*3.1.1 Mechanism*

*Multidisciplinary Approach for Colorectal Cancer*

populations with very low consumption [4].

and glucosinolates are found in cruciferous vegetables [4].

*2.6.1 Mechanism*

**2.7 Alcoholic beverages**

*2.7.1 Mechanism*

**3. Vitamins**

**3.1 Vitamin C**

CRC. Considering the well-establish cardiometabolic benefits of adequate fruit and vegetable intake, it would be reasonable to recommend increasing intake among

The consumption of vegetables provides a large number of potential anticarcinogenic components that include dietary fiber, carotenoids, vitamins C and E, selenium, folate, dithiolethiones, glucosinolates and indoles, isothiocyanates, flavonoids, polyphenols, protease inhibitors, plant sterols, allium compounds, and limonene [7, 29]. It is possible that a combination of these nutrients and phytochemicals is responsible for the lower CRC risks associated with vegetable consumption [8], due to their antioxidant and antiproliferative activities, modulating xenobiotic and hormonal metabolism and immunity [30, 31]. Vegetables are an important source of micronutrients, notably folate that plays an important role in DNA synthesis and methylation and in the expression of genes involved in carcinogenesis [32]. Anticarcinogenic compounds such as folate, vitamins, fiber, minerals, flavonoids,

Alcoholic beverages contain ethanol that is formed during fermentation. In epidemiological studies, exposure to alcoholic beverages is examined by measures such as drinking or not, the number of drinks/glasses or 10 g units consumed per day or per week [7]. Concerning CRC associations, the evidence is considered to be convincing in men and probable in women [7, 33], as there is convincing evidence that the consumption of approximately two or more alcoholic drinks per day (30 g) increases the risk of CRC with a significant risk being observed for colorectal, colon, and rectal cancer [8]. An intake of 30 g per day is associated with a 16% increase in CRC risk, whereas an intake of 45 g per day increases the risk by 41% [34], suggesting a doseresponse relationship in which the higher the intake, the higher the risk [33].

The mechanisms whereby chronic alcohol consumption has an effect on the development of CRC are diverse. Acetaldehyde (the first compound formed in ethanol metabolism) has mutagenic and carcinogenic activity. It is thought that it plays a critical role in CRC onset via toxic metabolites of ethanol oxidation that can be carcinogenic to colonocytes [35, 36]. Higher ethanol consumption can also induce oxidative stress through the increased production of reactive oxygen species which are genotoxic and carcinogenic [37]. Alcohol may also act as a solvent for cellular penetration of dietary or environmental (e.g., tobacco) carcinogens, affect hormone metabolism, and interfere with retinoid metabolism and with DNA repair mechanisms [38].

There is limited suggestive evidence that consuming foods containing vitamin C might

decrease the risk of colon cancer. However, no conclusion was drawn regarding rectal cancer [8]. Although the evidence was limited, it was generally consistent and the doseresponse meta-analysis showed a significant decreased risk at a level of 40 mg per day [8].

**14**

The biological plausibility to support a protective effect of vitamin C on CRC development is related to its potency as an antioxidant, thereby reducing levels of reactive oxygen species, inhibiting lipid peroxidation, and reducing nitrates [4, 28]. Vitamin C has also been shown to inhibit carcinogen formation in experimental models and to protect DNA from mutagenic effects [39]. Other mechanisms include inhibition of cell proliferation, pro-apoptosis, and a reduction in inflammation [4].
