Postpartum depression (PPD) adversely affects the health and well being of many new mothers, their infants, and their families. A comprehensive understanding of biopsychosocial precursors to PPD is needed to solidify the current evidence base for best practices in translation. We conducted a systematic review of research published from 2000 through 2013 on biological and psychosocial factors associated with PPD and postpartum depressive symptoms. Two hundred fourteen publications based on 199 investigations of 151,651 women in the first postpartum year met inclusion criteria. The biological and psychosocial literatures are largely distinct, and few studies provide integrative analyses. The strongest PPD risk predictors among biological processes are hypothalamic-pituitary-adrenal dysregulation, inflammatory processes, and genetic vulnerabilities. Among psychosocial factors, the strongest predictors are severe life events, some forms of chronic strain, relationship quality, and support from partner and mother. Fully integrated biopsychosocial investigations with large samples are needed to advance our knowledge of PPD etiology.

Background: Postpartum depression (PPD) poses a major global public health challenge. PPD is the most common complication associated with childbirth and exerts harmful effects on children. Although hundreds of PPD studies have been published, we lack accurate global or national PPD prevalence estimates and have no clear account of why PPD appears to vary so dramatically between nations. Accordingly, we conducted a meta-analysis to estimate the global and national prevalence of PPD and a meta-regression to identify economic, health, social, or policy factors associated with national PPD prevalence. Methods: We conducted a systematic review of all papers reporting PPD prevalence using the Edinburgh Postnatal Depression Scale. PPD prevalence and methods were extracted from each study. Random effects meta-analysis was used to estimate global and national PPD prevalence. To test for country level predictors, we drew on data from UNICEF, WHO, and the World Bank. Random effects meta-regression was used to test national predictors of PPD prevalence. Findings: 291 studies of 296284 women from 56 countries were identified. The global pooled prevalence of PPD was 17.7% (95% confidence interval: 16.6–18.8%), with significant heterogeneity across nations (Q = 16,823, p = 0.000, I² = 98%), ranging from 3% (2–5%) in Singapore to 38% (35–41%) in Chile. Nations with significantly higher rates of income inequality (R² = 41%), maternal mortality (R² = 19%), infant mortality (R² = 16%), or women of childbearing age working ≥40 h a week (R² = 31%) have higher rates of PPD. Together, these factors explain 73% of the national variation in PPD prevalence. Interpretation: The global prevalence of PPD is greater than previously thought and varies dramatically by nation. Disparities in wealth inequality and maternal-child-health factors explain much of the national variation in PPD prevalence.

OBJECTIVES: Breastfeeding rates differ among racial/ethnic groups in the United States. Our aim was to test whether racial/ethnic disparities in demographic characteristics, hospital use of infant formula, and family history of breastfeeding mediated racial/ethnic gaps in breastfeeding outcomes. METHODS: We analyzed data from the Community and Child Health Network study (N = 1636). Breastfeeding initiation, postnatal intent to breastfeed, and breastfeeding duration were assessed postpartum. Hierarchical linear modeling was used to estimate relative odds of breastfeeding initiation, postnatal intent, and duration among racial/ethnic groups and to test the candidate mediators of maternal age, income, household composition, employment, marital status, postpartum depression, preterm birth, smoking, belief that “breast is best,” family history of breastfeeding, in-hospital formula introduction, and WIC participation. RESULTS: Spanish-speaking Hispanic mothers were most likely to initiate (91%), intend (92%), and maintain (mean duration, 17.1 weeks) breastfeeding, followed by English-speaking Hispanic mothers (initiation 90%, intent 88%; mean duration, 10.4 weeks) and white mothers (initiation 78%, intent 77%; mean duration, 16.5 weeks); black mothers were least likely to initiate (61%), intend (57%), and maintain breastfeeding (mean duration, 6.4 weeks). Demographic variables fully mediated disparities between black and white mothers in intent and initiation, whereas demographic characteristics and in-hospital formula feeding fully mediated breastfeeding duration. Family breastfeeding history and demographic characteristics helped explain the higher breastfeeding rates of Hispanic mothers relative to white and black mothers. CONCLUSIONS: Hospitals and policy makers should limit in-hospital formula feeding and consider family history of breastfeeding and demographic characteristics to reduce racial/ethnic breastfeeding disparities.

Mothers in numerous species exhibit heightened aggression in defense of their young. This shift typically coincides with the duration of lactation in nonhuman mammals, which suggests that human mothers may display similarly accentuated aggressiveness while breast feeding. Here we report the first behavioral evidence for heightened aggression in lactating humans. Breast-feeding mothers inflicted louder and longer punitive sound bursts on unduly aggressive confederates than did formula-feeding mothers or women who had never been pregnant. Maternal aggression in other mammals is thought to be facilitated by the buffering effect of lactation on stress responses. Consistent with the animal literature, our results showed that while lactating women were aggressing, they exhibited lower systolic blood pressure than did formula-feeding or never-pregnant women while they were aggressing. Mediation analyses indicated that reduced arousal during lactation may disinhibit female aggression. Together, our results highlight the contributions of breast feeding to both protecting infants and buffering maternal stress.