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Glycemic index, glycemic load, and risk of digestive tract neoplasms: a systematic review and meta-analysis

¹ From the Cancer Epidemiology & Prevention Research Group, Centre for Clinical & Population Sciences, Queen's University Belfast, Mulhouse Building, Royal Victoria Hospital Site, Belfast, Northern Ireland (HGM, LJM, CRC, and MMC).

² Supported by a PhD studentship from the Department for Employment & Learning, Northern Ireland (to HGM).

³ Reprints not available. Address correspondence to HG Mulholland, Room 02040, Mulhouse Building, Royal Victoria Hospital Site, Grosvenor Rd, Belfast, Northern Ireland BT12 6BJ. E-mail: hmulholland04{at}qub.ac.uk.

Background: Habitual consumption of diets with a high glycemic index (GI) and a high glycemic load (GL) may influence cancer risk via hyperinsulinemia and the insulin-like growth factor axis.

Objective: The objective was to conduct a systematic review to assess the association between GI, GL, and risk of digestive tract cancers.

Design: Medline and Embase were searched for relevant publications from inception to July 2008. When possible, adjusted results from a comparison of cancer risk of the highest compared with the lowest category of GI and GL intake were combined by using random-effects meta-analyses.

Results: Cohort and case-control studies that examined the risk between GI or GL intake and colorectal cancer (n = 12) and adenomas (n = 2), pancreatic cancer (n = 6), gastric cancer (n = 2), and squamous-cell esophageal carcinoma (n = 1) were retrieved. Most case-control studies observed positive associations between GI and GL intake and these cancers. However, pooled cohort study results showed no associations between colorectal cancer risk and GI intake [relative risk (RR): 1.04; 95% CI: 0.92, 1.12; n = 7 studies] or GL intake (RR: 1.06; 95% CI: 0.95, 1.17; n = 8 studies). Furthermore, no significant associations were observed in meta-analyses of cohort study results of colorectal cancer subsites and GI and GL intake. Similarly, no significant associations emerged between pancreatic cancer risk and GI intake (RR: 0.99; 95% CI: 0.83, 1.19; n = 5 studies) or GL intake (RR: 1.01; 95% CI: 0.86, 1.19; n = 6 studies) in combined cohort studies.

Conclusions: The findings from our meta-analyses indicate that GI and GL intakes are not associated with risk of colorectal or pancreatic cancers. There were insufficient data available regarding other digestive tract cancers to make any conclusions about GI or GL intake and risk.