Sabina Sieri1, Claudia Agnoli1, Sara Grioni1, Elisabete Weiderpass2, Amalia Mattiello3, Ivonne Sluijs4, Maria Jose Sanchez5,6,7,8, Marianne Uhre Jakobsen9, Michael Sweeting10,11, Yvonne T van der Schouw4, Lena Maria Nilsson12, Patrik Wennberg13, Verena A Katzke14, Tilman Kühn14, Kim Overvad15, Tammy Y N Tong16, Moreno-Iribas Conchi17, José Ramón Quirós18, Juan Manuel García-Torrecillas19, Olatz Mokoroa20, Jesús-Humberto Gómez21, Anne Tjønneland22,23, Emiliy Sonestedt24, Antonia Trichopoulou25, Anna Karakatsani25,26, Elissavet Valanou25, Jolanda M A Boer27, W M Monique Verschuren27, Marie-Christine Boutron-Ruault28,29, Guy Fagherazzi28,29, Anne-Laure Madika28,29,30, Manuela M Bergmann31, Matthias B Schulze32,33,34, Pietro Ferrari2, Heinz Freisling2, Hannah Lennon2, Carlotta Sacerdote35, Giovanna Masala36, Rosario Tumino37, Elio Riboli38, Nicholas J Wareham39, John Danesh10, Nita G Forouhi39, Adam S Butterworth10, Vittorio Krogh1. 1. Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy. 2. International Agency for Research on Cancer, WHO, Lyon, France. 3. Department of Clinical Medicine and Surgery, Federico II University, Naples, Italy. 4. Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands. 5. Andalusian School of Public Health, Granada, Spain. 6. Centro de Investigación Biomédica en Red de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain. 7. Instituto de Investigación Biosanitaria (ibs.GRANADA), Granada, Spain. 8. Department of Preventive Medicine and Public Health, University of Granada, Granada, Spain. 9. National Food Institute, Division for Diet, Disease Prevention, and Toxicology, Technical University of Denmark, Kongens Lyngby, Denmark. 10. MRC/BHF Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom. 11. Department of Health Sciences, University of Leicester, Leicester, United Kingdom. 12. Department of Public Health and Clinical Medicine, Sustainable Health, Umeå University, Umeå, Sweden. 13. Department of Public Health and Clinical Medicine, Family Medicine, Umeå University, Umeå, Sweden. 14. Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany. 15. Department of Public Health, Aarhus University, Aarhus, Denmark. 16. Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom. 17. Public Health Institute of Navarra, IdiSNA, Pamplona, Spain. 18. Public Health Directorate, Asturias, Spain. 19. Hospital Universitario Torrecárdenas, Almería, Spain. 20. Public Health Division of Gipuzkoa, BioDonostia Research Institute, San Sebastian, Spain. 21. Department of Epidemiology, Murcia Regional Health Council, IMIB-Arrixaca, Murcia, Spain. 22. Diet, Genes, and Environment, Danish Cancer Society Research Center, Copenhagen, Denmark. 23. Department of Public Health, University of Copenhagen, Copenhagen, Denmark. 24. Nutritional Epidemiology, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden. 25. Hellenic Health Foundation, Athens, Greece. 26. 2nd Pulmonary Medicine Department, School of Medicine, National and Kapodistrian University of Athens, "ATTIKON" University Hospital, Haidari, Greece. 27. National Institute for Public Health and the Environment (RIVM), Bilthoven, Netherlands. 28. Center for Research in Epidemiology and Population Health, University Paris-South, Faculty of Medicine, University Versailles-St Quentin, National Institute for Health and Medical Research, Université Paris-Saclay, Villejuif, France. 29. Gustave Roussy, Villejuif, France. 30. Université Lille, CHU Lille, Lille, France. 31. Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbrücke, Nuthetal, Germany. 32. Department of Molecular Epidemiology, German Institute of Human Nutrition Potsdam-Rehbrücke, Nuthetal, Germany. 33. DZHK (German Center for Cardiovascular Research), partner site Berlin, Berlin, Germany. 34. University of Potsdam, Institute of Nutritional Sciences, Nuthetal, Germany. 35. Unit of Cancer Epidemiology, Città della Salute e della Scienza University-Hospital and Center for Cancer Prevention, Turin, Italy. 36. Cancer Risk Factors and Lifestyle Epidemiology Unit, Institute for Cancer Research, Prevention and Clinical Network, Florence, Italy. 37. Cancer Registry and Histopathology Department, "Civic-M.P.Arezzo" Hospital, ASP Ragusa, Ragusa, Italy. 38. Department of Epidemiology and Public Health, Imperial College London, London, United Kingdom. 39. MRC Epidemiology Unit, University of Cambridge School of Clinical Medicine, Cambridge, United Kingdom.
