Pharmacopsychiatry 2020; 53(02): 84
DOI: 10.1055/s-0039-3403002
P2 Biomarker
Georg Thieme Verlag KG Stuttgart · New York

No association between major depression with and without childhood adversity and the stress hormone copeptin

M Kaczmarczyk
1   Charité Universitätsmedizin, Berlin, Germany
,
C Spitzer
1   Charité Universitätsmedizin, Berlin, Germany
,
K Wingenfeld
1   Charité Universitätsmedizin, Berlin, Germany
,
K Wiedemann
1   Charité Universitätsmedizin, Berlin, Germany
,
L Kühl
1   Charité Universitätsmedizin, Berlin, Germany
,
K Schultebraucks
1   Charité Universitätsmedizin, Berlin, Germany
,
C Otte
1   Charité Universitätsmedizin, Berlin, Germany
› Author Affiliations
Further Information

Publication History

Publication Date:
24 February 2020 (online)

 

Introduction Major depressive disorder (MDD) is associated with adverse childhood experiences (ACE) and with hypothalamic-pituitary-adrenal (HPA) axis dysregulation. Copeptin, a cleavage product in the synthesis of arginine vasopressin, has been identified as a marker of the non-specific stress response. Children with ACE exhibit higher levels of copeptin compared to healthy controls (Krogh et al., 2013). In young adults, symptoms of depression and copeptin plasma concentrations were significantly associated (Thomsen et al., 2019). Our study aimed to disentangle the effects of MDD and ACE on copeptin in adults.

Methods We recruited 94 women (mean age: 34.03, SD: 10.9): 23 women with MDD and ACE, 24 women with MDD without ACE, 22 women with ACE without MDD, and 25 healthy controls. ACE was defined as repeated sexual or physical abuse at least once a month over at least one year before the age of 18. For MDD, all women had to meet MDD criteria according to DSM-IV. Copeptin plasma levels were measured with a radioimmunoassay.

Results The four groups did not differ in demographic variables. We found a significant effect of body mass index (BMI) on the plasma level of copeptin (r = -.210; p < .045), such that increasing BMI was associated with decreasing plasma levels of copeptin. After controlling for BMI, we found no significant main effect of MDD (F(1,85) = .017; p = .895) or of ACE (F(1,85) = .490; p = .486). The interaction between MDD and ACE was not significant, either.

Conclusion Neither MDD nor ACE were associated with altered plasma copeptin levels. Our results go in line with Krogh et al., 2013 and extend their findings by including ACE as an influencing factor. Our results contrast with Coelho et al., 2016 and Thomsen et al., 2019, indicating that altered copeptin levels after ACE or in MDD are predominantly found in children and young adults.