Header

UZH-Logo

Maintenance Infos

The association between the acute psychobiological stress response in second trimester pregnant women, amniotic fluid glucocorticoids, and neonatal birth outcome


La Marca-Ghaemmaghami, Pearl; Dainese, Sara M; La Marca, Roberto; Zimmermann, Roland; Ehlert, Ulrike (2014). The association between the acute psychobiological stress response in second trimester pregnant women, amniotic fluid glucocorticoids, and neonatal birth outcome. Developmental Psychobiology, 56(4):734-747.

Abstract

The underlying biological mechanism of prenatal stress in humans is poorly understood, but maternal cortisol (F) excess seems to play an important role. In pregnant rats, acute stress causes an up-regulation of placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), an enzyme present throughout the body (e.g., placenta, salivary glands) that inactivates F to cortisone (E), thereby protecting the fetus from maternal F overexposure. Whether acute stress influences human 11β-HSD2 is unclear. We aimed to explore the association between the maternal stress reactivity and amniotic fluid F, E, and the E/(E + F) ratio as a marker of fetoplacental 11β-HSD2. The predictive value of all markers for birth outcome was investigated. We examined 34 healthy pregnant women undergoing amniocentesis, which served as a standardized, real-life stressor. F, E, and E/(E + F) were determined from a single aliquot of amniotic fluid, and from saliva samples collected repeatedly. Subjects filled out state questionnaires repeatedly and were re-examined in a control condition after notification of a normal amniocentesis result. During amniocentesis, psychological stress, salivary F (SalF), and salivary E (SalE) increased significantly, whereas SalE/(E + F) decreased. The SalF reactivity was positively associated with amniotic E, while SalE/(E + F) was inversely associated with amniotic E/(E + F). SalF and SalE predicted lower and SalE/(E + F) higher birth weight. Psychological and amniotic fluid variables were unrelated to birth outcome. Findings indicate that maternal F is inactivated to E in the human fetoplacental unit during acute stress. Increased 11β-HSD2 activity within the maternal salivary glands following acute stress may mirror further stress protective mechanisms worthwhile investigating. © 2013 Wiley Periodicals, Inc. Dev Psychobiol.

Abstract

The underlying biological mechanism of prenatal stress in humans is poorly understood, but maternal cortisol (F) excess seems to play an important role. In pregnant rats, acute stress causes an up-regulation of placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), an enzyme present throughout the body (e.g., placenta, salivary glands) that inactivates F to cortisone (E), thereby protecting the fetus from maternal F overexposure. Whether acute stress influences human 11β-HSD2 is unclear. We aimed to explore the association between the maternal stress reactivity and amniotic fluid F, E, and the E/(E + F) ratio as a marker of fetoplacental 11β-HSD2. The predictive value of all markers for birth outcome was investigated. We examined 34 healthy pregnant women undergoing amniocentesis, which served as a standardized, real-life stressor. F, E, and E/(E + F) were determined from a single aliquot of amniotic fluid, and from saliva samples collected repeatedly. Subjects filled out state questionnaires repeatedly and were re-examined in a control condition after notification of a normal amniocentesis result. During amniocentesis, psychological stress, salivary F (SalF), and salivary E (SalE) increased significantly, whereas SalE/(E + F) decreased. The SalF reactivity was positively associated with amniotic E, while SalE/(E + F) was inversely associated with amniotic E/(E + F). SalF and SalE predicted lower and SalE/(E + F) higher birth weight. Psychological and amniotic fluid variables were unrelated to birth outcome. Findings indicate that maternal F is inactivated to E in the human fetoplacental unit during acute stress. Increased 11β-HSD2 activity within the maternal salivary glands following acute stress may mirror further stress protective mechanisms worthwhile investigating. © 2013 Wiley Periodicals, Inc. Dev Psychobiol.

Statistics

Citations

11 citations in Web of Science®
3 citations in Scopus®
Google Scholar™

Altmetrics

Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Obstetrics
06 Faculty of Arts > Institute of Psychology
Dewey Decimal Classification:150 Psychology
610 Medicine & health
Uncontrolled Keywords:Psychotherapeutisches Zentrum des Psychologischen Instituts UZH
Language:English
Date:2014
Deposited On:12 Jul 2013 14:26
Last Modified:05 Apr 2016 16:51
Publisher:Wiley-Blackwell
ISSN:0012-1630
Publisher DOI:https://doi.org/10.1002/dev.21142
PubMed ID:23775363

Download

Full text not available from this repository.
View at publisher

TrendTerms

TrendTerms displays relevant terms of the abstract of this publication and related documents on a map. The terms and their relations were extracted from ZORA using word statistics. Their timelines are taken from ZORA as well. The bubble size of a term is proportional to the number of documents where the term occurs. Red, orange, yellow and green colors are used for terms that occur in the current document; red indicates high interlinkedness of a term with other terms, orange, yellow and green decreasing interlinkedness. Blue is used for terms that have a relation with the terms in this document, but occur in other documents.
You can navigate and zoom the map. Mouse-hovering a term displays its timeline, clicking it yields the associated documents.

Author Collaborations