Abstract
BACKGROUND: High carbohydrate intake raises blood triglycerides, glucose, and insulin; reduces HDLs; and may increase risk of coronary heart disease (CHD). Epidemiological studies indicate that high dietary glycemic index (GI) and glycemic load (GL) are associated with increased CHD risk. OBJECTIVES: The aim of this study was to determine whether dietary GI, GL, and available carbohydrates are associated with CHD risk in both sexes. METHODS: This large prospective study-the European Prospective Investigation into Cancer and Nutrition-consisted of 338,325 participants who completed a dietary questionnaire. HRs with 95% CIs for a CHD event, in relation to intake of GI, GL, and carbohydrates, were estimated using covariate-adjusted Cox proportional hazard models. RESULTS: After 12.8 y (median), 6378 participants had experienced a CHD event. High GL was associated with greater CHD risk [HR 1.16 (95% CI: 1.02, 1.31) highest vs. lowest quintile, p-trend 0.035; HR 1.18 (95% CI: 1.07, 1.29) per 50 g/day of GL intake]. The association between GL and CHD risk was evident in subjects with BMI (in kg/m2) ≥25 [HR: 1.22 (95% CI: 1.11, 1.35) per 50 g/d] but not in those with BMI <25 [HR: 1.09 (95% CI: 0.98, 1.22) per 50 g/d) (P-interaction = 0.022). The GL-CHD association did not differ between men [HR: 1.19 (95% CI: 1.08, 1.30) per 50 g/d] and women [HR: 1.22 (95% CI: 1.07, 1.40) per 50 g/d] (test for interaction not significant). GI was associated with CHD risk only in the continuous model [HR: 1.04 (95% CI: 1.00, 1.08) per 5 units/d]. High available carbohydrate was associated with greater CHD risk [HR: 1.11 (95% CI: 1.03, 1.18) per 50 g/d]. High sugar intake was associated with greater CHD risk [HR: 1.09 (95% CI: 1.02, 1.17) per 50 g/d]. CONCLUSIONS: This large pan-European study provides robust additional support for the hypothesis that a diet that induces a high glucose response is associated with greater CHD risk.
BACKGROUND: High carbohydrate intake raises blood triglycerides, glucose, and insulin; reduces HDLs; and may increase risk of coronary heart disease (CHD). Epidemiological studies indicate that high dietary glycemic index (GI) and glycemic load (GL) are associated with increased CHD risk. OBJECTIVES: The aim of this study was to determine whether dietary GI, GL, and available carbohydrates are associated with CHD risk in both sexes. METHODS: This large prospective study-the European Prospective Investigation into Cancer and Nutrition-consisted of 338,325 participants who completed a dietary questionnaire. HRs with 95% CIs for a CHD event, in relation to intake of GI, GL, and carbohydrates, were estimated using covariate-adjusted Cox proportional hazard models. RESULTS: After 12.8 y (median), 6378 participants had experienced a CHD event. High GL was associated with greater CHD risk [HR 1.16 (95% CI: 1.02, 1.31) highest vs. lowest quintile, p-trend 0.035; HR 1.18 (95% CI: 1.07, 1.29) per 50 g/day of GL intake]. The association between GL and CHD risk was evident in subjects with BMI (in kg/m2) ≥25 [HR: 1.22 (95% CI: 1.11, 1.35) per 50 g/d] but not in those with BMI <25 [HR: 1.09 (95% CI: 0.98, 1.22) per 50 g/d) (P-interaction = 0.022). The GL-CHD association did not differ between men [HR: 1.19 (95% CI: 1.08, 1.30) per 50 g/d] and women [HR: 1.22 (95% CI: 1.07, 1.40) per 50 g/d] (test for interaction not significant). GI was associated with CHD risk only in the continuous model [HR: 1.04 (95% CI: 1.00, 1.08) per 5 units/d]. High available carbohydrate was associated with greater CHD risk [HR: 1.11 (95% CI: 1.03, 1.18) per 50 g/d]. High sugar intake was associated with greater CHD risk [HR: 1.09 (95% CI: 1.02, 1.17) per 50 g/d]. CONCLUSIONS: This large pan-European study provides robust additional support for the hypothesis that a diet that induces a high glucose response is associated with greater CHD risk.
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