Annals of Oncology Advance Access originally published online on June 24, 2009
Annals of Oncology 2009 20(11):1881-1885; doi:10.1093/annonc/mdp197
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epidemiology |
Glycemic index, glycemic load and renal cell carcinoma risk
1 Department of Epidemiology, Mario Negri Institute for Pharmacological Research, Milan
2 Institute of Medical Statistics and Biometry G. A. Maccacaro, University of Milan, Milan
3 Unit of Epidemiology and Biostatistics; National Cancer Institute, Aviano
4 Department of Epidemiology, Fondazione G. Pascale, National Cancer Institute, Naples
5 Department of Epidemiology, National Cancer Institute Regina Elena, Rome
6 Department of Statistics, University of Milano Bicocca, Milan, Italy
7 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
8 International Agency for Research on Cancer, Lyon Cedex, France
* Correspondence to: Dr C. Galeone, Dipartimento di Epidemiologia, Istituto di Ricerche Farmacologiche Mario Negri, Via Giuseppe La Masa 19, 20156 Milan, Italy. Tel: +39-02-39014656; Fax: +39-02-33200231; E-mail: galeone{at}marionegri.it
Background: The risk of renal cell carcinoma (RCC) has been related to refined cereals and starchy foods, but the association has not been studied in terms of glycemic index (GI) and glycemic load (GL). To provide information on this issue, we analyzed data from an Italian multicentric case–control study.
Materials and methods: Cases were 767 patients with histologically confirmed, incident RCC. Controls were 1534 subjects admitted to the same hospitals as cases for a wide spectrum of acute, non-neoplastic conditions, unrelated to known risk factors for RCC. Information on dietary habits was derived through a food-frequency questionnaire. Multivariate odds ratios (ORs) and 95% confidence intervals (CIs) for GI and GL intake were adjusted for major relevant covariates.
Results: Compared with the lowest quintile, the ORs for the highest quintile were 1.43 (95% CI 1.05–1.95) for GI and 2.56 (95% CI 1.78–3.70) for GL, with significant trends in risk. Compared with the lowest quintile, the risk of RCC for all subsequent levels of GL was higher in never drinkers than in ever drinkers.
Conclusions: We found direct relations between dietary levels of GI and GL and RCC risk. This can be related to mechanisms linked to insulin resistance and sensitivity.
Key words: cancer risk, case–control studies, diet, glycemic index, glycemic load, renal cell carcinoma
Received for publication November 26, 2008. Revision received March 6, 2009. Accepted for publication March 9, 2009.