HCP Live
Contagion LiveCGT LiveNeurology LiveHCP LiveOncology LiveContemporary PediatricsContemporary OBGYNEndocrinology NetworkPractical CardiologyRheumatology Netowrk

Arterial Stiffness Could Cause Insulin Resistance, Dyslipidemia

The largest study of its kind to date provides evidence suggesting a causal relationship between cfPWV and cIMT in adolescence with increased insulin resistance and dyslipidemia in young adulthood.

Data from an analysis of the Avon Longitudinal Study of Parents and Children (ALSPAC) suggests arterial stiffness in adolescence could cause insulin resistance and dyslipidemia in young adulthood.

The study, which investigators suggest is the largest of its kind to date, provide an overview of the associations between arterial stiffness, as measured by carotid-femoral pulse wave velocity (cfPWV), and carotid item-media thickness (cIMT) progression on the risk of dysglycemia, insulin resistance, and dyslipidemia.

“Our novel findings are clinically significant for pediatric and adolescent health, in that preventing and treating insulin resistance, young-onset type 2 diabetes mellitus, and dyslipidemia may necessitate strategies to concurrently reduce arterial stiffness, particularly from adolescence,” said Andrew Agbaje, MD, MPH, a physician and clinical epidemiologist at the University of Eastern Finland, in a statement.

As the diabetes epidemic continues to balloon in the US and abroad, understanding factors associated with increased risk of incident type 2 diabetes could prove beneficial in alleviating the burden of diabetes on individuals and health systems. Citing recent evidence suggesting arterial stiffness could be a novel risk factor in the causal pathway of type 2 diabetes, Agbaje and a team of investigators sought to further investigate potential associations using data from the ALSPAC birth cohort.

A cohort of more than 14,901 children surviving beyond 1 year, the ALSPAC cohort contained data from 3862 participants with data from cfPWV and cIMT assessments performed at 17.7 years. Using this cohort, investigators designed their study to assess temporal causal longitudinal associations of cfPWV and cIMT with fasting LDL-C, HDL-C, triglyceride, glucose, insulin, insulin resistance, and pancreatic beta-cell function at the 24.5-year follow-up.

Compared to their male counterparts, women included in the study had higher fasting total cholesterol, HDL-C, and insulin but lower glucose at both the 17.7-year and 24.5-year follow-up. Investigators noted 9.2%, 41.6%, 24.5%, 7.5%, and 10.3% of 3862 participants were at risk of high glucose, insulin, LDL, triglyceride, and low HDL, respectively, at 24.5 years.

Upon analysis, results suggested a higher cfPWV at 17.7 years was associated with increased insulin at 24.5 years, which investigators pointed out was slightly attenuated after adjustment for covariates. Higher cIMT at 17.7 years was associated with lower insulin at 24.5 years after adjustment for covariates.

In mixed-effect models, results indicated the 7-year progression of cfPWV was directly associated with an increase in triglycerides. Further analysis demonstrated cIMT progression was associated with increases in LDL-C, triglycerides, and glucose. In cross-lagged models suggested higher cfPWV at 17.7 years was associated with higher insulin (β=.06, SE, 0.12, P=.014), HOMA of insulin resistance, and HOMA-percent pancreatic beta-cell function at 24.5 years. However, in the same models, insulin, HOMA of insulin resistance, and HOMA-percent pancreatic beta-cell function at 17.7 years were not associated with cfPWV at 24.5 years.

Investigators pointed out higher cIMT at 17.7 years was associated with reduced insulin HOMA of insulin resistance, and HOMA-percent pancreatic beta-cell function at 24.5 years, but not vice versa. Additionally, higher glucose at 17.7 years was associated with higher cfPWV and cIMT at 24.5 years.

This study, “Effect of Arterial Stiffness and Carotid Intima-Media Thickness Progression on the Risk of Dysglycemia, Insulin Resistance, and Dyslipidemia: a Temporal Causal Longitudinal Study,” was published in Hypertension.