Dietary glycemic index and glycemic load and breast cancer risk

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

Romieu I, Ferrari P, Rinaldi S, Slimani N, Jenab M, Olsen A, Tjonneland A, Overvad K, Boutron-Ruault MC, Lajous M, Kaaks R, Teucher B, Boeing H, Trichopoulou A, Naska A, Vasilopoulo E, Sacerdote C, Tumino R, Masala G, Sieri S, Panico S, Bueno-de-Mesquita HB, Van-der-A D, van Gils CH, Peeters PH, Lund E, Skeie G, Asli LA, Rodriguez L, Navarro C, Amiano P, Sanchez MJ, Barricarte A, Buckland G, Sonestedt E, Wirfält E, Hallmans G, Johansson I, Key TJ, Allen NE, Khaw KT, Wareham NJ, Norat T, Riboli E, Clavel-Chapelon F.

Source

Nutrition and Metabolism Section, International Agency for Research on Cancer, Lyon, France, Barcelona, Spain.

Abstract

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 HR(Q5-Q1) (95% CI) = 1.36 (1.02, 1.82; P-trend = 0.010) and HR(Q5-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 [HR(Q5-Q1) (95% CI) = 1.48 (1.07, 2.05; P-trend = 0.010) for GL and HR(Q5-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.

High glycemic diet and breast cancer occurrence in the Italian EPIC cohort.

Sieri S, Pala V, Brighenti F, Agnoli C, Grioni S, Berrino F, Scazzina F, Palli D, Masala G, Vineis P, Sacerdote C, Tumino R, Giurdanella MC, Mattiello A, Panico S, Krogh V.

Source

Nutritional Epidemiology Unit, National Cancer Institute, Via Venezian 1, I-20133 Milan, Italy.

 

Abstract

BACKGROUND AND AIMS:

There are theoretical reasons for suspecting that a high glycemic index (GI) or glycemic load (GL) diet may increase breast cancer risk, perhaps via an effect on the insulin-like growth factor (IGF) axis. However observational studies have produced inconsistent findings and it is controversial whether breast cancer risk is influenced by the carbohydrate characteristics of the diet. We prospectively investigated the association between dietary GI and GL and breast cancer in the Italian section of the European Prospective Investigation into Cancer and Nutrition (EPIC).

METHODS AND RESULTS:

Women were recruited from 1993 to 1998 at five centers: Varese and Turin (north Italy), Florence (central Italy), and Ragusa and Naples (south Italy). Participants completed validated food frequency questionnaires from which GI and GL were estimated. Multivariable Cox proportional hazard regression models quantified the association between breast cancer risk and total carbohydrate intake, GI, and GL. During 11 years of follow-up, 879 breast cancer (797 invasive and 82 in situ) cases were indentified. High dietary GL was associated with increased breast cancer risk (RR 1.45, 95% CI = 1.06-1.99; highest vs. lowest quintile; p-trend 0.029), whereas dietary GI and total carbohydrate had no influence. The association was not modified by menopausal status or body mass index.

CONCLUSION:

Our data indicate that, in a Mediterranean population characterized by traditionally high and varied carbohydrate intake, a diet high in GL plays a role in the development of breast cancer.

Bron: 2012 Elsevier B.V.

American Society for Nutrition

 

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

 

1,2,3

 

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 HM Peeters,

Eiliv Lund,

Guri Skeie,

Lene Angell Asli,

Laudina Rodriguez,

Carmen Navarro,

Pilar Amiano,

Maria-José Sanchez,

Aurelio Barricarte,

Genevieve Buckland,

Emily Sonestedt,

Elisabet Wirfält,

Göran Hallmans,

Ingegerd Johansson,

Timothy J Key,

Naomi E Allen,

Kay-Tee Khaw,

Nicholas J Wareham,

Teresa Norat,

Elio Riboli, and

Françoise Clavel-Chapelon

 

