2. Dysregulation of psychoneuroimmune function in women symptomatic of postpartum depression

Abstract

500,000 U.S. women develop postpartum depression (PPD) annually. Although psychosocial risks are known, the underlying biology remains unclear. We hypothesized that exaggerated inflammation early after childbirth would increase PPD risk, alone or synergistically with abnormal cortisol secretion, indicating dysregulation of psychoneuroimmune function. Plasma pro- and anti-inflammatory cytokines were measured on Days 7 and 14, and Months 1, 2, 3, and 6 after childbirth. Saliva was collected 5 times the day preceding blood draws for cortisol area under the curve (AUC). Depressive symptoms were measured using the Edinburgh Postpartum Depression Survey (EPDS) and evaluated in light of cytokines and cortisol, independently and together. 152 women completed the EPDS; 18% scored symptomatic of depression (EPDS > 10) by 6-months. Cortisol AUC was higher in symptomatic women on Day 14 ( p = .017). Bivariate analysis indicated change in IFNγ/IL10 (pro- to anti-inflammatory cytokine) ratio on Day 14 from Day 7 and Day 14 cortisol AUC were important predictors of depressive symptoms. Multiple logistic regression indicated joint effects of cortisol AUC and change in IFN/IL10 ratio were highly significant in predicting symptoms. A unit increase in Day 14 IFN/IL10 was associated with 91% increase in odds (OR: 1.91, p = 0.036) of depressive symptoms while a 20-min increase in AUC was associated with a 33% increase in odds (cortisol AUC OR: 1.333, p = 0.012). Findings suggest dysregulation of psychoneuroimmune function is a biological risk for PPD.