Associations of trauma exposure and post-traumatic stress disorder with the activity of the renin-angiotensin-aldosterone-system in the general population.


Journal

Psychological medicine
ISSN: 1469-8978
Titre abrégé: Psychol Med
Pays: England
ID NLM: 1254142

Informations de publication

Date de publication:
04 2019
Historique:
pubmed: 19 6 2018
medline: 15 5 2020
entrez: 19 6 2018
Statut: ppublish

Résumé

Previous studies suggested that exposure to traumatic events during childhood and adulthood and post-traumatic stress disorder (PTSD) are associated with a dysregulation of different neuroendocrine systems. However, the activity of the renin-angiotensin-aldosterone-system (RAAS) in relation to trauma/PTSD has been largely neglected. Traumatization, PTSD, and plasma concentrations of renin and aldosterone were measured in 3092 individuals from the general population. Subgroups according to the status of traumatization ('without trauma'; 'trauma, without PTSD', 'PTSD') were formed and compared regarding renin and aldosterone concentrations. Additionally, we calculated the associations between the number of traumata, renin, and aldosterone concentrations. Finally, associations of PTSD with renin/aldosterone levels were controlled for the number of traumata ('trauma load'). Levels of renin, but not aldosterone, were increased in traumatized persons without PTSD (p = 0.02) and, even stronger, with PTSD (p < 0.01). Moreover, we found a dose-response relation between the number of traumata and renin levels (β = 0.065; p < 0.001). Regression analyses showed PTSD as a significant predictor of renin (β = 0.38; p < 0.01). This effect was only slightly attenuated when controlled for trauma load (β = 0.32; p < 0.01). Our results suggest that traumatization has lasting and cumulative effects on RAAS activity. Finding elevated renin levels in PTSD independent from trauma load supports the concept of PTSD as a disorder with specific neuroendocrine characteristics. Alternatively, elevated renin levels in traumatized persons may increase the risk for developing PTSD. Our findings contribute to explain the relationship between traumatic stress/PTSD and physical disorders.

Sections du résumé

BACKGROUND
Previous studies suggested that exposure to traumatic events during childhood and adulthood and post-traumatic stress disorder (PTSD) are associated with a dysregulation of different neuroendocrine systems. However, the activity of the renin-angiotensin-aldosterone-system (RAAS) in relation to trauma/PTSD has been largely neglected.
METHODS
Traumatization, PTSD, and plasma concentrations of renin and aldosterone were measured in 3092 individuals from the general population. Subgroups according to the status of traumatization ('without trauma'; 'trauma, without PTSD', 'PTSD') were formed and compared regarding renin and aldosterone concentrations. Additionally, we calculated the associations between the number of traumata, renin, and aldosterone concentrations. Finally, associations of PTSD with renin/aldosterone levels were controlled for the number of traumata ('trauma load').
RESULTS
Levels of renin, but not aldosterone, were increased in traumatized persons without PTSD (p = 0.02) and, even stronger, with PTSD (p < 0.01). Moreover, we found a dose-response relation between the number of traumata and renin levels (β = 0.065; p < 0.001). Regression analyses showed PTSD as a significant predictor of renin (β = 0.38; p < 0.01). This effect was only slightly attenuated when controlled for trauma load (β = 0.32; p < 0.01).
CONCLUSIONS
Our results suggest that traumatization has lasting and cumulative effects on RAAS activity. Finding elevated renin levels in PTSD independent from trauma load supports the concept of PTSD as a disorder with specific neuroendocrine characteristics. Alternatively, elevated renin levels in traumatized persons may increase the risk for developing PTSD. Our findings contribute to explain the relationship between traumatic stress/PTSD and physical disorders.

Identifiants

pubmed: 29909779
pii: S0033291718001496
doi: 10.1017/S0033291718001496
doi:

Substances chimiques

Aldosterone 4964P6T9RB
Renin EC 3.4.23.15

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

843-851

Auteurs

Jan Terock (J)

Department of Psychiatry and Psychotherapy,University Medicine Greifswald,Greifswald,Germany.

Anke Hannemann (A)

Institute of Clinical Chemistry and Laboratory Medicine, University Medicine Greifswald,Greifswald,Germany.

Deborah Janowitz (D)

Department of Psychiatry and Psychotherapy,University Medicine Greifswald,Greifswald,Germany.

Harald J Freyberger (HJ)

Department of Psychiatry and Psychotherapy,University Medicine Greifswald,Greifswald,Germany.

Stephan B Felix (SB)

Department of Internal Medicine B,University Medicine Greifswald,Greifswald,Germany.

Marcus Dörr (M)

Department of Internal Medicine B,University Medicine Greifswald,Greifswald,Germany.

Matthias Nauck (M)

Institute of Clinical Chemistry and Laboratory Medicine, University Medicine Greifswald,Greifswald,Germany.

Henry Völzke (H)

Institute for Community Medicine, University Medicine Greifswald,Greifswald,Germany.

Hans J Grabe (HJ)

Department of Psychiatry and Psychotherapy,University Medicine Greifswald,Greifswald,Germany.

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Classifications MeSH