Infant adrenocortical reactivity and behavioral functioning: Relation to early exposure to maternal intimate partner violence

Alytia A. Levendosky, G. Anne Bogat, Joseph S. Lonstein, Cecilia Martinez-Torteya, Maria Muzik, Douglas A. Granger, Alexander Von Eye

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

© 2015 Taylor & Francis. Prenatal stress negatively affects fetal development, which in turn may affect infant hypothalamic-pituitary-adrenal (HPA) axis regulation and behavioral functioning. We examined effects of exposure to a traumatic stressor in families [intimate partner violence (IPV)] on both infants HPA axis reactivity to stress and their internalizing and externalizing behaviors. Infants (n = 182, 50% girls, x age = 11.77 months) were exposed to a laboratory challenge task designed to induce frustration and anger (i.e. arm restraint). Saliva samples were taken pre-task and 20 and 40 min post-task and then assayed for cortisol. Mothers reported on their pregnancy and postpartum IPV history, current mental health, substance use and their infants behaviors. Structural equation modeling revealed that prenatal, but not postnatal, IPV was independently associated with infant cortisol reactivity and problem behavior. Maternal mental health predicted infant behavioral functioning but not infant HPA axis reactivity. These findings are consistent with the prenatal programing hypothesis; that is, early life stress affects later risk and vulnerability for altered physiological and behavioral regulation.
Original languageEnglish
Pages (from-to)37-44
Number of pages8
JournalStress
DOIs
Publication statusPublished - 2 Jan 2016
Externally publishedYes

Fingerprint

Maternal Exposure
Hydrocortisone
Mental Health
Embryonic and Fetal Development
Infant Behavior
Frustration
Anger
Fetal Development
Saliva
Psychological Stress
Postpartum Period
Intimate Partner Violence
History
Mothers
Pregnancy

All Science Journal Classification (ASJC) codes

  • Physiology
  • Neuropsychology and Physiological Psychology
  • Endocrine and Autonomic Systems
  • Psychiatry and Mental health
  • Behavioral Neuroscience

Cite this

Levendosky, Alytia A. ; Anne Bogat, G. ; Lonstein, Joseph S. ; Martinez-Torteya, Cecilia ; Muzik, Maria ; Granger, Douglas A. ; Von Eye, Alexander. / Infant adrenocortical reactivity and behavioral functioning: Relation to early exposure to maternal intimate partner violence. In: Stress. 2016 ; pp. 37-44.
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Infant adrenocortical reactivity and behavioral functioning: Relation to early exposure to maternal intimate partner violence. / Levendosky, Alytia A.; Anne Bogat, G.; Lonstein, Joseph S.; Martinez-Torteya, Cecilia; Muzik, Maria; Granger, Douglas A.; Von Eye, Alexander.

In: Stress, 02.01.2016, p. 37-44.

Research output: Contribution to journalArticle

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AU - Muzik, Maria

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AU - Von Eye, Alexander

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AB - © 2015 Taylor & Francis. Prenatal stress negatively affects fetal development, which in turn may affect infant hypothalamic-pituitary-adrenal (HPA) axis regulation and behavioral functioning. We examined effects of exposure to a traumatic stressor in families [intimate partner violence (IPV)] on both infants HPA axis reactivity to stress and their internalizing and externalizing behaviors. Infants (n = 182, 50% girls, x age = 11.77 months) were exposed to a laboratory challenge task designed to induce frustration and anger (i.e. arm restraint). Saliva samples were taken pre-task and 20 and 40 min post-task and then assayed for cortisol. Mothers reported on their pregnancy and postpartum IPV history, current mental health, substance use and their infants behaviors. Structural equation modeling revealed that prenatal, but not postnatal, IPV was independently associated with infant cortisol reactivity and problem behavior. Maternal mental health predicted infant behavioral functioning but not infant HPA axis reactivity. These findings are consistent with the prenatal programing hypothesis; that is, early life stress affects later risk and vulnerability for altered physiological and behavioral regulation.

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