© 2002 by Oxford University Press
Journal of the National Cancer Institute, Vol. 94, No. 17, 1293-1300,
September 4, 2002
© 2002 Oxford University Press
ARTICLE |
Dietary Sugar, Glycemic Load, and Pancreatic Cancer Risk in a Prospective Study
Affiliations of authors: D. S. Michaud, Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD; S. Liu, Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, and Department of Nutrition, Harvard School of Public Health, Boston; E. Giovannucci, W. C. Willett, Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, and Departments of Nutrition and Epidemiology, Harvard School of Public Health; G. A. Colditz, Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, and Department of Epidemiology, Harvard School of Public Health; C. S. Fuchs, Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, and Department of Adult Oncology, Dana-Farber Cancer Institute, Boston.
Correspondence to: Dominique Michaud, Sc.D., National Cancer Institute, 6120 Executive Blvd., EPS Rm. 3032, Rockville, MD 20852 (e-mail: michaudd{at}mail.nih.gov).
Background: Evidence from both animal and human studies suggests that abnormal glucose metabolism plays an important role in pancreatic carcinogenesis. We investigated whether diets high in foods that increase postprandial glucose levels are associated with an increased risk of pancreatic cancer. Methods: In a cohort of U.S. women (n = 88 802) participating in the Nurses' Health Study, 180 case subjects with pancreatic cancer were diagnosed during 18 years of follow-up. We used frequency of intake of individual foods as reported on a food-frequency questionnaire in 1980 to calculate sucrose, fructose, and carbohydrate intakes; glycemic index (postprandial blood glucose response as compared with a reference food); and glycemic load (glycemic index multiplied by carbohydrate content). Analyses of relative risk (RR) were performed by using multivariable Cox proportional hazards models to adjust for potential confounders. All statistical tests were two-sided. Results: Carbohydrate and sucrose intake were not associated with overall pancreatic cancer risk in this cohort. A statistically nonsignificant 53% increase in risk of pancreatic cancer (RR = 1.53, 95% confidence interval [CI] = 0.96 to 2.45) was observed among women with a high glycemic load intake, and a similar association was observed for fructose intake (RR = 1.57, 95% CI = 0.95 to 2.57). The associations of glycemic load and fructose intakes with pancreatic cancer risk were most apparent among women with elevated body mass index (
25 kg/m2) or with low physical activity. Among women who were both overweight and sedentary, a high glycemic load was associated with an RR of 2.67 (95% CI = 1.02 to 6.99; highest versus lowest quartile of intake; P for trend = .03), and high fructose was associated with an RR of 3.17 (95% CI = 1.13 to 8.91; P for trend = .04). Conclusion: Our data support other findings that impaired glucose metabolism may play a role in pancreatic cancer etiology. A diet high in glycemic load may increase the risk of pancreatic cancer in women who already have an underlying degree of insulin resistance.
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