Psychology

Warrior Gene

The "Warrior Gene" refers to a specific genetic variation in the MAOA gene that has been associated with aggressive behavior. This gene is thought to affect the regulation of neurotransmitters in the brain, potentially influencing an individual's response to stress and provocation. Research suggests that individuals with this genetic variation may be more predisposed to aggressive tendencies, particularly in certain environmental conditions.

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4 Key excerpts on "Warrior Gene"

  • Book cover image for: The Cambridge Handbook of Forensic Psychology
    A third genetic factor hypothesizes to play a role in violent behavior is monoamine oxidase (MAOA), an enzyme that plays a role in metabolizing neurotransmitters (Volavka et al., 2004). The MAOA gene codes for the production of the MAOA enzyme that breaks down serotonin and dopamine among other neurotransmitters. Previously, we mentioned popular media attention to a so-called murder gene. In fact, several studies have found links between low MAOA activity and violent behavior, which has resulted in some researchers labeling it the “Warrior Gene.” An early study of a Dutch family by Brunner and his colleagues (1993), for example, linked the MAOA gene to impulsive and serious forms of violence. In another landmark study, Caspi et al. (2002) examined the interrelationships among MAOA, childhood mal- treatment, and antisocial phenotypes in a sample of longitudinal sample of young boys from New Zealand. Though the results indicated that there were The Psychology of Violent Behaviour 133 no differences in violent behavior based on just the MAOA gene, further analysis revealed that MAOA was associated with aggression and violence in males who had been maltreated as child. Based on the results, Caspi and his colleagues (2002) concluded that low MAOA activity increases one’s suscepti- bility to environmental stressors. Work by neuropsychologist Jeffrey Gray (1981, 1987) offered one potential theoretical framework for understanding how genetics and neurotransmitter activity influences violent behavior. Gray proposed that learning and behavior are functions of two interacting biological systems. On one hand, the behav- ioral activation system activates behaviors in response to rewards and non- punishment in the environment. Conversely, the behavioral inhibition system (BIS) inhibits behaviors when aversive stimuli, such as punishment or threats, are signaled.
  • Book cover image for: Actor-Network Theory and Crime Studies
    eBook - ePub

    Actor-Network Theory and Crime Studies

    Explorations in Science and Technology

    • Dominique Robert, Martin Dufresne(Authors)
    • 2016(Publication Date)
    • Routledge
      (Publisher)
    Science in 2002, rekindled the debate over the intergenerational cycle of violence. Their work amalgamates two research streams, one on the intergenerational transmission of violence, the other on the genetics of neurotransmission involving the Monoamine oxidase-A gene and aggressive behaviour. Most North American Caucasian males have inherited one of two variants of the MAOA gene which is involved in neurotransmission, as it “encode[s] mitochondrial enzymes which catalyse the oxidative deamination of amines, such as dopamine, norepinephrine, and serotonin” (NCBI 2013). The conclusion of the study reads as follow:
    These findings provide initial evidence that a functional polymorphism in the MAOA gene moderates the impact of early childhood maltreatment on the development of antisocial behaviour in males. … Genes are assumed to create vulnerability to disease, but from an evolutionary perspective they are equally likely to protect against environmental insult (36). … Until this study’s findings are replicated, speculation about clinical implications is premature. … Both attributable risk and predictive sensitivity indicate that these findings could inform the development of future pharmacological treatments (Caspi et al. 2002a: 853).
    The study’s success is visible on the policy front. In France, the National Institute for Health and Medical Research published a report in which its findings are presented as reliable knowledge on antisocial behaviour, knowledge that should guide policy. But it provoked a powerful mobilization from a broad range of people interested in youth problematic behaviour and opposed to preventive genetic testing (Expertise collective 2005, Le Collectif Pas de zéro de conduite 2006). But overall, the policy issue continues to divide the scientific community. As Cunningham and Kerr (1999: 660) remind us, there is a tension over the usefulness of this science, a tension sometimes stated as an opposition between a neutral posture which allows the politicians to decide the faith of scientific knowledge (for example, Walsh 2009: 292), or a pragmatic posture where the scientist promotes his work through, for example, the development of chemical therapies to lower the risks of certain behaviours (for example, Vaughn and Broom 2011: 409, Tremblay 2010).
  • Book cover image for: Violence Rewired
    eBook - PDF

