TY - JOUR
T1 - Mother-infant dyadic dysregulation and postpartum depressive symptoms in low-income Mexican-origin women
AU - Luecken, Linda
AU - Crnic, Keith
AU - Gonzales, Nancy
AU - Winstone, Laura K.
AU - Somers, Jennifer A.
N1 - Funding Information:
Funded by the National Institute of Mental Health (R01 MH083173-01). The funding source had no role in study design, collection, analysis, interpretation, or writing of the report; or in the decision to submit the article for publication. We thank the mothers and infants for their participation; Anne Mauricio, Kirsten Letham, and Monica Gutierrez for their assistance with data collection and management; Dr. Dean Coonrod and the Maricopa Integrated Health Systems for their assistance with recruitment; and the interviewers for their commitment and dedication to this project.
Publisher Copyright:
© 2018 Elsevier B.V.
PY - 2019/10
Y1 - 2019/10
N2 - The current study evaluated a mechanistic pathway by which prenatal stress increases the risk of postpartum depressive (PPD) symptoms via observed dyadic emotional, behavioral, and attentional dysregulation and associated cortisol responses during mother-infant interactions. Methods: Participants included 322 low-income Mexican American mother-infant dyads. Depressive symptoms, economic hardship, and negative life events were assessed at a prenatal visit. Dysregulation in dyadic (mother-infant) interactions and cortisol responses to mother-infant interaction were evaluated at 12 weeks after the birth. Twenty-four weeks after the birth, PPD symptoms were predicted from prenatal stress (negative life events and economic hardship) and prenatal depressive symptoms, mediated through dyadic dysregulation and maternal and infant cortisol responses. Results: More negative life events in the prenatal period predicted more dyadic dysregulation at 12 weeks postpartum. Dyadic dysregulation and economic hardship predicted elevated 12-week infant cortisol total response and reactivity, and higher total infant cortisol response predicted higher maternal PPD symptoms at 24 weeks. Maternal cortisol response was not associated with dyadic dysregulation, either form of prenatal stress, or PPD symptoms. Conclusion: The results indicate the salience of early psychosocial processes and mother-infant relationship challenges for subsequent maternal affective well-being.
AB - The current study evaluated a mechanistic pathway by which prenatal stress increases the risk of postpartum depressive (PPD) symptoms via observed dyadic emotional, behavioral, and attentional dysregulation and associated cortisol responses during mother-infant interactions. Methods: Participants included 322 low-income Mexican American mother-infant dyads. Depressive symptoms, economic hardship, and negative life events were assessed at a prenatal visit. Dysregulation in dyadic (mother-infant) interactions and cortisol responses to mother-infant interaction were evaluated at 12 weeks after the birth. Twenty-four weeks after the birth, PPD symptoms were predicted from prenatal stress (negative life events and economic hardship) and prenatal depressive symptoms, mediated through dyadic dysregulation and maternal and infant cortisol responses. Results: More negative life events in the prenatal period predicted more dyadic dysregulation at 12 weeks postpartum. Dyadic dysregulation and economic hardship predicted elevated 12-week infant cortisol total response and reactivity, and higher total infant cortisol response predicted higher maternal PPD symptoms at 24 weeks. Maternal cortisol response was not associated with dyadic dysregulation, either form of prenatal stress, or PPD symptoms. Conclusion: The results indicate the salience of early psychosocial processes and mother-infant relationship challenges for subsequent maternal affective well-being.
KW - Cortisol
KW - Dyadic dysregulation
KW - Postpartum depression
KW - Prenatal stress
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U2 - 10.1016/j.biopsycho.2018.10.016
DO - 10.1016/j.biopsycho.2018.10.016
M3 - Article
C2 - 30391479
AN - SCOPUS:85056257320
VL - 147
JO - Biological Psychology
JF - Biological Psychology
SN - 0019-493X
M1 - 107614
ER -