title: Dietary glycemic load, added sugars, and carbohydrates as risk factors for pancreatic cancer: the Multiethnic Cohort Study.
abstract: BACKGROUND
  Because elevated blood glucose concentrations have been shown to be associated with greater risk of pancreatic cancer, a high dietary glycemic load, which is based on an empirical measure of blood glucose response after food consumption, has been hypothesized as a pancreatic cancer risk factor. However, results so far are scarce and inconsistent.
  
  
  OBJECTIVE
  We analyzed data for 162 150 participants in the Hawaii-Los Angeles Multiethnic Cohort Study to investigate associations between glycemic load, dietary carbohydrates, sucrose, fructose, total sugars, and added sugars and the risk of pancreatic cancer.
  
  
  METHODS
  Dietary intake was assessed at baseline by using a quantitative food-frequency questionnaire. During 8 y of follow-up, 434 incident pancreatic cancer cases occurred.
  
  
  RESULTS
  Glycemic load and added sugars were not significantly associated with pancreatic cancer risk. The risk increased with higher intakes of total sugars, fructose, and sucrose, and the association with fructose was significant when the highest and lowest quartiles were compared (relative risk: 1.35; 95% CI: 1.02, 1.80; P for trend = 0.046). A significant association was found with fruit and juices intake (1.37; 1.02, 1.84; P for trend = 0.04) but not with soda intake. Statistical evidence of a significant interaction with body mass index was present only for sucrose intake (P = 0.04). A comparison of the highest and lowest quartiles of sucrose intake in overweight or obese participants gave a relative risk of 1.46 (0.95-2.25; P for trend = 0.04), but the comparison was not significant in normal-weight participants.
  
  
  CONCLUSIONS
  High fructose and sucrose intakes may play a role in pancreatic cancer etiology. Conditions such as overweight or obesity in which a degree of insulin resistance may be present may also be important.
authors.affiliation: Cancer Research Center of Hawaii, University of Hawaii, Honolulu, HI, USA. ute.noethlings@difr.de
authors.forename: Ute
authors.initials: U
authors.lastname: Nöthlings
authors.forename: Suzanne P
authors.initials: SP
authors.lastname: Murphy
authors.forename: Lynne R
authors.initials: LR
authors.lastname: Wilkens
authors.forename: Brian E
authors.initials: BE
authors.lastname: Henderson
authors.forename: Laurence N
authors.initials: LN
authors.lastname: Kolonel
mesh_terms: D000368:Aged; D015992:Body Mass Index; D015331:Cohort Studies; D004040:Dietary Carbohydrates / Q000008:administration & dosage*; D005260:Female; D005632:Fructose / Q000008:administration & dosage*; D005638:Fruit; D006801:Humans; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D010190:Pancreatic Neoplasms / Q000208:ethnology / Q000209:etiology*; D012307:Risk Factors; D013395:Sucrose / Q000008:administration & dosage*
chemical_list: D004040:Dietary Carbohydrates; D005632:Fructose; D013395:Sucrose