    Violence Rewired

    Evidence and Strategies for Public Health Action

    translation into proteins. There is evidence that the environment is involved in this and can influence whether or not a gene is transcribed. This highlights the potential for rewiring our theories of violence to ensure the reciprocal relationships between levels in the biopsychosocial model are fully incorporated. Thus one widely discussed possibility with increasing evidential sup- port is that the effects of genes occur mainly through interaction with environmental variables (often labelled GxE). The impact of this is probably not directly on aggressiveness itself but on temperamental factors which, depending on socialisation experiences, could place people at risk of using aggression as a frequent means of responding. Research in this area needs to be approached with caution, as in an initial extensive review of candidate GxE studies in psychiatry, Duncan and Keller (2011) found evidence of publication bias and failures to replicate. Their review, however, did not cover studies of aggression or antisocial behaviour. Byrd and Manuck (2014) reported a meta-analysis of the interaction effect between the low MAOA gene and childhood maltreatment in rela- tion to later antisocial behaviour. The effect did not appear among females, but was found in sixteen of twenty studies with males. We will discuss this in a little more detail in Chapter 4. Weeland et al. (2015) reported a meta-analytic review of fifty-three studies of interaction effects between candidate gene polymorphisms (DAT1, DRD2, DRD4, 5HTTLPR, MAOA, COMT) and environmental variables (family adver- sity, child neglect/abuse, harsh parenting or neighbourhood disadvantage) in relation to externalising behaviours. They found an inconsistent pattern of results, and that methodological differences between studies, including poorly specified environmental and ASB measures, made comparisons difficult.
  • Book cover image for: The Societal Burden of Child Abuse
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    The Societal Burden of Child Abuse

    Long-Term Mental Health and Behavioral Consequences

    The clearest genetic link to aggressive behavior exists for the mono-amine oxidase A (MAOA) gene which plays a key role in the catabolism of monoamines, including dopamine (DA), norepinephrine (NE), and serotonin (5-HT) [7]. MAOA knockout (KO) mice display elevated lev-els of DA, NE and 5-HT and male KO mice exhibit increased aggres-sive behavior [8]. Forebrain-restricted transgenic expression of MAOA in MAOA KO mice results in lower levels of DA, NE and 5-HT and in a reversal of the aggressive phenotype, suggesting that lack of enzyme activity in the forebrain of MAOA KO mice underlies their behavioral phenotype [9]. In humans, a missense mutation was found in the MAOA gene (Xp11.23-11.4) in a Dutch kindred whose members exhibited a pat-tern of impulsively violent behavior for generations [10]. Since MAOA is an X-linked gene [11], hemizygous males from this family effectively represent functional gene knockouts. However, this mutation is extremely rare and has not been found in any other pedigree. More recently, a com-mon variable number tandem repeat (VNTR) polymorphism lying 1.2 kb upstream of the transcription initiation site of MAOA has been shown to affect transcriptional activity of the gene in transfected cells. The 3.5-and 4-repeat forms show high MAOA mRNA expression and high enzyme activity, while the 2-, 3-and 5-repeat forms show low MAOA mRNA ex-pression and low enzyme activity [12], [13]. Recently, a large longitudinal study of children followed for 26 years since birth showed that MAOA VNTR genotype moderates the association between childhood maltreatment and violent and antisocial behavior [14]. Although several studies have replicated this G×E effect [15]–[17], other studies have failed to replicate the original fi ndings reported by Caspi and co-workers [18]–[20]. Explanations for these con fl icting fi ndings are manifold, including the use of different measures of the behavioral pheno-type and of environmental risk factors.
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