R Cordova1, V Knaze2, V Viallon3, P Rust1, C G Schalkwijk4, E Weiderpass5, K-H Wagner1, A-L Mayen-Chacon3, E K Aglago3, C C Dahm6, K Overvad6,7, A Tjønneland8,9, J Halkjær8, F R Mancini10,11, M-C Boutron-Ruault10,11, G Fagherazzi10,11, V Katzke12, T Kühn12, M B Schulze13,14, H Boeing15, A Trichopoulou16, A Karakatsani16,17, P Thriskos16, G Masala18, V Krogh19, S Panico20, R Tumino21, F Ricceri22,23, A Spijkerman24, J Boer24, G Skeie25, C Rylander25, K B Borch25, J R Quirós26, A Agudo27, D Redondo-Sánchez28,29, P Amiano29,30, J-H Gómez-Gómez31, A Barricarte29,32,33, S Ramne34, E Sonestedt34, I Johansson35, A Esberg35, T Tong36, D Aune37, K K Tsilidis37,38, M J Gunter3, M Jenab3, Heinz Freisling39. 1. Department of Nutritional Sciences, University of Vienna, Vienna, Austria. 2. Section of Early Detection and Prevention, International Agency for Research on Cancer (IARC-WHO), Lyon, France. 3. Section of Nutrition and Metabolism, International Agency for Research on Cancer (IARC-WHO), Lyon, France. 4. Department of Internal Medicine, Laboratory of Metabolism and Vascular Medicine, Maastricht University Medical Center, Maastricht, The Netherlands. 5. International Agency for Research on Cancer (IARC-WHO), Lyon, France. 6. Department of Public Health, Aarhus University, Aarhus, Denmark. 7. Department of Cardiology, Aalborg University Hospital, Aalborg, Denmark. 8. Danish Cancer Society Research Center Copenhagen, Copenhagen, Denmark. 9. Department of Public Health, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. 10. CESP, Fac. de médecine, Univ. Paris-Sud, Fac. de médecine-UVSQ-INSERM, Université Paris-Saclay, Villejuif, France. 11. Institut Gustave Roussy, Villejuif, France. 12. Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. 13. Department of Molecular Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany. 14. Institute of Nutrition Science, University of Potsdam, Nuthetal, Germany. 15. Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany. 16. Hellenic Health Foundation, Athens, Greece. 17. 2nd Pulmonary Medicine Department, School of Medicine, National and Kapodistrian University of Athens, ATTIKON University Hospital, Haidari, Greece. 18. Cancer Risk Factors and Lifestyle Epidemiology Unit, Institute for Cancer Research, Prevention and Clinical Network-ISPRO, Florence, Italy. 19. Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy. 20. Dipartimento di Medicina Clinica E Chirurgia, Federico II University, Naples, Italy. 21. Cancer Registry and Histopathology Unit, Azienda Sanitaria Provinciale (ASP) Ragusa, Ragusa, Italy. 22. Department of Clinical and Biological Sciences, University of Turin, Turin, Italy. 23. Unit of Epidemiology, Regional Health Service ASL TO3, Turin, TO, Italy. 24. National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands. 25. Department of Community Medicine, Faculty of Health Sciences, UiT-The Arctic University of Norway, Tromsø, Norway. 26. Public Health Directorate, Asturias, Spain. 27. Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology-IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain. 28. Andalusian School of Public Health. Biomedical Research Institute ibs.GRANADA, University of Granada, Granada, Spain. 29. CIBER of Epidemiology and Public Health, Madrid, Spain. 30. Public Health Division of Gipuzkoa, BioDonostia Research Institute, San Sebastian, Spain. 31. Department of Epidemiology and Murcia Regional Health Council, Universidad de Murcia, Murcia, Spain. 32. Navarra Public Health Institute, Pamplona, Spain. 33. Navarra Institute for Health Research (IdiSNA), Pamplona, Spain. 34. Nutritional Epidemiology, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden. 35. Department of Odontology, Umeå University, Umeå, Sweden. 36. Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK. 37. Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK. 38. Department of Hygiene and Epidemiology, University of Ioannina School of Medicine University Campus Ioannina, Ioannina, Greece. 39. International Agency for Research on Cancer (IARC-WHO), 150 cours Albert Thomas, CEDEX 08, 69372, Lyon, France. freislingh@iarc.fr.
