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Age-dependent effect of the MAOA gene on childhood physical aggression

Molecular Psychiatry volume 18, pages 1151–1152 (2013)Cite this article

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Quantitative genetic studies suggest that genetic contributions account for a substantive part of a range of disruptive behaviors.1 At a molecular level, Caspi et al.2 reported no main effect of the monoamine oxidase A (MAOA) gene but an interactive effect with early maltreatment in the prediction of aggressive behavior. Later studies using different research designs as well as various measures of disruptive behavior and early adversity have yielded mixed results. These studies mainly relied on one or two time point assessments in adolescence or adulthood; few studies focused on childhood.3, 4 As such, no study has yet modeled explicitly an age-dependent contribution of MAOA. Suggestions have been made as to why the effect of genotype may decrease or increase with age.5 Accordingly, we examined the age-dependent contribution of MAOA alone or in interaction with family socioeconomic adversity to the frequency of physical aggression during the elementary school years.

We selected 436 boys from a longitudinal study of kindergarten children in Quebec (Canada). The study sample has been described elsewhere.6 The boys’ frequency of physical aggression was rated annually from age 6 to 12 years by teachers with the Social Behavior Questionnaire7 (each item rated on a three-point scale (0–2, from ‘never applies’ to ‘frequently applies’). Three items were used: (1) fights, (2) bullies and (3) kicks, bites, or hits (alphas ranging from 0.79 to 0.86). We used an index of family socioeconomic adversity based on information collected at the start of the study6 about: (1) family structure, (2) parents’ levels of education, (3) parents’ occupational status and 4) parents’ age at the birth of the first child. We imputed the values for 20 participants from the constituent variables of the index and from behavioral characteristics of the boys at 6 years. We assessed common tag single-nucleotide polymorphisms (SNPs; minor allele frequency >5%) and SNPs located up to 5-kbp upstream of the transcription site. Tag SNPs were obtained using HapMap and Tagger’s multimarker-tagging procedure (r2 >0.8).6 To reduce the number of statistical comparisons, only the most informative SNPs were selected from our genetic database using an algorithm based on r2 linkage disequilibrium.8 Table 1 presents the selected SNPs and their frequencies. Details on genetic assessments for this sample are provided elsewhere.6

Table 1 Contributions of family adversity and MAOA SNP’s to the initial level and slope of childhood physical aggression
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Authors and Affiliations

  1. Research Unit on Children’s Psychosocial Maladjustment, University of Montreal and Sainte–Justine Hospital, Montreal, QC, Canada

    J B Pingault, S M Côté, L Booij, I Ouellet-Morin, N Castellanos-Ryan, F Vitaro & R E Tremblay

  2. INSERM U669, Univ. Paris-Descartes and Paris-Sud, Paris, France

    J B Pingault, S M Côté & R E Tremblay

  3. Department of Psychiatry, University of Montreal, Montreal, QC, Canada

    L Booij

  4. Department of Psychiatry, McGill University, Montreal, QC, Canada

    L Booij

  5. School of Criminology, University of Montreal, Montreal, QC, Canada

    I Ouellet-Morin

  6. Mental Health Institute of Montreal Research Center, Montreal, QC, Canada

    I Ouellet-Morin

  7. The McGill Group for Suicide Studies, Douglas Hospital Research Centre, McGill University, Montreal, QC, Canada

    G Turecki

  8. School of Public Health, Physiotherapy and Population Science, University College, Dublin, Ireland

    R E Tremblay

  9. Departments of Pediatrics, Psychiatry and Psychology, University of Montreal, Montreal, QC, Canada

    R E Tremblay

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  1. J B Pingault
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  2. S M Côté
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  3. L Booij
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  6. F Vitaro
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  7. G Turecki
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  8. R E Tremblay
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Correspondence to J B Pingault or R E Tremblay.

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Pingault, J., Côté, S., Booij, L. et al. Age-dependent effect of the MAOA gene on childhood physical aggression. Mol Psychiatry 18, 1151–1152 (2013). https://doi.org/10.1038/mp.2012.173

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