Presented at the Society for Maternal Fetal Medicine Annual Meeting, Dallas, TX, February 2018.

Alison M. Stuebe1,3, Samantha Meltzer-Brody2, Brenda Pearson2, Cheryl Walker2, Karen Grewen2

1Department of Obstetrics and Gynecology, 2Department of Psychiatry, 3Department of Maternal and Child Health,
Gillings School of Global Public Health, University of North Carolina, Chapel Hill, North Carolina

Objective: Perinatal depression (PND) affects 1 in 8 women, making it the most common complication of childbirth. Hypothalamic Pituitary Adrenal (HPA) axis dysregulation has been implicated in the pathogenesis of PND, indexed by a blunted Cortisol (CRT) response to Adrenocorticotropic Hormone (ACTH). We hypothesized PND would be associated with dysregulated stress reactivity during lab stressors, indexed by loss of expected associations between ACTH and CRT.

Study Design: Women intending to breastfeed were recruited in the 3rd trimester for an ongoing longitudinal study. Past or current major depressive disorder or anxiety disorders were assessed via Structured Clinical Interview at enrollment; women with a history or current diagnosis of depression or anxiety were classified as high risk. At two months postpartum, dyads attended a lab visit. Following peripheral IV placement, women breastfed their infants and then participated in the Trier Social Stress Test (TSST), a standardized social stressor that includes a speech task and a math task. Blood samples for ACTH and CRT were collected prior to feeding, 10 minutes after feeding, during the speech and math tasks, and at 10, 20 and 30 minutes of recovery. We used repeated measures analysis to quantify associations between risk status and CRT and ACTH during the TSST, and we used linear regression to quantify the extent to which high risk status modified associations between ACTH at time j and cortisol at time j+1. P values <0.05 were considered statistically significant.

Results: ACTH and CRT data were available for 114 women, of whom 69 were high risk for PND and 45 were low risk. In repeated measures analysis (figure), high risk women had higher ACTH levels during the speech and math tasks (p<.05) and lower CRT levels during the recovery (p<.05) than low risk women. When we quantified associations between ACTH at time j and CRT at time j+1, we found that risk status modified this association: higher ACTH during the speech and math tasks, as well as during recovery, was associated with higher CRT among low-risk women, but not among high risk women (p for interaction < .05, figure).

Conclusion: We found a blunted association between ACTH and CRT among women with a history or current diagnosis of depression or anxiety. These findings support our hypothesis that the HPA axis is dysregulated in perinatal depression.