Dietary carbohydrate, glycemic index, and glycemic load and the risk of colorectal cancer in the BCDDP cohort
Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, 1300 South Second Street, Suite 300, Minneapolis, MN 55454, USA. Cancer Causes and Control
(Impact Factor: 2.74).
11/2007; 18(8):853-63. DOI: 10.1007/s10552-007-9030-8
There is considerable support for associations between insulin and IGF-I levels and colorectal cancer. Diet may relate to colorectal cancer through this mechanism, for example, diets high in glycemic index, glycemic load and/or carbohydrate are hypothesized to increase insulin load and the risk of insulin resistance, hyperinsulinemia. Case-control studies support this hypothesis, but prospective cohorts have had mixed results.
In the Breast Cancer Detection Demonstration Project (BCDDP) follow-up cohort of 45,561 women, we used Cox proportional hazards regression to assess the distribution of 490 incident cases of colorectal cancer ascertained during 8.5 years of follow-up across quintiles of carbohydrate intake, glycemic index, and glycemic load. We also stratified by combined BMI and physical activity levels.
We found reductions in colorectal cancer risk for diets high in carbohydrate (RR for Q5 vs. Q1 = 0.70, 95% CI: 0.50-0.97) and glycemic index (0.75, 95% CI: 0.56-1.00), and no significant association for glycemic load (0.91, 95% CI: 0.70-1.20). Inverse associations were weakest in normal weight active persons. The inverse association for glycemic index was strongest for the portion from dairy food.
These results do not support an association between diets high in carbohydrate, glycemic index or glycemic load and colorectal cancer.
Available from: Sara Gandini
- "Population M, F Franceschi et al, 2001 (53) Italy CC 1953 4154 Hospital M, F Levi et al, 2002 (54) Switzerland CC 323 661 Hospital M, F Terry et al, 2003 (63) Canada Cohort NBSS 616 49124 F Higginbotham et al, 2004 (64) USA Cohort WHS 174 38451 F Michaud et al, 2005 (20) USA Cohort HPFS, NHSI 1809 131349 M, F Larsson et al, 2007 (65) Sweden Cohort SMC 870 61433 F McCarl et al, 2006 (40) USA Cohort IWHS 954 35197 F Murtaugh et al, 2006 (29) USA CC KPMCP 1698 1861 Population M, F Strayer et al, 2007 (55) USA Cohort BCDDP 490 45561 F Weijenberg et al, 2007 (56) Netherlands Cohort NCS 1643 120852 M, F Pancreas Michaud et al, 2002 (36) USA Cohort NHS 180 88802 F Johnson et al, 2005 (42) USA Cohort IWHS 190 34699 F Silvera et al, 2005 (66) "
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ABSTRACT: Factors linked to glucose metabolism play an important role in the development of cancers, and both glycemic index (GI) and glycemic load (GL) have been investigated as potential etiologic factors.
A meta-analysis was performed to explore the association between GI and GL and cancer risk from published studies.
A comprehensive, systematic bibliographic search of the medical literature was conducted to identify relevant studies. Case-control and cohort studies published before October 2007 that reported cancer risk estimates for GI and GL were included. Pooled relative risks (RRs) were estimated for breast, colorectal, endometrial, and pancreatic cancer.
Thirty-nine studies were included in the meta-analysis. The interquantile ranges of GL were significantly wider in case-control studies, most of which were conducted in European countries, than in cohort studies. Cohort studies that presented lower ranges of GL also reported lower risk estimates. Overall, both GL and GI were significantly associated with a greater risk of colorectal (summary RR = 1.26; 95% CI: 1.11, 1.44 and RR = 1.18; 95% CI: 1.05, 1.34, respectively) and endometrial (RR = 1.36; 95% CI: 1.14, 1.62 and RR = 1.22; 95% CI: 1.01, 1.49) cancer than of breast and pancreatic cancer. There was, however, a significant between-study heterogeneity for colorectal cancer (P < 0.0001). The association between GL and breast cancer disappeared when publication bias was taken into account. No association was found for pancreatic cancer.
This comprehensive meta-analysis of GI and GL and cancer risk suggested an overall direct association with colorectal and endometrial cancer.
American Journal of Clinical Nutrition 07/2008; 87(6):1793-801. · 6.77 Impact Factor
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ABSTRACT: Evidence implicating hyperinsulinemia and insulin resistance in the etiology of colorectal cancer suggests that a diet characterized
by a high glycemic index and load may increase the risk of this disease, but previous studies have yielded inconsistent results.
We assessed the association between intake of total carbohydrates, sugars, fiber, and the glycemic index (GI) and glycemic
load (GL) of individual diets, and risk of developing colorectal cancer among 158,800 participants in the Women’s Health Initiative
(WHI). We used a GI/GL database developed specifically for the WHI food-frequency questionnaire. Over an average of 7.8years
of follow-up, 1,476 incident cases of colorectal cancer were identified. Cox proportional hazards models were used to estimate
the association between dietary factors classified by quintiles and risk of colorectal cancer, with adjustment for covariates.
Total carbohydrate intake, glycemic index, glycemic load, and intake of sugars and fiber showed no association with colorectal
cancer. Analyses by cancer subsite also yielded null results, with the exception of a borderline positive association between
glycemic load and rectal cancer (HR for the highest versus lowest quintile 1.84, 95% confidence interval 0.95–3.56, p for trend 0.05). Analyses stratified by tertiles of body mass index and physical activity showed no evidence of effect modification
by these factors. Results of this large study do not support of a role of a diet characterized by high glycemic index or load
in colorectal carcinogenesis in postmenopausal women.
Cancer Causes and Control 12/2008; 19(10):1291-1298. DOI:10.1007/s10552-008-9200-3 · 2.74 Impact Factor
Available from: Seamus J Murphy
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ABSTRACT: ObjectiveTo examine the association between dietary glycemic index (GI), glycemic load (GL), total carbohydrate, sugars, starch, and
fiber intakes and the risk of reflux esophagitis, Barrett’s esophagus, and esophageal adenocarcinoma.
MethodsIn an all-Ireland study, dietary information was collected from patients with esophageal adenocarcinoma (n=224), long-segment Barrett’s esophagus (n=220), reflux esophagitis (n=219), and population-based controls (n=256). Multiple logistic regression analysis examined the association between dietary variables and disease risk by tertiles
of intake and as continuous variables, while adjusting for potential confounders.
ResultsReflux esophagitis risk was positively associated with starch intake and negatively associated with sugar intake. Barrett’s
esophagus risk was significantly reduced in people in the highest versus the lowest tertile of fiber intake (OR 0.44 95%CI
0.25–0.80). Fiber intake was also associated with a reduced risk of esophageal adenocarcinoma, as was total carbohydrate intake
(OR 0.45 95%CI 0.33–0.61 per 50g/d increase). However, an increased esophageal adenocarcinoma risk was detected per 10 unit
increase in GI intake (OR 1.42 95%CI 1.07–1.89).
ConclusionsOur findings suggest that fiber intake is inversely associated with Barrett’s esophagus and esophageal adenocarcinoma risk.
Esophageal adenocarcinoma risk is inversely associated with total carbohydrate consumption but positively associated with
high GI intakes.
Cancer Causes and Control 04/2008; 20(3):279-288. DOI:10.1007/s10552-008-9242-6 · 2.74 Impact Factor
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