Dietary Glycemic Index and Load and the Risk of Type 2 Diabetes: Assessment of Causal Relations.
Plain language summary
It is generally accepted that certain diet and lifestyle choices contribute to a person’s risk of developing type 2 diabetes (T2D). In this meta-analysis, researchers set out to review previous studies and assess whether there is any evidence that the amount and type of carbohydrate (measured by Glycaemic Index (GI) and Glycaemic Load (GL)) in a person’s diet has a direct influence on their risk of developing T2D. The authors concluded with a high level of confidence that eating high GI and GL foods can lead to a higher risk of developing T2D. They suggest that nutrition advice that favours low GI and GL foods could produce significant cost savings for public healthcare.
While dietary factors are important modifiable risk factors for type 2 diabetes (T2D), the causal role of carbohydrate quality in nutrition remains controversial. Dietary glycemic index (GI) and glycemic load (GL) have been examined in relation to the risk of T2D in multiple prospective cohort studies. Previous meta-analyses indicate significant relations but consideration of causality has been minimal. Here, the results of our recent meta-analyses of prospective cohort studies of 4 to 26-y follow-up are interpreted in the context of the nine Bradford-Hill criteria for causality, that is: (1) Strength of Association, (2) Consistency, (3) Specificity, (4) Temporality, (5) Biological Gradient, (6) Plausibility, (7) Experimental evidence, (8) Analogy, and (9) Coherence. These criteria necessitated referral to a body of literature wider than prospective cohort studies alone, especially in criteria 6 to 9. In this analysis, all nine of the Hill's criteria were met for GI and GL indicating that we can be confident of a role for GI and GL as causal factors contributing to incident T2D. In addition, neither dietary fiber nor cereal fiber nor wholegrain were found to be reliable or effective surrogate measures of GI or GL. Finally, our cost-benefit analysis suggests food and nutrition advice favors lower GI or GL and would produce significant potential cost savings in national healthcare budgets. The high confidence in causal associations for incident T2D is sufficient to consider inclusion of GI and GL in food and nutrient-based recommendations.
Glycemic Index, Glycemic Load and Cancer Risk: An Updated Meta-Analysis.
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.
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.