Negative Affect-Related Autonomic Arousal Mediates the Association between Baroreflex Dysfunction and Insulin Resistance in Non-Diabetic Young Adults.

Published

Journal Article

Autonomic dysfunction, in particular under-regulation of heart rate (HR) by the baroreflex, is implicated in development of insulin resistance (IR). According to reactivity hypothesis, sympathetic response to stressors may be more sensitive at predicting IR than baroreceptor sensitivity (BRS), a baseline measure of baroreflex functioning. Using ecological momentary assessment (EMA) of negative affect coupled with minute-to-minute HR and heart-rate variability (HRV) monitoring, we examined whether negative affect (NA)-related autonomic arousal mediates the association of BRS with IR. At baseline, BRS was measured, and fasting serum glucose and insulin levels were collected from 178 young adults (18-39 years old), from which homeostasis model assessment of IR (HOMA-IR) and beta-cell functioning (HOMA %B) were derived. Participants subsequently underwent one day of Holter HR and HRV monitoring while reporting negative affect levels via EMA. Multilevel modeling was used to assess the associations of momentary negative affect with HR and low- (LF) and high-frequency (HF) HRV during the 5-minute intervals following each EMA reading. Structural equation modeling was then used to determine whether individual differences in these associations mediated the association of BRS with IR, measured by HOMA-IR, HOMA %B, and insulin levels. As predicted, BRS was negatively associated with the IR (β = -.17, p = .024). However, NA-related autonomic arousal mediated their association, accounting for 56% of the covariance between BRS and IR. Not only do these results provide support for reactivity hypothesis, they reveal a potential point of intervention in the treatment of affective dysregulation.

Full Text

Duke Authors

Cited Authors

  • Dennis, PA; Neal, JM; Travis, E; Watkins, LL; Calhoun, PS; Dennis, MF; Beckham, JC

Published Date

  • October 2019

Published In

Volume / Issue

  • 33 / 4

Start / End Page

  • 243 - 253

PubMed ID

  • 31666757

Pubmed Central ID

  • 31666757

International Standard Serial Number (ISSN)

  • 0269-8803

Digital Object Identifier (DOI)

  • 10.1027/0269-8803/a000226

Language

  • eng

Conference Location

  • United States