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Dietary Insulin Load and Cancer Recurrence and Survival in Patients With Stage III Colon Cancer: Findings From CALGB 89803 (Alliance).
Morales-Oyarvide, V, Yuan, C, Babic, A, Zhang, S, Niedzwiecki, D, Brand-Miller, JC, Sampson-Kent, L, Ye, X, Li, Y, Saltz, LB, et al
Journal of the National Cancer Institute. 2019;(2):170-179
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Abstract
BACKGROUND Evidence suggests that diets inducing postprandial hyperinsulinemia may be associated with increased cancer-related mortality. The goal of this study was to assess the influence of postdiagnosis dietary insulin load and dietary insulin index on outcomes of stage III colon cancer patients. METHODS We conducted a prospective observational study of 1023 patients with resected stage III colon cancer enrolled in an adjuvant chemotherapy trial who reported dietary intake halfway through and six months after chemotherapy. We evaluated the association of dietary insulin load and dietary insulin index with cancer recurrence and survival using Cox proportional hazards regression adjusted for potential confounders; statistical tests were two-sided. RESULTS High dietary insulin load had a statistically significant association with worse disease-free survival (DFS), comparing the highest vs lowest quintile (adjusted hazard ratio [HR] = 2.77, 95% confidence interval [CI] = 1.90 to 4.02, Ptrend < .001). High dietary insulin index was also associated with worse DFS (highest vs lowest quintile, HR = 1.75, 95% CI = 1.22 to 2.51, Ptrend= .01). The association between higher dietary insulin load and worse DFS differed by body mass index and was strongest among patients with obesity (HR = 3.66, 95% CI = 1.88 to 7.12, Pinteraction = .04). The influence of dietary insulin load on cancer outcomes did not differ by mutation status of KRAS, BRAF, PIK3CA, TP53, or microsatellite instability. CONCLUSIONS Patients with resected stage III colon cancer who consumed a high-insulinogenic diet were at increased risk of recurrence and mortality. These findings support the importance of dietary management following resection of colon cancer, and future research into underlying mechanisms of action is warranted.
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Prediction of postprandial glycemia and insulinemia in lean, young, healthy adults: glycemic load compared with carbohydrate content alone.
Bao, J, Atkinson, F, Petocz, P, Willett, WC, Brand-Miller, JC
The American journal of clinical nutrition. 2011;(5):984-96
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Abstract
BACKGROUND Dietary glycemic load (GL; defined as the mathematical product of the glycemic index and carbohydrate content) is increasingly used in nutritional epidemiology. Its ability to predict postprandial glycemia and insulinemia for a wide range of foods or mixed meals is unclear. OBJECTIVE Our objective was to assess the degree of association between calculated GL and observed glucose and insulin responses in healthy subjects consuming isoenergetic portions of single foods and mixed meals. DESIGN In study 1, groups of healthy subjects consumed 1000-kJ portions of 121 single foods in 10 food categories. In study 2, healthy subjects consumed 2000-kJ servings of 13 mixed meals. Foods and meals varied widely in macronutrient content, fiber, and GL. Glycemia and insulinemia were quantified as area under the curve relative to a reference food (= 100). RESULTS Among the single foods, GL was a more powerful predictor of postprandial glycemia and insulinemia than was the available carbohydrate content, explaining 85% and 59% of the observed variation, respectively (P < 0.001). Similarly, for mixed meals, GL was also the strongest predictor of postprandial glucose and insulin responses, explaining 58% (P = 0.003) and 46% (P = 0.01) of the variation, respectively. Carbohydrate content alone predicted the glucose and insulin responses to single foods (P < 0.001) but not to mixed meals. CONCLUSION These findings provide the first large-scale, systematic evidence of the physiologic validity and superiority of dietary GL over carbohydrate content alone to estimate postprandial glycemia and insulin demand in healthy individuals. This trial was registered at ANZCTR.org as ACTRN12610000484044.