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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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Association between cholesterol intake and pancreatic cancer risk: evidence from a meta-analysis.
Chen, H, Qin, S, Wang, M, Zhang, T, Zhang, S
Scientific reports. 2015;:8243
Abstract
Quantification of the association between the intake of cholesterol and risk of pancreatic cancer is still conflicting. We therefore conducted a meta-analysis to summarize the evidence from epidemiological studies of cholesterol intake and the risk of pancreatic cancer. Pertinent studies were delivered by PubMed and Web of Knowledge issued through April of 2014. A random effects model was used to process the data for analysis. Sensitivity analysis and publication bias were conducted. Dose-response relationship was assessed by restricted cubic spline and variance-weighted least squares regression analysis. With 4513 pancreatic cases exemplified, 16 articles were applied in the meta-analysis. Pooled results suggest that cholesterol intake level was significantly associated with the risk of pancreatic cancer [summary relative risk (RR) = 1.371, 95%CI = 1.155-1.627, I(2) = 58.2%], especially in America [summary RR = 1.302, 95%CI = 1.090-1.556]. A linear dose-response relation was attested that the risk of pancreatic cancer rises by 8% with 100 mg/day of cholesterol intake. [summary RR = 1.08, 95% CI = 1.04-1.13]. In conclusion, our analysis suggests that a high intake of cholesterol might increase the risk of pancreatic cancer, especially in America.
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Diets high in carbohydrate may not be appropriate for rs328 G carriers with the metabolic syndrome.
Zhang, S, Ma, Y, Guo, H, Wan, W, Xue, K
Asia Pacific journal of clinical nutrition. 2015;(3):546-54
Abstract
The objective of this study was to test how the genetic polymorphisms located within the lipoprotein lipase (LPL) locus would modulate the relationship between a diet high in carbohydrate and insulin resistance related traits in metabolic syndrome adults. A one year nutritional intervention study focusing on education to increase dietary intake of whole grain, vegetable and fruit, and to reduce the intake of sodium, simple sugar and dietary fat (especially cooking oil and pork lard) was conducted. Two districts in Shanghai, China were randomly selected to be the intervention and control group, and patients (n=235) with metabolic syndrome within these two districts were selected based on a multistage sampling method. Fasting glucose was reduced in rs328 CC homozygotes (p=0.028) but not G carriers (p=0.686) within the intervention group. Also an ancillary study with greater statistical power by combining the baseline measurements across both the intervention and control groups was conducted to test the cross-sectional statistical interactions between carbohydrate/fat and lipoprotein lipase genotypes for homeostasis model assessment of insulin resistance/insulin/fasting glucose. Increased carbohydrate intakes were positively associated with homeostasis model assessment of insulin resistance and insulin in rs328 G carriers but not CC homozygotes (p for interaction was 0.025). These results indicate that diet high in carbohydrate may not be suitable for metabolic syndrome rs328 G carriers, calling for the development of personalized dietary intervention for metabolic syndrome subjects.