TY - JOUR
T1 - Course of ante-and postnatal depressive symptoms related to mothers' HPA axis regulation
AU - Laurent, Heidemarie
AU - Goodman, Sherryl H.
AU - Stowe, Zachary N.
AU - Halperin, Meeka
AU - Khan, Faaiza
AU - Wright, Dorianne
AU - Nelson, Benjamin W.
AU - Jeffrey Newport, D.
AU - Ritchie, James C.
AU - Monk, Catherline
AU - Knight, Bettina
N1 - Funding Information:
D. Jeffrey Newport has received research support from Eli Lilly, Glaxo SmithKline, Janssen, the National Alliance for Research on Schizophrenia and Depression (NARSAD), the National Institutes of Health (NIH), Takeda Pharmaceuticals, and Wyeth. He has served on speakers’ bureaus and/or received honoraria from Astra-Zeneca, Eli Lilly, Glaxo SmithKline, Pfizer, and Wyeth. He has served on advisory boards for Glaxo SmithKline, Janssen, and Sage Therapeutics. He has never served as a consultant to any biomedical or pharmaceutical corporations. Neither he nor family members have ever held equity positions in biomedical or pharmaceutical corporations. Zachary N. Stowe has served as a study clinician for Janssen Pharmaceuticals. Bettina Knight has a son employed by GlaxoSmith Kline and has stock options in the company.
Funding Information:
D. Jeffrey Newport has received research support from Eli Lilly, Glaxo SmithKline, Janssen, the National Alliance for Research on Schizophrenia and Depression (NARSAD), the National Institutes of Health (NIH), Takeda Pharmaceuticals, and Wyeth. He has served on speakers' bureaus and/or received honoraria from Astra-Zeneca, Eli Lilly, Glaxo SmithKline, Pfizer, and Wyeth. He has served on advisory boards for Glaxo SmithKline, Janssen, and Sage Therapeutics. He has never served as a consultant to any biomedical or pharmaceutical corporations. Neither he nor family members have ever held equity positions in biomedical or pharmaceutical corporations. Zachary N. Stowe has served as a study clinician for Janssen Pharmaceuticals. Bettina Knight has a son employed by GlaxoSmith Kline and has stock options in the company.
Publisher Copyright:
© 2018 American Psychological Association.
PY - 2018/5
Y1 - 2018/5
N2 - Given high health costs of depression during pregnancy and the first postnatal year, it is important to understand mechanisms involved in the emergence and perpetuation of symptoms during this time. In a series of 2 studies, we aim to clarify bidirectional relations between mothers' physiological stress regulation-stress-related activation of the hypothalamic-pituitary-adrenal (HPA) axis-and their course of depressive symptoms. In Study 1, 230 pregnant women recruited from a women's mental health program gave 3 saliva samples in the context of psychosocial stress at 24, 30, and 36-weeks gestation. They self-reported depressive symptoms across the three trimesters of pregnancy and first year postpartum. Multilevel models revealed women with elevated salivary cortisol during pregnancy showed a course of escalating ante- and postnatal symptoms, implicating HPA hyperactivation as a precursor to worsening mood problems. In Study 2, 54 mothers from a community sample self-reported depressive symptoms at 3, 6, 12, and 18 months postnatal. At 18 months, they participated in a dyadic stress task with their infant and gave 4 saliva samples for cortisol assay. For mothers with a lifetime depression diagnosis, an escalating course of postnatal symptoms predicted a higher, flatter cortisol response profile. Together, the results of these studies suggest that for high-risk mothers, a trajectory of worsening depression may both follow from and give rise to neuroendocrine stress hyperactivation. These findings suggest greater attention is warranted to course of depressive symptoms across the ante- and postnatal period, rather than symptom levels at any given time, to characterize health risks.
AB - Given high health costs of depression during pregnancy and the first postnatal year, it is important to understand mechanisms involved in the emergence and perpetuation of symptoms during this time. In a series of 2 studies, we aim to clarify bidirectional relations between mothers' physiological stress regulation-stress-related activation of the hypothalamic-pituitary-adrenal (HPA) axis-and their course of depressive symptoms. In Study 1, 230 pregnant women recruited from a women's mental health program gave 3 saliva samples in the context of psychosocial stress at 24, 30, and 36-weeks gestation. They self-reported depressive symptoms across the three trimesters of pregnancy and first year postpartum. Multilevel models revealed women with elevated salivary cortisol during pregnancy showed a course of escalating ante- and postnatal symptoms, implicating HPA hyperactivation as a precursor to worsening mood problems. In Study 2, 54 mothers from a community sample self-reported depressive symptoms at 3, 6, 12, and 18 months postnatal. At 18 months, they participated in a dyadic stress task with their infant and gave 4 saliva samples for cortisol assay. For mothers with a lifetime depression diagnosis, an escalating course of postnatal symptoms predicted a higher, flatter cortisol response profile. Together, the results of these studies suggest that for high-risk mothers, a trajectory of worsening depression may both follow from and give rise to neuroendocrine stress hyperactivation. These findings suggest greater attention is warranted to course of depressive symptoms across the ante- and postnatal period, rather than symptom levels at any given time, to characterize health risks.
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U2 - 10.1037/abn0000348
DO - 10.1037/abn0000348
M3 - Article
C2 - 29745705
AN - SCOPUS:85046996297
SN - 0021-843X
VL - 127
SP - 404
EP - 416
JO - Journal of Abnormal Psychology
JF - Journal of Abnormal Psychology
IS - 4
ER -