PMID- 30068406
OWN - NLM
STAT- MEDLINE
DCOM- 20181031
LR  - 20190214
IS  - 1469-2198 (Electronic)
IS  - 0954-5794 (Linking)
VI  - 30
IP  - 3
DP  - 2018 Aug
TI  - Prenatal intimate partner violence exposure predicts infant biobehavioral 
      regulation: Moderation by the brain-derived neurotrophic factor (BDNF) gene.
PG  - 1009-1021
LID - 10.1017/S0954579418000329 [doi]
AB  - The ability to regulate stress is a critical developmental milestone of early 
      childhood that involves a set of interconnected behavioral and physiological 
      processes and is influenced by genetic and environmental stimuli. Prenatal 
      exposure to traumatic stress and trauma, including intimate partner violence 
      (IPV), increases risk for offspring biobehavioral regulation problems during 
      childhood and adolescence. Although individual differences in susceptibility to 
      prenatal stress have been largely unexplored, a handful of studies suggest 
      children with specific genetic characteristics are most vulnerable to prenatal 
      stress. We evaluated the brain-derived neurotrophic factor Val66Met gene (BDNF) 
      as a moderator of the effect of prenatal IPV exposure on infant temperamental and 
      cortisol regulation in response to a psychosocial challenge. Ninety-nine 
      mother-infant dyads recruited from the community were assessed when infants (51% 
      female) were 11 to 14 months. Maternal reports of IPV during pregnancy and infant 
      temperament were obtained, and infant saliva was collected for genotyping and to 
      assess cortisol reactivity (before and after the Strange Situation Task). 
      Significant genetic moderation effects were found. Among infants with the BDNF 
      Met allele, prenatal IPV predicted worse temperamental regulation and 
      mobilization of the cortisol response, while controlling for infant postnatal 
      exposure to IPV, other maternal traumatic experiences, and infant sex. However, 
      prenatal IPV exposure was not associated with temperamental or cortisol outcomes 
      among infant carriers of the Val/Val genotype. Findings are discussed in relation 
      to prenatal programming and biological susceptibility to stress.
FAU - Martinez-Torteya, Cecilia
AU  - Martinez-Torteya C
AD  - DePaul University.
FAU - Figge, Caleb J
AU  - Figge CJ
AD  - DePaul University.
FAU - Gilchrist, Michelle A
AU  - Gilchrist MA
AD  - DePaul University.
FAU - Muzik, Maria
AU  - Muzik M
AD  - University of Michigan.
FAU - King, Anthony P
AU  - King AP
AD  - University of Michigan.
FAU - Sorenson, Matthew
AU  - Sorenson M
AD  - DePaul University.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Dev Psychopathol
JT  - Development and psychopathology
JID - 8910645
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - WI4X0X7BPJ (Hydrocortisone)
SB  - IM
EIN - Dev Psychopathol. 2019 Oct;31(4):1603. PMID: 31304896
MH  - Adult
MH  - Brain-Derived Neurotrophic Factor/*genetics
MH  - Child
MH  - Female
MH  - Gene-Environment Interaction
MH  - Humans
MH  - Hydrocortisone/analysis
MH  - Infant
MH  - Infant Behavior/*psychology
MH  - Intimate Partner Violence/*psychology
MH  - Male
MH  - Mothers/psychology
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects/*psychology
MH  - Saliva
MH  - Stress, Psychological/genetics/*psychology
MH  - Temperament/physiology
EDAT- 2018/08/03 06:00
MHDA- 2018/11/01 06:00
CRDT- 2018/08/03 06:00
PHST- 2018/08/03 06:00 [entrez]
PHST- 2018/08/03 06:00 [pubmed]
PHST- 2018/11/01 06:00 [medline]
AID - S0954579418000329 [pii]
AID - 10.1017/S0954579418000329 [doi]
PST - ppublish
SO  - Dev Psychopathol. 2018 Aug;30(3):1009-1021. doi: 10.1017/S0954579418000329.