Several evidences suggest that the positive association between meat intake and colorectal adenoma (CRA) and cancer (CRC) risk is mediated by mutagenic compounds generated during cooking at high temperature. A number of epidemiological studies have estimated the effect of meat-related mutagens intake on CRC/CRA risk with contradictory and sometime inconsistent results. A literature search was carried out (PubMed, Web of Science and Scopus) to identify articles reporting the relationship between the intake of meat-related mutagens (2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine: PhIP, 2-amino-3,8-dimethylimidazo[4,5-f] quinoxaline: MeIQx, 2-amino-3,4,8-trimethylimidazo[4,5-f] quinoxaline: DiMeIQx, benzo(a) pyrene: (B(a)P) and “meat derived mutagenic activity”: MDM) and CRC/CRA risk. A random-effect model was used to calculate the risk association. Thirty-nine studies were included in the systematic review and meta-analysis. Polled CRA risk (15229 cases) was significantly increased by intake of PhIP (OR=1.20; 95%CI:1.13,1.28; p<0.001), MeIQx (OR=1.14; 95%CI:1.05,1.23; p=0.001), DiMeIQx (OR=1.13; 95%CI:1.05,1.21; p=0.001), B(a)P (OR=1.10; 95%CI:1.02,1.19; p=0.017) and MDM (OR=1.17; 95%CI:1.07,1.28; p=0.001). A linear and curvilinear trend was observed in dose-response meta-analisis between CRA risk in association with PhIP and MDM, MeIQx, respectively. CRC risk (21344 cases) was increased by uptake of MeIQx (OR=1.14; 95%CI:1.04,1.25; p=0.004), DiMeIQx (OR=1.12; 95%CI:1.02,1.22; p=0.014) and MDM (OR=1.12; 95%CI:1.06,1.19; p<0.001). No publication bias could be detected whereas heterogeneity was in some cases rather high. Mutagenic compounds formed during cooking of meat at high temperature may be responsible of its carcinogenicity.

Dietary patterns were recently applied to examine the relationship between eating habits and prostate cancer (PC) risk. While the associations between PC risk with glycemic index and Mediterranean score have been reviewed, no meta-analysis is currently available on dietary patterns defined by “a posteriori” methods. Search was carried out (PubMed, Web of Science) to identify studies reporting the relationship between dietary patterns and PC risk. Relevant dietary patterns were selected and the risk estimated were calculated by a random-effect model. Multivariable-adjusted odds ratios (ORs) for a 1st-percentile increase in dietary pattern score were combined by a dose response meta-analysis. 12 observational studies were included in the meta-analysis which identified “Healthy pattern” and “Western pattern”. The Healthy pattern was not related to PC risk (OR=0.96; 95% CI: 0.88-1.04) while the Western pattern significantly increased it (OR=1.34; 95% CI: 1.08-1.65). In addition, a “Carbohydrate pattern”, identified in four articles, was positively associated with a higher PC risk (OR=1.64; 95% CI: 1.35-2.00). A significant linear trend between the Western (p=0.011) and the Carbohydrate (p=0.005) pattern and the increment of PC risk was observed. The small numbers of studies included suggest that further investigations are necessary to support these findings.