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.

BackgroundPostpartum 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.MethodsWe 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.Findings291 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.InterpretationThe 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.

The SARS-CoV-2 immune response in human milk has not yet been examined, though protecting infants and young children from COVID-19 is critical for limiting community transmission, and preventing serious illness and death. Here, milk samples from 8 COVID-19-recovered and 7 COVID-19-suspected donors were tested for antibody (Ab) binding to the SARS-CoV-2 Spike protein. All samples exhibited significant specific IgA reactivity to the full Spike, while 80% exhibited significant IgA and secretory (s)Ab binding to the receptor binding domain (RBD). Additionally, 67% of samples exhibited IgG and/or IgM binding to RBD. IgA and sAb titers were highly correlated, indicating most IgA to be sIgA. Overall, these data indicate that a robust sIgA-dominant SARS-CoV-2 Ab response in human milk after infection should be expected in a significant majority of individuals. Further research is highly warranted to determine Ab functionality, and the potential for exploiting extracted milk sIgA for therapeutic use.

on behalf of the Community Child Health Research Network abstract 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. Dr McKinney conceptualized the research questions, helped design the data collection instruments, conducted data collection, helped conduct the analyses, and drafted the initial and revised manuscripts; Dr Hahn-Holbrook helped conceptualize the research questions, draft the initial and revised manuscripts, and conduct the analyses; Dr Chase-Lansdale critically reviewed the initial manuscript; Dr Ramey helped design the data collection instruments, coordinated and supervised data collection, and critically reviewed the initial and revised manuscripts; Mrs Krohn helped design the data collection instruments and critically reviewed the initial manuscript; Mrs Vance helped design the data collection instruments, coordinated and supervised data collection, NIH

Mothers who breastfeed typically exhibit lower levels of depressive symptomatology than mothers who do not. However, very few studies have investigated the directionality of this relationship. Of the prospective studies published, all but one focus exclusively on whether maternal depression reduces rates of subsequent breastfeeding. This study again examines this relationship, but also the reverse—that breastfeeding might predict lower levels of later depression. Using multilevel modeling, we investigated the relationship between breastfeeding and self-reported depressive symptomatology in 205 women followed prenatally and at 3, 6, 12, and 24 months after birth. Consistent with previous research, women with prenatal depressive symptomatology weaned their infants 2.3 months earlier, on average, than women without such symptomatology. We also found, however, that women who breastfed more frequently at 3 months postpartum showed greater subsequent declines in depressive symptomatology over time compared to women who breastfed less frequently, resulting in lower absolute levels of depressive symptoms by 24 months postpartum, controlling for important confounds. In sum, these findings are consistent with a bidirectional association between breastfeeding and depression, with prenatal depression predicting less breastfeeding soon after birth and breastfeeding predicting declines in maternal depression up to 2 years after birth. We discuss mechanisms that could potentially explain these associations and avenues for future research.

SARS-CoV-2, commonly termed COVID-19 for the illness it causes, has infected >3.2 million people, including >220,000 deaths. Human milk IgG originates mainly from blood, therefore a SARS-CoV-2-reactive antibody (Ab) response in milk would be expected (1). However, IgG comprises only ~2% of milk Ab, with most milk Abs originating from mucosa-associated

Objective Breastfeeding is linked to lower rates of childhood obesity. Human milk contains cortisol, known to regulate glucose storage and metabolism. We aimed to test the hypothesis that early exposure to cortisol in human breast milk helps to modulate infant BMI trajectories over the first two years of life. Methods Growth curve modeling was used to examine whether infant exposure to cortisol in human milk at 3 months predicted changes in child body mass index percentile (BMIP) at 6, 12, and 24 months of age in 51 breastfeeding mother-child pairs. Results Infants exposed to higher milk cortisol levels at 3 months were less likely to exhibit BMIP gains over the first 2 years of life, compared to infants exposed to lower milk cortisol. By age 2, infants exposed to higher milk cortisol levels had lower BMIPs then infants exposed to lower milk cortisol. Milk cortisol was a stronger predictor of BMIP change in girls than boys. Conclusions Cortisol exposure through human milk may help to program metabolic functioning and childhood obesity risk. Further, because infant formula contains only trace amounts of glucocorticoids, this finding represents a novel biological pathway through which breastfeeding may protect against later obesity.

Three decades of research point to both biological and psychological risk factors for postpartum depression, but very little research integrates the two. This study bridged this gap by testing whether prenatal social support predicted depressive symptoms at 8 weeks postpartum in a multiethnic sample of 210 women and whether the stress hormone placental corticotropin-releasing hormone (pCRH), measured at 19, 29, and 37 weeks’ gestation, mediated this relationship. We found that prenatal family support predicted significantly fewer depressive symptoms postpartum and more gradual increases in pCRH from 29 to 37 weeks’ gestation. Furthermore, steeper increases in pCRH during this same period predicted more depressive symptoms postpartum. Finally, these changes in pCRH in late pregnancy mediated the relationship between prenatal family support and postpartum depressive symptoms. These results suggest that social and biological risk factors for postpartum depressive symptoms are intertwined and move us closer to an integrated biopsychosocial understanding of postpartum depression.