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. 2010 Feb;9(1):65-74.
doi: 10.1111/j.1601-183X.2009.00535.x. Epub 2009 Sep 9.

Early life stress, MAOA, and gene-environment interactions predict behavioral disinhibition in children

M-A Enoch  1 , C D Steer, T K Newman, N Gibson, D Goldman
Affiliations

Early life stress, MAOA, and gene-environment interactions predict behavioral disinhibition in children

M-A Enoch et al. Genes Brain Behav. 2010 Feb.

Abstract

Several, but not all, studies have shown that the monoamine oxidase A functional promoter polymorphism (MAOA-LPR) interacts with childhood adversity to predict adolescent and adult antisocial behavior. However, it is not known whether MAOA-LPR interacts with early life (pre-birth-3 years) stressors to influence behavior in prepubertal children. The Avon Longitudinal Study of Parents and Children, UK, is a community-representative cohort study of children followed from pre-birth onwards. The impact of family adversity from pre-birth to age 3 years and stressful life events from 6 months to 7 years on behavioral disinhibition was determined in 7500 girls and boys. Behavioral disinhibition measures were: mother-reported hyperactivity and conduct disturbances (Strengths and Difficulties Questionnaire) at ages 4 and 7 years. In both sexes, exposure to family adversity and stressful life events in the first 3 years of life predicted behavioral disinhibition at age 4, persisting until age 7. In girls, MAOA-LPR interacted with stressful life events experienced from 6 months to 3.5 years to influence hyperactivity at ages 4 and 7. In boys, the interaction of MAOA-LPR with stressful life events between 1.5 and 2.5 years predicted hyperactivity at age 7 years. The low activity MAOA-LPR variant was associated with increased hyperactivity in girls and boys exposed to high stress. In contrast, there was no MAOA-LPR interaction with family adversity. In a general population sample of prepubertal children, exposure to common stressors from pre-birth to 3 years predicted behavioral disinhibition, and MAOA-LPR- stressful life event interactions specifically predicted hyperactivity.

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Figures

FIGURE 1
FIGURE 1. The Effects of Stressful Life Events and MAOA-LPR Genotype on Hyperactivity in Girls Aged 4 and 7 Years
MAOA-LPR alleles: L = low activity, H = high activity. The maximum possible hyperactivity score is 10. No difference in genotype distribution between number of stressful life events. A1, A2: Graphs showing means (+ SEs) for the 3 genotypes derived from analyses in which cumulative life events experienced from 0.5 to 3.5 years were dichotomized into low stress (LS) and high stress (HS) (defined as the upper quartile of the sample). A1: LL: LS, N = 228; HS, N = 88. LH: LS, N = 862; HS, N = 327. HH: LS, N = 822; HS, N = 286. Interaction p value = 0.003. A2: LL: LS, N = 211; HS, N = 74. LH: LS, N = 810; HS, N = 298. HH: LS, N = 779; HS, N = 262. Interaction p value = 0.01. B1, B2: graphs showing predicted values for the linear trend using the dose response model where the strongest differences are observed.
FIGURE 2
FIGURE 2. The Effects of Stressful Life Events and MAOA-LPR Genotype on Hyperactivity in Boys at Age 7 Years
MAOA-LPR alleles: L = low activity, H = high activity. The maximum possible hyperactivity score is 10. No difference in genotype distribution between number of stressful life events. A1, A2: Graphs showing means (+ SEs) for the H and L alleles derived from analyses using the dichotomous life event variable: low stress (LS); high stress (HS) (upper quartile of sample). A1: L allele: LS, N = 712; HS, N = 225. H allele: LS, N = 1375; HS, N = 467. Interaction p value = 0.03. A2: L allele: LS, N = 637; HS, N = 249. H allele: LS, N = 1268; HS, N = 502. Interaction p value = 0.1. B1, B2: graphs showing predicted values for the linear trend using the dose response model.
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