Prenatal Risk and Infant Regulation: Indirect Pathways via Fetal Growth and Maternal Prenatal Stress and Anger

Pamela Schuetze, Rina Das Eiden, Craig R. Colder, Marilyn A. Huestis, Kenneth E. Leonard

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Pathways from maternal tobacco, marijuana, stress, and anger in pregnancy to infant reactivity and regulation (RR) at 9 months of infant age were examined in a low-income, diverse sample beginning in the first trimester of pregnancy, with fetal growth and postnatal stress/anger as potential mediators, and infant sex as a moderator. Participants were 247 dyads (173 substance-exposed infants). There were no direct effects of prenatal risk on RR and no moderation by sex. However, there were significant indirect effects on RR via poor fetal growth and higher postnatal anger. The study adds to the sparse literature on joint effects of tobacco and marijuana, and highlights the role of fetal growth and maternal anger as important pathways from prenatal risk to infant RR.

Original languageEnglish (US)
Pages (from-to)e123-e137
JournalChild development
Volume89
Issue number2
DOIs
StatePublished - Mar 1 2018

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Anger
Fetal Development
anger
infant
Mothers
regulation
Cannabis
nicotine
Tobacco
pregnancy
First Pregnancy Trimester
moderator
dyad
low income
Pregnancy

All Science Journal Classification (ASJC) codes

  • Pediatrics, Perinatology, and Child Health
  • Education
  • Developmental and Educational Psychology

Cite this

Schuetze, Pamela ; Das Eiden, Rina ; Colder, Craig R. ; Huestis, Marilyn A. ; Leonard, Kenneth E. / Prenatal Risk and Infant Regulation : Indirect Pathways via Fetal Growth and Maternal Prenatal Stress and Anger. In: Child development. 2018 ; Vol. 89, No. 2. pp. e123-e137.
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Prenatal Risk and Infant Regulation : Indirect Pathways via Fetal Growth and Maternal Prenatal Stress and Anger. / Schuetze, Pamela; Das Eiden, Rina; Colder, Craig R.; Huestis, Marilyn A.; Leonard, Kenneth E.

In: Child development, Vol. 89, No. 2, 01.03.2018, p. e123-e137.

Research output: Contribution to journalArticle

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