RT Journal Article
T1 Dietary Advanced Glycation End-Products and Colorectal Cancer Risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) Study.
A1 Aglago, Elom K
A1 Mayén, Ana-Lucia
A1 Knaze, Viktoria
A1 Freisling, Heinz
A1 Fedirko, Veronika
A1 Hughes, David J
A1 Jiao, Li
A1 Eriksen, Anne Kirstine
A1 Tjønneland, Anne
A1 Boutron-Ruault, Marie-Christine
A1 Rothwell, Joseph A
A1 Severi, Gianluca
A1 Kaaks, Rudolf
A1 Katzke, Verena
A1 Schulze, Matthias B
A1 Birukov, Anna
A1 Palli, Domenico
A1 Sieri, Sabina
A1 Santucci de Magistris, Maria
A1 Tumino, Rosario
A1 Ricceri, Fulvio
A1 Bueno-de-Mesquita, Bas
A1 Derksen, Jeroen W G
A1 Skeie, Guri
A1 Gram, Inger Torhild
A1 Sandanger, Torkjel
A1 Quirós, J Ramón
A1 Luján-Barroso, Leila
A1 Sánchez, Maria-Jose
A1 Amiano, Pilar
A1 Chirlaque, María-Dolores
A1 Gurrea, Aurelio Barricarte
A1 Johansson, Ingegerd
A1 Manjer, Jonas
A1 Perez-Cornago, Aurora
A1 Weiderpass, Elisabete
A1 Gunter, Marc J
A1 Heath, Alicia K
A1 Schalkwijk, Casper G
A1 Jenab, Mazda
K1 advanced glycation end-products
K1 colorectal cancer
K1 dietary exposure
K1 dietary glycation compounds
AB 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.
YR 2021
FD 2021-09-08
LK https://hdl.handle.net/10668/24708
UL https://hdl.handle.net/10668/24708
LA en
DS RISalud
RD Apr 11, 2025