**3.1 Vitamin C**

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].

**15**

*Effectivity and Modulating Pathways for the Prevention of Colorectal Cancer: Diet, Body Fatness…*

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].

There is limited suggestive evidence that foods containing vitamin D, serum vitamin D, and supplemental vitamin D might decrease the risk of CRC [8]. For foods containing vitamin D, a dose-response meta-analysis showed a significant decreased risk for CRC. For supplemental vitamin D, the dose-response meta-analysis showed a significant decreased risk for colon cancer, whereas for plasma/serum vitamin D, the dose-response meta-analysis did not exhibit a significant association with CRC. Two published meta-analyses reported significant inverse associations. Hence, the WCRF/AICR, Continuous Update Project report, noted that plasma/serum vitamin D status can be influenced by sun exposure, obesity, seasonality, smoking, and measurement error. There is evidence of plausible mechanisms in humans [8]. Convincing data from epidemiologic and experimental studies support the potential chemopreventive effects of vitamin D against CRC development, although the

Underlying mechanisms for an effect of vitamin D on CRC have been predominantly studied in vitro and experimental models. Hence, limited data is available in humans [8]. However, these studies suggest a role of circulating vitamin D through its active form, 1 α, 12-dihydroxyvitamin D3 [1,12(OH)2D3], in controlling cell growth, by reducing proliferation and by inducing differentiation and apoptosis [4, 40]. Other alleged mechanisms related to a higher vitamin D status are related to improved innate and adaptive immune function, inhibition of angiogenesis, reduced inflammation, and regulation of microRNA expression [4, 40–42], as well as inhibition of invasion and metastasis and suppression of angiogenesis [4].

Body fatness and abdominal obesity is normally estimated by body mass index (BMI), waist circumference, and waist-to-hip ratio [7]. There is strong convincing evidence that body fatness increases the risk of colorectal, colon, and rectum cancer [7]. However, cognizance should be taken of the fact that these anthropometric measurements have limitations as they do not distinguish between lean and fat mass [8]. Evidence supporting a clear dose-response association was related to showing a significant increased risk of CRC with an increased BMI [8, 43, 44]. There is evidence of a nonlinear dose response, whereby the increased risk is higher at a BMI

in the dose-response analysis for waist circumference and waist-to-hip ratio [8]; hence, the level of evidence is being referred to as convincing for abdominal obesity [33]. In contrast to the vague findings regarding the role of individual nutrients or foods, the strong consistent association between obesity and CRC (at least in men)

for CRC. Significant positive associations were observed for CRC

evidence from randomized controlled trials (RCTs) is inconclusive [4].

*DOI: http://dx.doi.org/10.5772/intechopen.84764*

*3.1.1 Mechanism*

**3.2 Vitamin D**

*3.2.1 Mechanism*

**4. Body fatness**

beyond 27 kg/m2

*Effectivity and Modulating Pathways for the Prevention of Colorectal Cancer: Diet, Body Fatness… DOI: http://dx.doi.org/10.5772/intechopen.84764*
