Does MAOA increase susceptibility to prenatal stress in young children?

Suena H. Massey, Amalia E. Hatcher, Caron A.C. Clark, James L. Burns, Daniel S. Pine, Andrew D. Skol, Daniel K. Mroczek, Kimberly Andrews Espy, David Goldman, Edwin Cook, Lauren S. Wakschlag

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Background We previously demonstrated a gene-by-prenatal-environment interaction whereby the monoamine oxidase A gene (MAOA) modified the impact of prenatal tobacco exposure (PTE) on adolescent disruptive behavior (DB), with the MAOA risk genotype varying by sex. We extend this work by examining whether this mechanism is evident with another common adversity, prenatal stress exposure (PSE), and whether sex differences are present earlier in development in closer proximity to exposure. Methods Participants were 281 mothers and their 285 children derived from a prenatal cohort with in-depth prospective measures of PSE and PTE. We assessed DB at age 5 via dimensional developmentally-sensitive measurement. Analyses were stratified by sex based on prior evidence for sex differences. Results Concurrent stress exposure predicted DB in children (β = 0.310, p = 0.001), while main effects of prenatal exposures were seen only in boys. We found a three-way interaction of MAOA × PSE × sex on DB (β = 0.813, p = 0.022). Boys with MAOA-H had more DB as a function of PSE, controlling for PTE (β = 0.774, p = 0.015), and as a function of PTE, controlling for PSE (β = 0.362, p = 0.037). Boys with MAOA-L did not show this susceptibility. MAOA did not interact with PSE (β = − 0.133, p = 0.561) nor PTE (β = − 0.144; p = 0.505) in predicting DB in girls. Examination of gene-environment correlation (rGE) showed a correlation between paternal MAOA-L and daughters' concurrent stress exposure (r = − 0.240, p = 0.013). Discussion Findings underscore complex mechanisms linking genetic susceptibility and early adverse exposures. Replication in larger cohorts followed from the pregnancy through adolescence is suggested to elucidate mechanisms that appear to have varying developmental expression.

Original languageEnglish (US)
Pages (from-to)82-91
Number of pages10
JournalNeurotoxicology and Teratology
Volume61
DOIs
StatePublished - May 1 2017

Fingerprint

Monoamine Oxidase
Genes
Tobacco
Sex Characteristics
Gene-Environment Interaction
Adolescent Behavior
Genetic Predisposition to Disease
Nuclear Family
Problem Behavior
Genotype
Mothers
Pregnancy

Keywords

  • Disruptive behavior
  • Early adversity
  • Gene × environment interaction
  • Monoamine oxidase A
  • Pregnancy smoking
  • Sex differences

ASJC Scopus subject areas

  • Toxicology
  • Developmental Neuroscience
  • Cellular and Molecular Neuroscience

Cite this

Massey, S. H., Hatcher, A. E., Clark, C. A. C., Burns, J. L., Pine, D. S., Skol, A. D., ... Wakschlag, L. S. (2017). Does MAOA increase susceptibility to prenatal stress in young children? Neurotoxicology and Teratology, 61, 82-91. https://doi.org/10.1016/j.ntt.2017.01.005

Does MAOA increase susceptibility to prenatal stress in young children? / Massey, Suena H.; Hatcher, Amalia E.; Clark, Caron A.C.; Burns, James L.; Pine, Daniel S.; Skol, Andrew D.; Mroczek, Daniel K.; Espy, Kimberly Andrews; Goldman, David; Cook, Edwin; Wakschlag, Lauren S.

In: Neurotoxicology and Teratology, Vol. 61, 01.05.2017, p. 82-91.

Research output: Contribution to journalArticle

Massey, SH, Hatcher, AE, Clark, CAC, Burns, JL, Pine, DS, Skol, AD, Mroczek, DK, Espy, KA, Goldman, D, Cook, E & Wakschlag, LS 2017, 'Does MAOA increase susceptibility to prenatal stress in young children?', Neurotoxicology and Teratology, vol. 61, pp. 82-91. https://doi.org/10.1016/j.ntt.2017.01.005
Massey, Suena H. ; Hatcher, Amalia E. ; Clark, Caron A.C. ; Burns, James L. ; Pine, Daniel S. ; Skol, Andrew D. ; Mroczek, Daniel K. ; Espy, Kimberly Andrews ; Goldman, David ; Cook, Edwin ; Wakschlag, Lauren S. / Does MAOA increase susceptibility to prenatal stress in young children?. In: Neurotoxicology and Teratology. 2017 ; Vol. 61. pp. 82-91.
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AU - Hatcher, Amalia E.

