Vagal control moderates the association between endothelial function and PTSD symptoms in women with T2DM

Antonia V. Seligowski, Ida T. Fonkoue, Natalie C. Noble, Drew Dixon, Rachel Gluck, Ye Ji Kim, Abigail Powers, Thaddeus W.W. Pace, Tanja Jovanovic, Guillermo Umpierrez, Kerry J. Ressler, Arshed A. Quyyumi, Vasiliki Michopoulos, Charles F. Gillespie

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Background: Individuals with posttraumatic stress disorder (PTSD) are more likely to present with metabolic diseases such as type-2 diabetes mellitus (T2DM), and cardiovascular dysfunction has been implicated in this link. These diseases disproportionately affect women and individuals exposed to chronic environmental stressors (e.g., community violence, poverty). We examined associations among PTSD, cardiovascular indices, and metabolic function in highly trauma-exposed Black women with T2DM. Methods: Participants (N = 80) were recruited for a follow-up study of stress and T2DM as part of the Grady Trauma Project. PTSD symptoms were assessed with the Clinician Administered PTSD Scale (CAPS-IV). Cardiovascular indices included heart rate (HR), blood pressure (BP), respiratory sinus arrhythmia (RSA), and endothelial function (assessed via flow-mediated dilation; FMD). An oral glucose tolerance test was used as an indicator of metabolic function. Results: Of the cardiovascular indices, only FMD was significantly associated with PTSD symptoms (CAPS Avoidance symptoms; β = −0.37, p = .042), and glucose tolerance (β = −0.44, p = .019), controlling for age and body mass index. The association between FMD and PTSD Avoidance was moderated by RSA such that the effect of FMD was only significant at low levels of RSA (simple slopes β = −0.87, p = .004). Conclusions: Our results indicate that endothelial function is significantly related to PTSD and glucose tolerance, over and above other cardiovascular measures (HR, BP, RSA). Further, our results suggest that low RSA may be a risk factor for the link between poor endothelial function and PTSD in women with T2DM.

Original languageEnglish (US)
Article number100527
JournalBrain, Behavior, and Immunity - Health
Volume26
DOIs
StatePublished - Dec 2022

Bibliographical note

Funding Information:
This study was supported by the National Center for Advancing Translational Sciences of the National Institutes of Health under Award Number UL1TR002378. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. CFG also supported by MH099211, the Georgia Clinical and Translational Science Alliance (Georgia CTSA), the NIH National Centers for Research Resources (M01 RR00039), the Woodruff Health Sciences IT Division (UL1 TR000424) and the Emory University General Clinical Research Center at Grady Hospital. AVS supported by NIH K23MH125920 and AHA 20CDA35310031. ITF supported by NIH UL1TR002378, KL2TR002381 and UL1TR002494. KJR supported by NIH R21MH112956, P50MH115874, R01MH094757 and R01MH106595, the Frazier Foundation Grant for Mood and Anxiety Research, and Partners Healthcare Biobank.KJR has received consulting income from Alkermes, research support from NIH, Genomind and Brainsway, and he is on scientific advisory boards for Janssen and Verily, all of which is unrelated to the present work. CFG has received consulting income from Cohen Veterans Bioscience which is unrelated to the present work.

Funding Information:
This study was supported by the National Center for Advancing Translational Sciences of the National Institutes of Health under Award Number UL1TR002378 . The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. CFG also supported by MH099211 , the Georgia Clinical and Translational Science Alliance ( Georgia CTSA ), the NIH National Centers for Research Resources ( M01 RR00039 ), the Woodruff Health Sciences IT Division ( UL1 TR000424 ) and the Emory University General Clinical Research Center at Grady Hospital . AVS supported by NIH K23MH125920 and AHA 20CDA35310031 . ITF supported by NIH UL1TR002378 , KL2TR002381 and UL1TR002494 . KJR supported by NIH R21MH112956 , P50MH115874 , R01MH094757 and R01MH106595 , the Frazier Foundation Grant for Mood and Anxiety Research , and Partners Healthcare Biobank .

Publisher Copyright:
© 2022 The Authors

Keywords

  • Cardiovascular
  • Metabolic
  • PTSD
  • Trauma
  • Type-II diabetes Mellitus

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