell proliferation, differentiation, apoptosis and angiogenesis. Elevated intracellular calcium, together with diacyl glycerol (DAG), results in the activation of protein kinase C (PKC) that can inhibit cell proliferation and promote differentiation through multiple downstream signals. CaR signaling may also inhibit cell proliferation through inactivation of the β-catenin pathway. Vitamin D is an essential regulator of calcium homeostasis through the negative feedback system involving parathyroid hormone (PTH). The secretion of PTH is enhanced as circulating calcium concentration decreases, resulting in increased synthesis of 1,25(OH)2D3. Elevated 1,25(OH)2D3 in turn promotes calcium absorption in the intestine and calcium release from bone, which suppresses PTH production.
Figure 3
Figure 3. Folate, methionine and other B vitamins in DNA methylation and synthesis
Folate from dietary intake, supplement use and synthesis by gut bacteria is converted to its predominant circulating form, 5-methyl tetrahydrofolate (THF), which can be metabolized by methionine synthase (MS) to form methionine from homocysteine. Vitamin B6 and B12 are also critical cofactors in DNA methylation and synthesis. Dysregulated DNA methylation and DNA synthesis contribute to colorectal carcinogenesis. Abbreviations: DNMT, DNA methyltransferase; MAT, S-adenosylmethonine synthase; SAH, S-adenosylhomocysteine; TS, thymidylate synthase; VDRE, vitamin D response element.
Figure 4
Figure 4. Proposed mechanisms relating sulfur-containing foods to colorectal cancer
Sulfur-containing amino acids and inorganic sulfur may have procarcinogenic properties, whereas glucosinolates and allyl sulfur compounds possess antineoplastic activities. Gut bacteria can ferment sulfur-containing amino acids to produce hydrogen sulfide (H2S). Gut sulfate-reducing bacteria can reduce inorganic sulfur in processed food and beverages to produce H2S. Several mechanisms that may mediate the pro-carcinogenic effects of H2S include: impaired fuel utilization of butyrate by colonocytes, increased cell proliferation, DNA damage, and inflammation. 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. These metabolites and their downstream products have a wide diversity of anticarcinogenic effects. Allium vegetables have high levels of allyl sulfur compounds, mainly γ-glutamylcysteines, which can be converted to S-allylcysteine, or hydrolyzed and oxidized to form alliin. After processing, alliin decomposes to diallyl disulfide (DADS), diallyl sulfide (DAS), and diallyl trisulfide (DAT), which have been related to garlic's cancer-preventive effects.
Figure 5
Figure 5. Biologic mechanisms relating foods to colorectal cancer
Red and processed meat may contribute to CRC through generation of carcinogens, including N-nitroso compounds (NOC), heme iron, sulfur-containing amino acids, and saturated fat. Overweight or obesity as well as chronically increased levels of insulin may also have a critical role. Despite high saturated fat content and its role in increasing insulin-like growth factor 1 (IGF1), dairy products may inhibit colorectal carcinogenesis via a variety of bioactive constituents: calcium, vitamin D (when fortified), conjugated linoleic acid (CLA), butyric acid, lactose, and lactic acid bacteria in fermented milk products. Fruits and vegetables contain various components with antineoplastic potential: fiber, antioxidants, B vitamins, and glucosinolates (in cruciferous vegetables). Potential anti-cancer mechanisms of fiber include: binding or diluting secondary bile acids, increased stool weight, decreased transit time, and bacterial fermentation leading to reduced colonic luminal pH and production of butyrate which has antineoplastic properties. Fiber, fruits and vegetables may also influence carcinogenesis through decreased adiposity.
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