Shannon K Crowley1, Todd K O'Buckley2, Crystal E Schiller1, Alison Stuebe3,4, A Leslie Morrow1,2,5, Susan S Girdler6. 1. Department of Psychiatry, CB#7175, UNC School of Medicine, Psychiatry Wing C, Chapel Hill, NC, 27599-7175, USA. 2. Bowles Center for Alcohol Studies, Chapel Hill, NC, 27599-7175, USA. 3. Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, Chapel Hill, NC, 27599-7175, USA. 4. Department of Maternal and Child Health, Gillings School of Global Public Health, Chapel Hill, NC, 27599-7175, USA. 5. Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599-7175, USA. 6. Department of Psychiatry, CB#7175, UNC School of Medicine, Psychiatry Wing C, Chapel Hill, NC, 27599-7175, USA. susan_girdler@med.unc.edu.
Abstract
RATIONALE: Anxiety during pregnancy has been linked to adverse maternal health outcomes, including postpartum depression (PPD). However, there has been limited study of biological mechanisms underlying behavioral predictors of PPD during pregnancy. OBJECTIVES: Considering the shared etiology of chronic stress amongst antenatal behavioral predictors, the primary goal of this pilot study was to examine associations among stress-related physiological factors (including GABA-ergic neurosteroids) and stress-related behavioral indices of anxiety during pregnancy. METHODS: Fourteen nulliparous women in their second trimester of a singleton pregnancy underwent speech and mental arithmetic stress, following a 2-week subjective and objective recording of sleep-wake behavior. RESULTS: Lower cortisol, progesterone, and a combined measure of ALLO + pregnanolone throughout the entire stressor protocol (area under the curve, AUC) were associated with greater negative emotional responses to stress, and lower cortisol AUC was associated with worse sleep quality. Lower adrenocorticotropic hormone was associated with greater anxious and depressive symptoms. Stress produced paradoxical reductions in cortisol, progesterone, and a combined measure of allopregnanolone + pregnanolone, while tetrahydrodeoxycorticosterone levels were elevated. CONCLUSIONS: These data suggest that cortisol, progesterone, and ALLO + pregnanolone levels in the second trimester of pregnancy are inversely related to negative emotional symptoms, and the negative impact of acute stress challenge appears to exert its effects by reducing these steroids to further promote negative emotional responses.
RATIONALE: Anxiety during pregnancy has been linked to adverse maternal health outcomes, including postpartum depression (PPD). However, there has been limited study of biological mechanisms underlying behavioral predictors of PPD during pregnancy. OBJECTIVES: Considering the shared etiology of chronic stress amongst antenatal behavioral predictors, the primary goal of this pilot study was to examine associations among stress-related physiological factors (including GABA-ergic neurosteroids) and stress-related behavioral indices of anxiety during pregnancy. METHODS: Fourteen nulliparous women in their second trimester of a singleton pregnancy underwent speech and mental arithmetic stress, following a 2-week subjective and objective recording of sleep-wake behavior. RESULTS: Lower cortisol, progesterone, and a combined measure of ALLO + pregnanolone throughout the entire stressor protocol (area under the curve, AUC) were associated with greater negative emotional responses to stress, and lower cortisol AUC was associated with worse sleep quality. Lower adrenocorticotropic hormone was associated with greater anxious and depressive symptoms. Stress produced paradoxical reductions in cortisol, progesterone, and a combined measure of allopregnanolone + pregnanolone, while tetrahydrodeoxycorticosterone levels were elevated. CONCLUSIONS: These data suggest that cortisol, progesterone, and ALLO + pregnanolone levels in the second trimester of pregnancy are inversely related to negative emotional symptoms, and the negative impact of acute stress challenge appears to exert its effects by reducing these steroids to further promote negative emotional responses.
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