Postpartum depression (PPD) is a common, morbid condition that affects 10-15% of mothers. Recent work implicates reductions in oxytocin, a neuropeptide that plays a central role in mothering and social behavior, in the pathophysiology of this disorder. The proposed study will use lactation as a novel physiologic challenge to determine the extent to which low oxytocin mediates associations between PPD and impaired development of the mother-infant dyad. The long-term goal of this research is to identify mother-infant dyads at risk of PPD and implement targeted interventions to address their personal neuroendocrine vulnerabilities, thereby improving the health of mother and child. The objective here is to define the role of oxytocin and dysregulated stress reactivity in the psychobiology of PPD and impaired dyadic development, indexed by maternal sensitivity, infant emotional regulation, and insecure attachment. The central hypothesis is that PPD is associated with reduced oxytocin and maternal HPA axis dysregulation, indexed by loss of expected associations between ACTH and cortisol. These changes reduce maternal sensitivity, impairing dyadic development and increasing risk for insecure attachment. This hypothesis has been formulated based on published literature and preliminary data showing diminished oxytocin and dysregulation of the HPA axis among women with PPD symptoms. The rationale for this work is that as the underlying mechanisms of PPD are identified, interventions can be developed to target at-risk dyads and diminish PPD and its sequelae for mother and infant. Guided by strong preliminary data, the central hypothesis will be tested by pursuing three specific aims: 1. Use lactation as a physiologic challenge to quantify the extent to which PPD reduces oxytocin, dysregulates stress reactivity, and diminishes maternal sensitivity; 2. Use standardized mother-infant interactions to determine the extent to which PPD and reduced maternal sensitivity impair development of infant emotional regulation and increase risk for insecure attachment; 3. Determine the extent to which diminished maternal oxytocin and reduced sensitivity mediate associations between PPD, impaired infant emotional regulation, and insecure attachment.
These aims will be achieved through a longitudinal study of 200 mother-infant dyads spanning late pregnancy through 12 months postpartum, half with a history of depression and/or anxiety and half with no psychiatric history, confirmed by diagnostic interview. Mother-infant dyads will be assessed during visits to the Mother-Infant Biobehavioral Lab. The approach is innovative, because this project will use lactation as a physiologic challenge to quantify intersections among maternal oxytocin physiology, stress reactivity, care giving, emotional regulation, and attachment, thereby shedding light on both maternal mental health and infant emotional development. The proposed research is significant, because it is expected to define the role of oxytocin in PPD and impaired dyadic development. Ultimately, such knowledge has the potential to inform novel therapies to prevent PPD and reduce its sequelae for mother and child.
The proposed research is relevant to public health because it will define the role of a potentially modifiable mechanism underlying postpartum depression, a common and morbid condition that impacts the health of more than 400,000 mother-infant dyads every year. The project is relevant to NICHD's mission because it will inform new strategies to support optimal dyadic development, ensuring that all children have the chance to achieve their full potential for healthy and productive lives.
|Wouk, Kathryn; Stuebe, Alison M; Meltzer-Brody, Samantha (2017) Postpartum Mental Health and Breastfeeding Practices: An Analysis Using the 2010-2011 Pregnancy Risk Assessment Monitoring System. Matern Child Health J 21:636-647|
|Crowley, Shannon K; O'Buckley, Todd K; Schiller, Crystal E et al. (2016) Blunted neuroactive steroid and HPA axis responses to stress are associated with reduced sleep quality and negative affect in pregnancy: a pilot study. Psychopharmacology (Berl) 233:1299-310|
|Stuebe, Alison M (2015) Does breastfeeding prevent the metabolic syndrome, or does the metabolic syndrome prevent breastfeeding? Semin Perinatol 39:290-5|
|Stuebe, Alison (2015) Associations Among Lactation, Maternal Carbohydrate Metabolism, and Cardiovascular Health. Clin Obstet Gynecol 58:827-39|
|Cox, E Q; Stuebe, A; Pearson, B et al. (2015) Oxytocin and HPA stress axis reactivity in postpartum women. Psychoneuroendocrinology 55:164-72|
|Stuebe, Alison M; Horton, Bethany J; Chetwynd, Ellen et al. (2014) Prevalence and risk factors for early, undesired weaning attributed to lactation dysfunction. J Womens Health (Larchmt) 23:404-12|