+ Author Affiliations

1From the Nutrition and Metabolism Section, International Agency for Research on Cancer, Lyon, France (IR, PF, SR, NS, and MJ); the Danish Cancer Society, Institute of Cancer Epidemiology, Diet, Cancer, and Health, Copenhagen, Denmark (AO and A Tjonneland); the Department of Cardiology, Aarhus University Hospital, Aalborg, Denmark (KO); the Department of Epidemiology, School of Public Health, Aarhus University, Aarhus, Denmark (KO); INSERM, Centre for Research in Epidemiology and Population Health, U1018, Institut Gustave Roussy, Villejuif, France (M-CB-R, ML, and FC-C); the Instituto Nacional de Salud Publica, Cuernavaca, Mexico (ML); the Department of Cancer Epidemiology, German Cancer Research Centre, Heidelberg, Germany (RK and BT); the Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany (HB); the WHO Collaborating Center for Food and Nutrition Policies, Department of Hygiene, Epidemiology, and Medical Statistics, University of Athens Medical School, Athens, Greece (A Trichopoulou, AN, and EV); the Hellenic Health Foundation, Athens, Greece (A Trichopoulou and AN); the Center for Cancer Prevention (CPO-Piemonte), Turin, Italy (CS); the Human Genetic Foundation (HuGeF), Turin, Italy (CS); the Cancer Registry and Histopathology Unit, Ragusa, Italy (RT); the Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute–ISPO, Florence, Italy (GM); the Nutritional Epidemiology Unit, Fondazione IRCCS Institute Nazionale Tumori, Milan, Italy (SS); the Department of Clinical and Experimental Medicine, Federico II University, Naples, Italy (SP); the National Institute for Public Health and the Environment (RIVM), Bilthoven, Netherlands (HBB-d-M and DV-d-A); the Department of Gastroenterology and Hepatology, University Medical Centre Utrecht (UMCU), Utrecht, Netherlands (HBB-d-M); the Julius Centre for Health Sciences and Primary Care, University Medical Centre Utrecht, Utrecht, Netherlands (CHvG and PHMP); the Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom (PHMP, TN, and ER); the Institute of Community Medicine, University of Tromsø, Tromsø, Norway (EL, GS, and LAA); the Public Health and Participation Directorate, Health and Health Care Services Council, Asturias, Spain (LR); the Murcia Regional Health Authority, Murcia, Spain (CN); the Public Health Division of Gipuzkoa, Investigation Institute IISS BioDonostia, Basque Country Health Department, San Sebastian, Spain (PA); the Andalusian School of Public Health, Granada, Spain (M-JS); the Navarre Public Health Institute, Pamplona, Spain (AB); the Consortium for Biomedical Research in Epidemiology and Public Health (CIBERESP), Spain (CN, PA, M-JS, and AB); the Unit of Nutrition, Environment, and Cancer, Cancer Epidemiology Research Programme, Catalan Institute of Oncology (ICO-IDIBELL), Barcelona, Spain (GB); the Department of Clinical Sciences in Malmö/Nutrition Epidemiology, Lund University, Malmö, Sweden (ES and EW); the Department of Public Health and Clinical Medicine, Nutritional Research, Umeå University, Umeå, Sweden (GH); the Department of Odontology, Umeå University, Umeå, Sweden (IJ); the Cancer Epidemiology Unit, University of Oxford, Nuffield Department of Clinical Medicine, Oxford, United Kingdom (TJK and NEA); the Department of Public Health and Primary Care, University of Cambridge Addenbrooke’s Hospital, Cambridge, United Kingdom (K-TK); and the MRC Epidemiology Unit, Institute of Metabolic Science, Addenbrooke’s Hospital, Cambridge, United Kingdom (NJW).


+ Author Notes

2 The coordination of EPIC is financially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The national cohorts are supported by the Danish Cancer Society (Denmark); Ligue Contre le Cancer, Institut Gustave Roussy, Mutuelle Générale de l’Education Nationale, Institut National de la Santé et de la Recherche Médicale (INSERM) (France); Deutsche Krebshilfe, Deutsches Krebsforschungszentrum and Federal Ministry of Education and Research (Germany); the Hellenic Health Foundation, the Stavros Niarchos Foundation, and the Hellenic Ministry of Health and Social Solidarity (Greece); the Italian Association for Research on Cancer (AIRC) and National Research Council (Italy); the Dutch Ministry of Public Health, Welfare, and Sports (VWS), Netherlands Cancer Registry (NKR), LK Research Funds, Dutch Prevention Funds, Dutch ZON (Zorg Onderzoek Nederland), World Cancer Research Fund (WCRF), and Statistics Netherlands (Netherlands); ERC-2009-AdG 232997 and Nordforsk, Nordic Centre of Excellence Programme on Food, Nutrition and Health (Norway); the Health Research Fund (FIS), Regional Governments of Andalucía, Asturias, Basque Country, Murcia (project no. 6236) and Navarra, ISCIII RETIC (RD06/0020) (Spain); the Swedish Cancer Society, Swedish Scientific Council and Regional Government of Skåne and Västerbotten (Sweden); Cancer Research UK, Medical Research Council, Stroke Association, British Heart Foundation, Department of Health, Food Standards Agency, and Wellcome Trust (United Kingdom).

3 Address correspondence to I Romieu, International Agency for Research on Cancer, 150 Cours Albert Thomas, 69372 Lyon Cedex 08, France. E-mail: romieui@iarc.fr

 

Abstract

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.

Footnotes

Received September 26, 2011.

Accepted April 27, 2012.

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