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Articles

Effect of Dietary Insulinemia on All-Cause and Cause-Specific Mortality: Results From a Cohort Study

, , , &
Pages 407-413 | Received 09 Oct 2018, Accepted 16 Jul 2019, Published online: 25 Nov 2019
 

Abstract

Background: Insulin response to diet might predict the risk of mortality; however, the evidence is limited. We prospectively evaluated the link between the dietary hyperinsulinemia index (DHI) and dietary insulin resistance index (DIRI) with all-cause and cause-specific (cardiovascular disease [CVD] and cancer) mortality.

Methods: The National Health and Nutrition Examination Survey (1999–2010) database was used. Vital status through December 31, 2011, was ascertained. Stepwise linear regression models consisted of 39 macro/micronutrients applied, and fasting plasma C-peptide for the DHI and triglyceride/high-density lipoprotein cholesterol ratio (TG/HDL-C) for the DIRI were used. Adjusted Cox regression (followed by propensity score matching) was performed to determine the hazard ratios (HRs) and 95% confidence interval (95% CIs).

Results: Overall, 22,246 participants were included (mean age = 47.8 years; 48.9% men). There was a significant increasing risk of mortality across the quartiles of DHI, i.e., participants with a highest score of DHI (Q4) had a greater risk of all-cause (HR: 1.21, 95% CI: 1.17–1.26), CVD (HR: 1.17, 95% CI: 1.07–1.29), and cancer (HR: 1.15, 95% CI: 1.08–1.23) mortality compared with the first quartile (Q1; p < 0.001 for all comparisons). Similarly, participants in the highest DIRI quartile (Q4) had 23% and 31% higher risk of all-cause and CVD mortality, respectively, compared with Q1, while the association between cancer mortality and DIRI was non-significant (HR: 0.88, 95% CI: 0.35–2.61).

Conclusions: These findings highlight, for the first time, the detrimental role (association) of insulinemia and insulin resistance potential of diet on all-cause and cause-specific mortality. Our findings support the role of C-peptide and TG/HDL-C ratio as cost-effective and practical biomarkers in clinical settings. These results need to be confirmed to establish their implications.

Acknowledgments

None.

Disclosure statement

NK has given talks, attended conferences, and participated in trials sponsored by Amgen, Angelini, AstraZeneca, Boehringer Ingelheim, MSD, Novartis, Novo Nordisk, Sanofi, and WinMedica. DPM has given talks and attended conferences sponsored by Amgen, AstraZeneca, and Libytec. The other authors have no conflict of interest to declare.

Funding

None.

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