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The association of dietary glycemic index and glycemic load on ovarian cancer incidence and survival in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) cohort

Principal Investigator
Name
Jennifer Mongiovi
Degrees
MS
Institution
University at Buffalo
Position Title
Pre-doctoral Trainee
Email
About this CDAS Project
Study
PLCO (Learn more about this study)
Project ID
PLCO-427
Initial CDAS Request Approval
Dec 11, 2018
Title
The association of dietary glycemic index and glycemic load on ovarian cancer incidence and survival in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) cohort
Summary
In order to keep up with the high demand for energy, cancer cells reprogram their energy production from respiration to aerobic glycolysis (1). This process results in an overall lower yield of adenosine triphosphate but at rate 10-100 times faster than typical oxidation (1, 2). Increased glucose uptake, a hallmark of cancer (1), is required to sustain proliferation, migration, invasion, and recurrence (3). Increasing availability of glucose may provide cancer cells with additional resources to sustain tumor metabolism. In vitro, hyperglycemia been shown to lead to increased levels of glucose metabolism and expression of genes associated with proliferation, invasion, and migration (4).
Hyperglycemia is a state of excess glucose concentration in the blood (5) that occurs when the body either cannot use insulin properly or has too little available (3). Glucose is obtained through carbohydrate consumption. Foods vary on amount and nature of carbohydrates, which in turn influences the extent of the postprandial glycemic response (6). The glycemic index (GI) is a scale used to quantify this anticipated response and is measured as the area under the curve (AUC) 2 hours after consuming 50g of carbohydrate from a particular food compared to the AUC for the same amount of carbohydrate from either sugar or white bread (6-8). Consumption of high GI foods, such potatoes and white bread (6), can lead to increased blood glucose, insulin, glycosylated hemoglobin, and C-peptide excretion following consumption (9, 10). To better estimate the actual rise in blood glucose, glycemic load (GL) factors in a food’s percent energy from carbohydrates and serving size (6). GI is a measure of carbohydrate quality while GL is a measure of both quality and quantity (11, 12).
Adopting a low GI and GL diet has been encouraged for management of several chronic diseases including diabetes, cardiovascular disease, and some cancers (13). This may be especially true for hormone-related and digestive tract cancers which have been shown to have a moderate increase in risk associated with high GI/GL diets (12). Additional evidence suggests a connection between lowered blood glucose and remission of malignancy (14). For ovarian cancer (OvCa), hyperglycemia was associated with increased growth rate of tumors and decreased overall survival in mouse models (15). Glucose levels may also have prognostic value among OvCa patients where higher levels were associated with shorter survival times (16).
To our knowledge, there is a limited number of epidemiologic studies regarding GI/GL and OvCa in the United States, where OvCa is the fifth most common cause of female cancer death (17). Using data from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial cohort, we aim to assess the association between GI/GL and OvCa incidence/ mortality. We hypothesize that higher GI/GL will be associated with greater incident and fatal disease compared to lower GI/GL. This analysis will strengthen the current evidence on GI/GL and OvCa (12, 15, 18-20) and provide further insight on whether pre-diagnostic diet may play a role in the development and prognosis of OvCa.
Aims

1. To determine the association between GI and GL on OvCa incidence.
2. To determine the association between GI and GL on OvCa mortality.

References:
1. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144(5):646-74.
2. Liberti MV, Locasale JW. The Warburg Effect: How Does it Benefit Cancer Cells? Trends in biochemical sciences. 2016;41(3):211-8.
3. Duan W, Shen X, et al. Hyperglycemia, a neglected factor during cancer progression. BioMed research international. 2014;2014:461917.
4. Masur K, Vetter C, et al. Diabetogenic glucose and insulin concentrations modulate transcriptome and protein levels involved in tumour cell migration, adhesion and proliferation. British journal of cancer. 2011;104(2):345-52.
5. Ryu TY, Park J, Scherer PE. Hyperglycemia as a risk factor for cancer progression. Diabetes & metabolism journal. 2014;38(5):330-6.
6. Ludwig DS. The glycemic index: physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. Jama. 2002;287(18):2414-23.
7. Jenkins DJ, Wolever TM, et al. Glycemic index of foods: a physiological basis for carbohydrate exchange. Am J Clin Nutr. 1981;34(3):362-6.
8. Ebbeling CB, Ludwig DS. Treating obesity in youth: should dietary glycemic load be a consideration? Advances in pediatrics. 2001;48:179-212.
9. Miller JC. Importance of glycemic index in diabetes. Am J Clin Nutr. 1994;59(3 Suppl):747s-52s.
10. Jenkins DJ, Wolever TM, et al. Metabolic effects of a low-glycemic-index diet. Am J Clin Nutr. 1987;46(6):968-75.
11. Foster-Powell K, et al. International table of glycemic index and glycemic load values: 2002. Am J Clin Nutr. 2002;76(1):5-56.
12. Turati F, Galeone C, et al. High glycemic index and glycemic load are associated with moderately increased cancer risk. Molecular nutrition & food research. 2015;59(7):1384-94.
13. Kitahara CM. Low-glycemic load diets: how does the evidence for prevention of disease measure up? Journal of the American Dietetic Association. 2010;110(12):1818-9.
14. Krone CA, Ely JT. Controlling hyperglycemia as an adjunct to cancer therapy. Integrative cancer therapies. 2005;4(1):25-31.
15. Kellenberger LD, Petrik J. Hyperglycemia promotes insulin-independent ovarian tumor growth. Gynecologic oncology. 2018;149(2):361-70.
16. Lamkin DM, Spitz DR, et al. Glucose as a prognostic factor in ovarian carcinoma. Cancer. 2009;115(5):1021-7.
17. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2018. CA: A Cancer Journal for Clinicians. 2018;68(1):7-30.
18. Nagle CM, Kolahdooz F, et al. Carbohydrate intake, glycemic load, glycemic index, and risk of ovarian cancer. Annals of oncology : official journal of the European Society for Medical Oncology. 2011;22(6):1332-8.
19. Silvera SA, Jain M, et al. Glycaemic index, glycaemic load and ovarian cancer risk: a prospective cohort study. Public health nutrition. 2007;10(10):1076-81.
20. Augustin LS, Polesel J, et al. Dietary glycemic index, glycemic load and ovarian cancer risk: a case-control study in Italy. Annals of oncology : official journal of the European Society for Medical Oncology. 2003;14(1):78-84.

Collaborators

Kirsten Moysich, MS, PhD (Roswell Park Comprehensive Care Center)
Susan McCann, PhD, RD (Roswell Park Comprehensive Care Center)
Jo Freudenheim, PhD (University at Buffalo)

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