Dietary carbohydrate, fibre, glycaemic index, glycaemic load and the risk of postmenopausal breast cancer

Authors

  • Graham G. Giles,

    Corresponding author
    1. Cancer Epidemiology Centre, The Cancer Council Victoria, Melbourne, Australia
    2. Centre for Genetic Epidemiology, University of Melbourne, Melbourne, Australia
    3. Department of Epidemiology & Preventive Medicine, Monash University, Melbourne, Australia
    • Cancer Epidemiology Centre, The Cancer Council Victoria, 1 Rathdowne Street, Carlton South, VIC 3053, Australia
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    • Fax: +61-3-9635-5330.

  • Julie A. Simpson,

    1. Cancer Epidemiology Centre, The Cancer Council Victoria, Melbourne, Australia
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  • Dallas R. English,

    1. Cancer Epidemiology Centre, The Cancer Council Victoria, Melbourne, Australia
    2. Centre for Genetic Epidemiology, University of Melbourne, Melbourne, Australia
    3. Department of Epidemiology & Preventive Medicine, Monash University, Melbourne, Australia
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  • Allison M. Hodge,

    1. Cancer Epidemiology Centre, The Cancer Council Victoria, Melbourne, Australia
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  • Dorota M. Gertig,

    1. Centre for Genetic Epidemiology, University of Melbourne, Melbourne, Australia
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  • Robert J. MacInnis,

    1. Cancer Epidemiology Centre, The Cancer Council Victoria, Melbourne, Australia
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  • John L. Hopper

    1. Centre for Genetic Epidemiology, University of Melbourne, Melbourne, Australia
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Abstract

Evidence that the insulin pathway may be involved in breast carcinogenesis has increased the interest in dietary factors that influence insulin secretion and resistance. We investigated dietary carbohydrate, fibre, glycaemic index (GI) and glycaemic load (GL) in a prospective study of 324 breast cancers diagnosed in 12,273 post-menopausal women. Although an increase of 1 standard deviation in carbohydrate was marginally associated with risk of breast cancer, relative risk (RR) 1.31 (95% CI, 0.98, 1.75), there were no significant associations with fibre, 1.08 (0.92, 1.26), GI, 0.98 (0.88, 1.10) or GL, 1.19 (0.93, 1.52) or with carbohydrate foods (bread, rice, pasta). The RR for carbohydrate and localized disease was elevated, 1.40 (1.02, 1.92), but like those for fibre, GI and GL did not differ significantly between localized and non-localized disease. RRs for grade I, but not grade II or III, tumours were elevated for fibre, 1.38 (1.08, 1.75), carbohydrate, 1.56 (1.08, 2.25) and GL, 1.41 (1.01, 1.98) but not for GI, 0.84 (0.65, 1.09). The RRs for fibre and oestrogen receptor (ER) positive (+) and progesterone receptor (PR) positive (+) tumours, 1.36 (1.10, 1.67), differed significantly from those for ER positive (+) and PR negative (−) tumours, 1.01 (0.61, 1.69) and ER−/PR− tumours, 0.65 (0.43, 0.99), p = 0.005. Our data do not support a strong role for GI and GL in breast carcinogenesis but suggest that increased intake of fibre and carbohydrate may be associated with the diagnosis of cancers of more favourable prognosis. © 2005 Wiley-Liss, Inc.

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