Available carbohydrates, glycemic load, and pancreatic cancer: is there a link?

National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, Maryland 20852, USA.
American journal of epidemiology (Impact Factor: 4.98). 06/2010; 171(11):1174-82. DOI: 10.1093/aje/kwq061
Source: PubMed

ABSTRACT High-carbohydrate diets have been linked to pancreatic cancer risk in case-control studies, but prospective studies have shown mostly null results. The authors investigated the associations of glycemic load, glycemic index, and carbohydrate intake with pancreatic cancer risk in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Dietary intake was assessed by using a self-administered questionnaire. Between 1998 and 2006 (median follow-up = 6.5 years), 266 incident, confirmed pancreatic cancers were identified among 109,175 participants. Hazards ratios and 95% confidence intervals were adjusted for sex, smoking, body mass index, and total energy. Overall, elevated risks for pancreatic cancer were observed in the 90th versus 10th percentile of glycemic load (hazards ratio (HR) = 1.45, 95% confidence interval (CI): 1.05, 2.00), available carbohydrate (HR = 1.47, 95% CI: 1.05, 2.06), and sucrose (HR = 1.37, 95% CI: 0.99, 1.89) intake. The positive association for available carbohydrate intake was observed during the first 4 years of follow-up (HR(<2 years) = 2.60, 95% CI: 1.34, 5.06; HR(2-<4 years) = 1.94, 95% CI: 1.06, 3.55) but not subsequently (HR = 0.86, 95% CI: 0.52, 1.44); the opposite pattern was observed for total fat and saturated fat intake. Rather than being causal, the short-term increase in pancreatic cancer risk associated with high available carbohydrate and low fat intake may be capturing dietary changes associated with subclinical disease.

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    ABSTRACT: Background Dietary glycemic index (GI) and glycemic load (GL) have been related to the risk of selected cancers, but the issue remains open.Patients and methodsMailed questionnaires were completed between 1994 and 1997 in eight Canadian provinces for incident, histologically confirmed cases of the stomach (n = 1182), colon (n = 1727), rectum (n = 1447), liver (n = 309), pancreas (n = 628), lung (n = 3341), breast (n = 2362), ovary (n = 442), prostate (n = 1799), testis (n = 686), kidney (n = 1345), bladder (n = 1029), brain (n = 1009), non-Hodgkin's lymphomas (NHL, n = 1666), leukemias (n = 1069), multiple myelomas (n = 343), and 5039 population controls. Dietary information on eating habits 2 years before participants' enrollment in the study was obtained using a validated food frequency questionnaire (FFQ). Odds ratios (ORs) and 95% confidence intervals (CI) were derived by unconditional logistic regression including recognized confounding factors.ResultsDietary GI was positively associated with the risk of prostate cancer (OR, 1.26 for the highest versus the lowest quartile). A higher dietary GL significantly increased the risk of colorectal (OR, 1.28), rectal (OR, 1.44) and pancreatic (OR, 1.41) cancers. No other significant associations were found.Conclusions Our findings suggest that a diet high in GI and GL is associated with increased risk of selected cancers.
    Annals of Oncology 07/2012; 24(1). DOI:10.1093/annonc/mds235 · 6.58 Impact Factor
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    ABSTRACT: Although previous studies have linked intake of sugars with incidence of cancer and other chronic diseases, its association with mortality remains unknown. We investigated the association of total sugars, added sugars, total fructose, added fructose, sucrose, and added sucrose with the risk of all-cause, cardiovascular disease, cancer, and other-cause mortality in the NIH-AARP Diet and Health Study. The participants (n = 353,751), aged 50-71 y, were followed for up to 13 y. Intake of individual sugars over the previous 12 mo was assessed at baseline by using a 124-item NIH Diet History Questionnaire. In fully adjusted models (fifth quartile compared with first quartile), all-cause mortality was positively associated with the intake of total sugars [HR (95% CI): 1.13 (1.06, 1.20); P-trend < 0.0001], total fructose [1.10 (1.04, 1.17); P-trend < 0.0001], and added fructose [1.07 (1.01, 1.13); P-trend = 0.005) in women and total fructose [1.06 (1.01, 1.10); P-trend = 0.002] in men. In men, a weak inverse association was found between other-cause mortality and dietary added sugars (P-trend = 0.04), sucrose (P-trend = 0.03), and added sucrose (P-trend = 0.006). Investigation of consumption of sugars by source showed that the positive association with mortality risk was confined only to sugars from beverages, whereas the inverse association was confined to sugars from solid foods. In this large prospective study, total fructose intake was weakly positively associated with all-cause mortality in both women and men, whereas added sugars, sucrose, and added sucrose intakes were inversely associated with other-cause mortality in men. In our analyses, intake of added sugars was not associated with an increased risk of mortality. The NIH-AARP Diet and Health Study was registered at as NCT00340015.
    American Journal of Clinical Nutrition 02/2014; 99(5). DOI:10.3945/ajcn.113.069369 · 6.92 Impact Factor
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    ABSTRACT: Sucrose is the principal carbohydrate in cane, beet, sweetener and drinking juice. It has many functional roles in foods preparation. It is used as a preservative, for flavor and for texture. It is an important source for supplying pure energy. However, a high-sucrose diet can increase the appetite, resulting in many detrimental effects upon metabolism of the body health. This chapter focuses on the sucrose effects that include its effect on body weight, lipid profile and blood glucose levels. This chapter also deals with the role of a high sucrose diet on antioxidant/oxidative stress in different tissues such as renal and cardiac tissue and emphasize in the significance of HSD in vitamin E and vascular antioxidant ability.
    Dietary Sugars : Chemistry, Edited by Victor R Preedy, 01/2012: chapter 44: pages 770-778; Royal Society of Chemistry., ISBN: 978-1-84973-370-0

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