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Physiological stress response in postpartum women with obsessive–compulsive disorder: A pilot study

Authors
Journal
Psychoneuroendocrinology
0306-4530
Publisher
Elsevier
Publication Date
Volume
36
Issue
1
Identifiers
DOI: 10.1016/j.psyneuen.2010.04.014
Keywords
  • Obsessive–Compulsive Disorder
  • Postpartum
  • Stress
  • Cortisol
  • Alpha-Amylase
  • Cold Pressor
Disciplines
  • Biology
  • Medicine

Abstract

Summary Postpartum onset and/or worsening of anxiety disorders, particularly of obsessive–compulsive disorder (OCD) are scarcely reported in the literature although frequently observed in the clinical setting. These obsessions and compulsions focus primarily on the newborn and create immense distress in the mother. Research on the stress response in postpartum mothers is limited and the neuroendocrine correlates of OCD in particular are unclear. The aim of this pilot study was to compare the physiological and subjective responses to a physical stressor, the Cold Pressor Test (CPT), in postpartum women with OCD in comparison to healthy controls. Saliva samples were collected during the CPT and analyzed for cortisol and alpha-amylase (AA). Statistical analyses demonstrated a significant main effect of time with the CPT eliciting an increase in cortisol ( p = 0.002) and alpha-amylase ( p = 0.02) with a lot of variance in cortisol and AA stress responses in women suffering from OCD; in addition, postpartum women with OCD had higher cortisol levels compared to controls (main effect of group t: p = 0.001). Overall, women with OCD reported experiencing more subjective stress and anxiety ( p = 0.006 and p = 0.002, respectively) and found the CPT more stressful than healthy postpartum women ( p = 0.05). This is the first study investigating the subjective and endocrine stress responses in postpartum women suffering from OCD. Our findings demonstrate cortisol hyperactivity and higher CPT-related subjective stress ratings in postpartum OCD women but no group difference in adrenergic activity and in the magnitude of the stress-related endocrine increases following a physical stressor.

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