The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here:

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

Emily Sonestedt

Emily Sonestedt

Associate senior lecturer

Emily Sonestedt

Dietary glycemic index and glycemic load and breast cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC)


  • Isabelle Romieu
  • Pietro Ferrari
  • Sabina Rinaldi
  • Nadia Slimani
  • Mazda Jenab
  • Anja Olsen
  • Anne Tjonneland
  • Kim Overvad
  • Marie-Christine Boutron-Ruault
  • Martin Lajous
  • Rudolf Kaaks
  • Birgit Teucher
  • Heiner Boeing
  • Antonia Trichopoulou
  • Androniki Naska
  • Effie Vasilopoulo
  • Carlotta Sacerdote
  • Rosario Tumino
  • Giovanna Masala
  • Sabina Sieri
  • Salvatore Panico
  • H. Bas Bueno-de-Mesquita
  • Daphne Van-der-A
  • Carla H. van Gils
  • Petra H. M. Peeters
  • Eiliv Lund
  • Guri Skeie
  • Lene Angell Asli
  • Laudina Rodriguez
  • Carmen Navarro
  • Pilar Amiano
  • Maria-Jose Sanchez
  • Aurelio Barricarte
  • Genevieve Buckland
  • Emily Sonestedt
  • Elisabet Wirfält
  • Goran Hallmans
  • Ingegerd Johansson
  • Timothy J. Key
  • Naomi E. Allen
  • Kay-Tee Khaw
  • Nicholas J. Wareham
  • Teresa Norat
  • Elio Riboli
  • Francoise Clavel-Chapelon

Summary, in English

Background: The glycemic potential of a diet is associated with chronically elevated insulin concentrations, which may augment breast cancer (BC) risk by stimulating insulin receptor or by affecting insulin-like growth factor I (IGF-I)-mediated mitogenesis. It is unclear whether this effect differs by BC phenotype. Objective: The objective was to investigate the relation between glycemic index (GI), glycemic load (GL), and total carbohydrate intake with BC by using data from the European Prospective Investigation into Cancer and Nutrition (EPIC). Design: We identified 11,576 women with invasive BC among 334,849 EPIC women aged 34-66 y (5th to 95th percentiles) at baseline over a median follow-up of 11.5 y. Dietary GI and GL were calculated from country-specific dietary questionnaires. We used multivariable Cox proportional hazards models to quantify the association between GI. GL, and carbohydrate intake and BC risk. BC tumors were classified by receptor status. Results: Overall GI, GL, and carbohydrates were not related to BC. Among postmenopausal women, GL and carbohydate intake were significantly associated with an increased risk of estrogen receptor negative (ER-) BC when extreme quintiles (Q) were compared [multivariable HRQ5-Q1 (95% CI) = 1.36 (1.02, 1.82; P-trend = 0.010) and HRQ5-Q1 = 1.41 (1.05, 1.89; P-trend = 0.009), respectively]. Further stratification by progesterone receptor (PR) status showed slightly stronger associations with ER (-)/PR- BC [HRQ5-Q1 (95% CI) = 1.48 (1.07, 2.05; P-trend = 0.010) for GL and HRQ5-Q1 = 1.62 (1.15, 2.30; P-trend = 0.005) for carbohydrates]. No significant association with ER-positive BC was observed. Conclusion: Our results indicate that a diet with a high GL and carbohydrate intake is positively associated with an increased risk of developing ER- and ER-/PR- BC among postmenopausal women. Am J Clin Nutr 2012;96:345-55.


  • Nutrition Epidemiology
  • EXODIAB: Excellence of Diabetes Research in Sweden
  • EpiHealth: Epidemiology for Health

Publishing year







American Journal of Clinical Nutrition





Document type

Journal article


Oxford University Press


  • Nutrition and Dietetics



Research group

  • Nutrition Epidemiology


  • ISSN: 1938-3207