AU - Clark, Caron A.C.

AU - Burns, James L.

AU - Pine, Daniel S.

AU - Skol, Andrew D.

AU - Mroczek, Daniel K.

AU - Espy, Kimberly Andrews

AU - Goldman, David

AU - Cook, Edwin

AU - Wakschlag, Lauren S.

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N2 - Background We previously demonstrated a gene-by-prenatal-environment interaction whereby the monoamine oxidase A gene (MAOA) modified the impact of prenatal tobacco exposure (PTE) on adolescent disruptive behavior (DB), with the MAOA risk genotype varying by sex. We extend this work by examining whether this mechanism is evident with another common adversity, prenatal stress exposure (PSE), and whether sex differences are present earlier in development in closer proximity to exposure. Methods Participants were 281 mothers and their 285 children derived from a prenatal cohort with in-depth prospective measures of PSE and PTE. We assessed DB at age 5 via dimensional developmentally-sensitive measurement. Analyses were stratified by sex based on prior evidence for sex differences. Results Concurrent stress exposure predicted DB in children (β = 0.310, p = 0.001), while main effects of prenatal exposures were seen only in boys. We found a three-way interaction of MAOA × PSE × sex on DB (β = 0.813, p = 0.022). Boys with MAOA-H had more DB as a function of PSE, controlling for PTE (β = 0.774, p = 0.015), and as a function of PTE, controlling for PSE (β = 0.362, p = 0.037). Boys with MAOA-L did not show this susceptibility. MAOA did not interact with PSE (β = − 0.133, p = 0.561) nor PTE (β = − 0.144; p = 0.505) in predicting DB in girls. Examination of gene-environment correlation (rGE) showed a correlation between paternal MAOA-L and daughters' concurrent stress exposure (r = − 0.240, p = 0.013). Discussion Findings underscore complex mechanisms linking genetic susceptibility and early adverse exposures. Replication in larger cohorts followed from the pregnancy through adolescence is suggested to elucidate mechanisms that appear to have varying developmental expression.

AB - Background We previously demonstrated a gene-by-prenatal-environment interaction whereby the monoamine oxidase A gene (MAOA) modified the impact of prenatal tobacco exposure (PTE) on adolescent disruptive behavior (DB), with the MAOA risk genotype varying by sex. We extend this work by examining whether this mechanism is evident with another common adversity, prenatal stress exposure (PSE), and whether sex differences are present earlier in development in closer proximity to exposure. Methods Participants were 281 mothers and their 285 children derived from a prenatal cohort with in-depth prospective measures of PSE and PTE. We assessed DB at age 5 via dimensional developmentally-sensitive measurement. Analyses were stratified by sex based on prior evidence for sex differences. Results Concurrent stress exposure predicted DB in children (β = 0.310, p = 0.001), while main effects of prenatal exposures were seen only in boys. We found a three-way interaction of MAOA × PSE × sex on DB (β = 0.813, p = 0.022). Boys with MAOA-H had more DB as a function of PSE, controlling for PTE (β = 0.774, p = 0.015), and as a function of PTE, controlling for PSE (β = 0.362, p = 0.037). Boys with MAOA-L did not show this susceptibility. MAOA did not interact with PSE (β = − 0.133, p = 0.561) nor PTE (β = − 0.144; p = 0.505) in predicting DB in girls. Examination of gene-environment correlation (rGE) showed a correlation between paternal MAOA-L and daughters' concurrent stress exposure (r = − 0.240, p = 0.013). Discussion Findings underscore complex mechanisms linking genetic susceptibility and early adverse exposures. Replication in larger cohorts followed from the pregnancy through adolescence is suggested to elucidate mechanisms that appear to have varying developmental expression.

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KW - Pregnancy smoking

KW - Sex differences

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