Biological aging mediates the associations of metabolic score for insulin resistance with all‐cause and cardiovascular disease mortality among US adults: A nationwide cohort study

Jun 10, 2024Diabetes, obesity & metabolism

Biological aging links insulin resistance to death from all causes and heart disease in US adults

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Abstract

During a median follow-up of 9.17 years, 2818 deaths were observed, with 875 being CVD-specific.

Higher levels of insulin resistance, indicated by the metabolic score for insulin resistance (METS-IR), are associated with increased all-cause (hazard ratio 1.38) and cardiovascular disease (CVD) mortality (hazard ratio 1.52).
A nonlinear relationship exists between METS-IR and all-cause mortality, with levels above 41.02 μg/L positively correlated with increased risk of death.
METS-IR shows a linear positive relationship with CVD mortality.
Biological ageing markers, particularly phenotypic age, mediate a significant portion of the association between METS-IR and mortality, accounting for 51.32% of all-cause deaths and 41.77% of CVD-specific deaths.
Biological age also plays a role in mediating the relationship, with phenotypic age accounting for 21.33% of all-cause mortality and 15.88% of CVD mortality.

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AIM: To investigate the associations of metabolic score for insulin resistance (METS-IR) with all-cause and cardiovascular disease (CVD)-specific mortality and the potential mediating role of biological ageing.

METHODS: A cohort of 19 204 participants from the National Health and Nutrition Examination Survey (NHANES) 1999-2018 was recruited for this study. Cox regression models, restricted cubic splines, and Kaplan-Meier survival curves were used to determine the relationships of METS-IR with all-cause and CVD-specific mortality. Mediation analyses were performed to explore the possible intermediary role of biological ageing markers, including phenotypic age (PhenoAge) and biological age (BioAge).

RESULTS: During a median follow-up of 9.17 years, we observed 2818 deaths, of which 875 were CVD-specific. Multivariable Cox regression showed that the highest METS-IR level (Q4) was associated with increased all-cause (hazard ratio [HR] 1.38, 95% confidence interval [CI] 1.14-1.67) and CVD mortality (HR 1.52, 95% CI 1.10-2.12) compared with the Q1 level. Restricted cubic splines showed a nonlinear relationship between METS-IR and all-cause mortality. Only METS-IR above the threshold (41.02 μg/L) was positively correlated with all-cause death. METS-IR had a linear positive relationship with CVD mortality. In mediation analyses, we found that PhenoAge mediated 51.32% (p < 0.001) and 41.77% (p < 0.001) of the association between METS-IR and all-cause and CVD-specific mortality, respectively. For BioAge, the mediating proportions of PhenoAge were 21.33% (p < 0.001) and 15.88% (p < 0.001), respectively.

CONCLUSIONS: This study highlights the detrimental effects of insulin resistance, as measured by METS-IR, on all-cause and CVD mortality. Moreover, it underscores the role of biological ageing in mediating these associations, emphasizing the need for interventions targeting both insulin resistance and ageing processes to mitigate mortality risks in metabolic disorders.

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Biological aging mediates the associations of metabolic score for insulin resistance with all‐cause and cardiovascular disease mortality among US adults: A nationwide cohort study

Abstract

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