title: Dietary insulin load, dietary insulin index, and risk of pancreatic cancer.
abstract: BACKGROUND
  Although hyperinsulinemia and insulin resistance have been hypothesized to be involved in pancreatic carcinogenesis, studies that have examined glycemic load or individual dietary components that influence glucose concentrations yielded inconclusive results.
  
  
  OBJECTIVE
  Our objective was to investigate whether dietary insulin load and dietary insulin index are associated with the risk of pancreatic cancer.
  
  
  METHODS
  We prospectively followed 86,740 women and 46,147 men who were free of cancer and diabetes at baseline in the Nurses' Health Study and the Health Professionals Follow-Up Study. During ≤26 y of follow-up, 691 pancreatic cancer cases were documented. Dietary insulin load was calculated as a function of the food insulin index, and the energy content of individual foods was reported on food-frequency questionnaires. The dietary insulin index was calculated by dividing the dietary insulin load by the total energy intake.
  
  
  RESULTS
  Dietary insulin load and dietary insulin index were not associated with the overall risk of pancreatic cancer. In a comparison of the highest with the lowest quintiles, the pooled multivariate RRs of pancreatic cancer were 1.05 (95% CI: 0.82, 1.34) for dietary insulin load and 0.96 (95% CI: 0.75, 1.23) for dietary insulin index. In individuals with an elevated BMI (in kg/m(2); ≥27.5) or with low physical activity, a high insulin load was associated with small, nonsignificant increases in the risk of pancreatic cancer; in a comparison of the highest with the lowest tertile of intake, the positive association became more apparent in those who were both overweight and inactive (RR: 2.03; 95% CI: 1.05, 3.93; P-trend = 0.04).
  
  
  CONCLUSIONS
  A diet that induces an elevated postprandial insulin response does not influence the overall risk of pancreatic cancer. However, a diet with a high insulin load may increase the risk in individuals with a preexisting state of insulin resistance.
authors.affiliation: Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. ying.bao@channing.harvard.edu
authors.forename: Ying
authors.initials: Y
authors.lastname: Bao
authors.forename: Katharina
authors.initials: K
authors.lastname: Nimptsch
authors.forename: Brian M
authors.initials: BM
authors.lastname: Wolpin
authors.forename: Dominique S
authors.initials: DS
authors.lastname: Michaud
authors.forename: Jennie C
authors.initials: JC
authors.lastname: Brand-Miller
authors.forename: Walter C
authors.initials: WC
authors.lastname: Willett
authors.forename: Edward
authors.initials: E
authors.lastname: Giovannucci
authors.forename: Charles S
authors.initials: CS
authors.lastname: Fuchs
mesh_terms: D000328:Adult; D050260:Carbohydrate Metabolism; D004040:Dietary Carbohydrates / Q000378:metabolism*; D002149:Energy Intake; D005260:Female; D006801:Humans; D015994:Incidence; D007328:Insulin / Q000097:blood*; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000150:complications*; D010190:Pancreatic Neoplasms / Q000097:blood / Q000453:epidemiology / Q000209:etiology*; D019518:Postprandial Period; D011446:Prospective Studies; D012307:Risk Factors; D057185:Sedentary Behavior; D011795:Surveys and Questionnaires
chemical_list: D004040:Dietary Carbohydrates; D007328:Insulin