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JNCI Journal of the National Cancer Institute 2004 96(3):229-233; doi:10.1093/jnci/djh020
© 2004 by Oxford University Press
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© 2004 Oxford University Press

BRIEF COMMUNICATION

Dietary Glycemic Load and Risk of Colorectal Cancer in the Women's Health Study

Susan Higginbotham, Zuo-Feng Zhang, I-Min Lee, Nancy R. Cook, Edward Giovannucci, Julie E. Buring, Simin Liu

Affiliations of authors: Department of Epidemiology, University of California at Los Angeles, Los Angeles (SH, ZFZ); Division of Preventive Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, MA (IML, NRC, JEB, SL); Departments of Epidemiology (IML, EG, JEB, SL) and Nutrition (EG), Harvard School of Public Health, Boston.

Correspondence to: Simin Liu, MD, ScD, Division of Preventive Medicine, Harvard Medical School and Brigham and Women's Hospital, 900 Commonwealth Ave., Boston, MA 02215 (e-mail: simin.liu{at}channing.harvard.edu)

Although diet is believed to influence colorectal cancer risk, the long-term effects of a diet with a high glycemic load are unclear. The growing recognition that colorectal cancer may be promoted by hyperinsulinemia and insulin resistance suggests that a diet inducing high blood glucose levels and an elevated insulin response may contribute to a metabolic environment conducive to tumor growth. We prospectively followed a cohort of 38 451 women for an average of 7.9 years and identified 174 with incident colorectal cancer. We used baseline dietary intake measurements, assessed with a semiquantitative food-frequency questionnaire, to examine the associations of dietary glycemic load, overall dietary glycemic index, carbohydrate, fiber, nonfiber carbohydrate, sucrose, and fructose with the subsequent development of colorectal cancer. Cox proportional hazards models were used to estimate relative risks (RRs). Dietary glycemic load was statistically significantly associated with an increased risk of colorectal cancer (adjusted RR = 2.85, 95% confidence interval [CI] = 1.40 to 5.80, comparing extreme quintiles of dietary glycemic load; Ptrend = .004) and was associated, although not statistically significantly, with overall glycemic index (corresponding RR = 1.71, 95% CI = 0.98 to 2.98; Ptrend = .04). Total carbohydrate (adjusted RR = 2.41, 95% CI = 1.10 to 5.27, comparing extreme quintiles of carbohydrate; Ptrend = .02), nonfiber carbohydrate (corresponding RR = 2.60, 95% CI = 1.22 to 5.54; Ptrend = .02), and fructose (corresponding RR = 2.09, 95% CI = 1.13 to 3.87; Ptrend = .08) were also statistically significantly associated with increased risk. Thus, our data indicate that a diet with a high dietary glycemic load may increase the risk of colorectal cancer in women.



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