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The effects of MAOA genotype, childhood trauma, and sex on trait and state-dependent aggression

Monoamine oxidase A (MAOA) genotypic variation has been associated with variation in aggression, especially in interaction with childhood trauma or other early adverse events. Male carriers of the low-expressing variant (MAOA-L) with childhood trauma or other early adverse events seem to be more agg...

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Autores principales: Verhoeven, Floor E A, Booij, Linda, Kruijt, Anne-Wil, Cerit, Hilâl, Antypa, Niki, Does, Willem
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Inc 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3500467/
https://www.ncbi.nlm.nih.gov/pubmed/23170243
http://dx.doi.org/10.1002/brb3.96
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author Verhoeven, Floor E A
Booij, Linda
Kruijt, Anne-Wil
Cerit, Hilâl
Antypa, Niki
Does, Willem
author_facet Verhoeven, Floor E A
Booij, Linda
Kruijt, Anne-Wil
Cerit, Hilâl
Antypa, Niki
Does, Willem
author_sort Verhoeven, Floor E A
collection PubMed
description Monoamine oxidase A (MAOA) genotypic variation has been associated with variation in aggression, especially in interaction with childhood trauma or other early adverse events. Male carriers of the low-expressing variant (MAOA-L) with childhood trauma or other early adverse events seem to be more aggressive, whereas female carriers with the high-expressing variant (MAOA-H) with childhood trauma or other early adverse events may be more aggressive. We further investigated the effects of MAOA genotype and its interaction with sex and childhood trauma or other early adverse events on aggression in a young adult sample. We hypothesized that the association between genotype, childhood trauma, and aggression would be different for men and women. We also explored whether this association is different for dispositional (trait) aggression versus aggression in the context of dysphoric mood. In all, 432 Western European students (332 women, 100 men; mean age 20.2) were genotyped for the MAOA gene. They completed measures of childhood trauma, state and trait measures of aggression-related behaviors (STAXI), and cognitive reactivity to sad mood (LEIDS-R), including aggression reactivity. Women with the MAOA-H had higher aggression reactivity scores than women with the MAOA-L. This effect was not observed in men, although the nonsignificant findings in men may be a result of low power. Effects on the STAXI were not observed, nor were there gene by environment interactions on any of the aggression measures. A protective effect of the low-expression variant in women on aggression reactivity is consistent with previous observations in adolescent girls. In females, the MAOA-H may predispose to aggression-related problems during sad mood.
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spelling pubmed-35004672012-11-20 The effects of MAOA genotype, childhood trauma, and sex on trait and state-dependent aggression Verhoeven, Floor E A Booij, Linda Kruijt, Anne-Wil Cerit, Hilâl Antypa, Niki Does, Willem Brain Behav Original Research Monoamine oxidase A (MAOA) genotypic variation has been associated with variation in aggression, especially in interaction with childhood trauma or other early adverse events. Male carriers of the low-expressing variant (MAOA-L) with childhood trauma or other early adverse events seem to be more aggressive, whereas female carriers with the high-expressing variant (MAOA-H) with childhood trauma or other early adverse events may be more aggressive. We further investigated the effects of MAOA genotype and its interaction with sex and childhood trauma or other early adverse events on aggression in a young adult sample. We hypothesized that the association between genotype, childhood trauma, and aggression would be different for men and women. We also explored whether this association is different for dispositional (trait) aggression versus aggression in the context of dysphoric mood. In all, 432 Western European students (332 women, 100 men; mean age 20.2) were genotyped for the MAOA gene. They completed measures of childhood trauma, state and trait measures of aggression-related behaviors (STAXI), and cognitive reactivity to sad mood (LEIDS-R), including aggression reactivity. Women with the MAOA-H had higher aggression reactivity scores than women with the MAOA-L. This effect was not observed in men, although the nonsignificant findings in men may be a result of low power. Effects on the STAXI were not observed, nor were there gene by environment interactions on any of the aggression measures. A protective effect of the low-expression variant in women on aggression reactivity is consistent with previous observations in adolescent girls. In females, the MAOA-H may predispose to aggression-related problems during sad mood. Blackwell Publishing Inc 2012-11 2012-10-05 /pmc/articles/PMC3500467/ /pubmed/23170243 http://dx.doi.org/10.1002/brb3.96 Text en © 2012 Published by Wiley Periodicals, Inc. http://creativecommons.org/licenses/by/2.5/ Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.
spellingShingle Original Research
Verhoeven, Floor E A
Booij, Linda
Kruijt, Anne-Wil
Cerit, Hilâl
Antypa, Niki
Does, Willem
The effects of MAOA genotype, childhood trauma, and sex on trait and state-dependent aggression
title The effects of MAOA genotype, childhood trauma, and sex on trait and state-dependent aggression
title_full The effects of MAOA genotype, childhood trauma, and sex on trait and state-dependent aggression
title_fullStr The effects of MAOA genotype, childhood trauma, and sex on trait and state-dependent aggression
title_full_unstemmed The effects of MAOA genotype, childhood trauma, and sex on trait and state-dependent aggression
title_short The effects of MAOA genotype, childhood trauma, and sex on trait and state-dependent aggression
title_sort effects of maoa genotype, childhood trauma, and sex on trait and state-dependent aggression
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3500467/
https://www.ncbi.nlm.nih.gov/pubmed/23170243
http://dx.doi.org/10.1002/brb3.96
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