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Title: Dietary Advanced Glycation End-Products and Colorectal Cancer Risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) Study.
Authors: Aglago, Elom K
Mayén, Ana-Lucia
Knaze, Viktoria
Freisling, Heinz
Fedirko, Veronika
Hughes, David J
Jiao, Li
Eriksen, Anne Kirstine
Tjønneland, Anne
Boutron-Ruault, Marie-Christine
Rothwell, Joseph A
Severi, Gianluca
Kaaks, Rudolf
Katzke, Verena
Schulze, Matthias B
Birukov, Anna
Palli, Domenico
Sieri, Sabina
Santucci de Magistris, Maria
Tumino, Rosario
Ricceri, Fulvio
Bueno-de-Mesquita, Bas
Derksen, Jeroen W G
Skeie, Guri
Gram, Inger Torhild
Sandanger, Torkjel
Quirós, J Ramón
Luján-Barroso, Leila
Sánchez, Maria-Jose
Amiano, Pilar
Chirlaque, María-Dolores
Gurrea, Aurelio Barricarte
Johansson, Ingegerd
Manjer, Jonas
Perez-Cornago, Aurora
Weiderpass, Elisabete
Gunter, Marc J
Heath, Alicia K
Schalkwijk, Casper G
Jenab, Mazda
Keywords: advanced glycation end-products;colorectal cancer;dietary exposure;dietary glycation compounds
metadata.dc.subject.mesh: Adult
Colorectal Neoplasms
Diet Surveys
Glycation End Products, Advanced
Middle Aged
Proportional Hazards Models
Prospective Studies
Risk Assessment
Issue Date: 8-Sep-2021
Abstract: Dietary advanced glycation end-products (dAGEs) have been hypothesized to be associated with a higher risk of colorectal cancer (CRC) by promoting inflammation, metabolic dysfunction, and oxidative stress in the colonic epithelium. However, evidence from prospective cohort studies is scarce and inconclusive. We evaluated CRC risk associated with the intake of dAGEs in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Dietary intakes of three major dAGEs: Nε-carboxy-methyllysine (CML), Nε-carboxyethyllysine (CEL), and Nδ-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine (MG-H1) were estimated in 450,111 participants (median follow-up = 13 years, with 6162 CRC cases) by matching to a detailed published European food composition database. Hazard ratios (HRs) and 95% confidence intervals (CIs) for the associations of dAGEs with CRC were computed using multivariable-adjusted Cox regression models. Inverse CRC risk associations were observed for CML (HR comparing extreme quintiles: HRQ5vs.Q1 = 0.92, 95% CI = 0.85-1.00) and MG-H1 (HRQ5vs.Q1 = 0.92, 95% CI = 0.85-1.00), but not for CEL (HRQ5vs.Q1 = 0.97, 95% CI = 0.89-1.05). The associations did not differ by sex or anatomical location of the tumor. Contrary to the initial hypothesis, our findings suggest an inverse association between dAGEs and CRC risk. More research is required to verify these findings and better differentiate the role of dAGEs from that of endogenously produced AGEs and their precursor compounds in CRC development.
metadata.dc.identifier.doi: 10.3390/nu13093132
Appears in Collections:Escuela Andaluza de Salud Pública
Instituto de Investigación Biosanitaria de Granada (ibsGRANADA)

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