Abstract
PURPOSE: Advanced glycation end products (AGEs) can be formed in foods by the reaction of reducing sugars with proteins, and have been shown to induce insulin resistance and obesity in experimental studies. We examined the association between dietary AGEs intake and changes in body weight in adults over an average of 5 years of follow-up. METHODS: A total of 255,170 participants aged 25-70 years were recruited in ten European countries (1992-2000) in the PANACEA study (Physical Activity, Nutrition, Alcohol, Cessation of smoking, Eating out of home in relation to Anthropometry), a sub-cohort of the EPIC (European Prospective Investigation into Cancer and Nutrition). Body weight was measured at recruitment and self-reported between 2 and 11 years later depending on the study center. A reference database for AGEs was used containing UPLC-MS/MS-measured Nε-(carboxymethyl)-lysine (CML), Nε-(1-carboxyethyl)-lysine (CEL), and Nδ-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine (MG-H1) in 200 common European foods. This reference database was matched to foods and decomposed recipes obtained from country-specific validated dietary questionnaires in EPIC and intake levels of CEL, CML, and MG-H1 were estimated. Associations between dietary AGEs intake and body weight change were estimated separately for each of the three AGEs using multilevel mixed linear regression models with center as random effect and dietary AGEs intake and relevant confounders as fixed effects. RESULTS: A one-SD increment in CEL intake was associated with 0.111 kg (95% CI 0.087-0.135) additional weight gain over 5 years. The corresponding additional weight gain for CML and MG-H1 was 0.065 kg (0.041-0.089) and 0.034 kg (0.012, 0.057), respectively. The top six food groups contributing to AGEs intake, with varying proportions across the AGEs, were cereals/cereal products, meat/processed meat, cakes/biscuits, dairy, sugar and confectionary, and fish/shellfish. CONCLUSION: In this study of European adults, higher intakes of AGEs were associated with marginally greater weight gain over an average of 5 years of follow-up.
PURPOSE: Advanced glycation end products (AGEs) can be formed in foods by the reaction of reducing sugars with proteins, and have been shown to induce insulin resistance and obesity in experimental studies. We examined the association between dietary AGEs intake and changes in body weight in adults over an average of 5 years of follow-up. METHODS: A total of 255,170 participants aged 25-70 years were recruited in ten European countries (1992-2000) in the PANACEA study (Physical Activity, Nutrition, Alcohol, Cessation of smoking, Eating out of home in relation to Anthropometry), a sub-cohort of the EPIC (European Prospective Investigation into Cancer and Nutrition). Body weight was measured at recruitment and self-reported between 2 and 11 years later depending on the study center. A reference database for AGEs was used containing UPLC-MS/MS-measured Nε-(carboxymethyl)-lysine (CML), Nε-(1-carboxyethyl)-lysine (CEL), and Nδ-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine (MG-H1) in 200 common European foods. This reference database was matched to foods and decomposed recipes obtained from country-specific validated dietary questionnaires in EPIC and intake levels of CEL, CML, and MG-H1 were estimated. Associations between dietary AGEs intake and body weight change were estimated separately for each of the three AGEs using multilevel mixed linear regression models with center as random effect and dietary AGEs intake and relevant confounders as fixed effects. RESULTS: A one-SD increment in CEL intake was associated with 0.111 kg (95% CI 0.087-0.135) additional weight gain over 5 years. The corresponding additional weight gain for CML and MG-H1 was 0.065 kg (0.041-0.089) and 0.034 kg (0.012, 0.057), respectively. The top six food groups contributing to AGEs intake, with varying proportions across the AGEs, were cereals/cereal products, meat/processed meat, cakes/biscuits, dairy, sugar and confectionary, and fish/shellfish. CONCLUSION: In this study of European adults, higher intakes of AGEs were associated with marginally greater weight gain over an average of 5 years of follow-up.
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