Plain language summary
This 2019 meta-analysis is an update of an earlier 2015 study on the relationship between high Glycemic Index (GI) and Glycemic load (GL) diets and cancer risk. Twenty new epidemiological reports were added to the original seventy-five studies covering a total of 169,00 cancer cases. The theory is that elevated insulin levels, triggered by a high GI diet, increase bioactive chemicals which promote cancer development by inhibiting cell apoptosis and stimulating cell proliferation. This study collated cancers into 3 subgroups of hormonal cancers (breast, endometrium, ovary and prostate), digestive tract cancers (cancers, stomach, colorectum and pancreas) and other (lung, bladder and kidney). The combined results showed that the risk ratio for hormonal-related cancers and GI/GL were modestly elevated but not significant except for a possible moderate positive association between GL and endometrial cancer (RR1.12). There was a positive significant association between high GI intake and colorectal cancer risk (RR 1.20) but not with the other digestive-tract cancers. A high GI was associated with small increased risks of bladder (RR 1.25) and kidney (RR 1.16) cancers. The researchers conclude that the high number of studies and cancer types included provide high statistical power. Although the results show only moderate association this may be relevant at population level given the high incidence of cancers.
Abstract
Diets high in glycemic index (GI) and glycemic load (GL) have been related to an increased risk of selected cancers, but additional quantification is required. We updated a systematic review and meta-analysis published in 2015 to May 2019 to provide quantitative information on GI/GL and cancer risk. Relative risks (RR) and the corresponding 95 % confidence intervals (CI) for the highest versus the lowest categories of GI and GL were extracted from selected studies and pooled using random-effects models. Twenty reports (>22,000 cancer cases) have become available after January 2015, and 15 were added to the meta-analyses by cancer sites, which considered a total of 88 investigations. The five additional reports were reviewed, but not included in the meta-analyses, since data were inadequate to be pooled. For hormone-related cancers, summary RRs for the highest versus lowest GI and GL intakes were moderately increased. They ranged from 1.04 (breast) to 1.12 (endometrium) for GI and from 1.03 (prostate) to 1.22 (ovary) for GL, of borderline significance. High GI was associated with small increased risks of colorectal (summary RR for GI: 1.20, 95% CI, 1.07-1.34-GL: 1.09, 95% CI, 0.97-1.22, 19 studies), bladder (GI: 1.25, 95% CI, 1.11-1.41-GL: 1.10, 95% CI, 0.85-1.42, four studies) and kidney cancers (GI: 1.16, 95% CI, 1.02-1.32-GL: 1.14, 95% CI, 0.81-1.60, five studies). GL was not significantly related to those cancer sites. Stomach, prostate and lung cancers were not associated with GI and GL. The present analysis, based on an updated comprehensive evaluation of the epidemiological literature, indicates moderate unfavorable effects of high versus low GI on colorectal, and possibly bladder and kidney cancers, and a possible moderate positive association between GL and endometrial cancer.
Methodological quality
Jadad score
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3
Allocation concealment
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Not applicable
