Task 1 of the course PSY3377 Legal Psychology in a Nutshell, followed at Maastricht University. The task is comprehensive and well organized. All research papers are summarized and everything discussed during the tutorials is included. Using my tasks, I got an 8.5 for the final exam :).
LEARNING GOALS:
PART A
1. What is MAOA? Low vs high MAOA
Guy (2016) – The Warrior Gene: Genetics and Criminology
Monoamine oxidase A (MAOA): an enzyme produced by these genes, breaking down DA, 5-HT, NE.
The MAOA gene can be found on the X chromosome.
- In rare cases this gene can be missing completely, or individuals can have different variants
o MAOA-L: a low activity variant; present in 30-40% of the male population
o MAOA-H: a high activity variant
- Women have 2 X chromosomes, so they’re more likely to have at least 1 high functioning
variant and are therefore less affected, although studies on women so far have been few
- Men only have 1 X chromosome, so they will either have MAOA-L or MAOA-H
o The presence of MAOA-L translates to a vulnerability toward violent behaviour,
particularly when provoked or challenged, hence the term warrior gene
The crucial neurotransmitters in the brain are not being mobilized correctly
5-HT is of particular importance to behaviour as it is most closely associated
with stabilizing mood + calming us down in anger
Low 5-HT => less communication with the amygdala (the emotional
brain area); so people with low 5-HT may find it more difficult to
control emo responses to anger in the PFC that have been generated
within the amygdala => lack of impulse control
The warrior gene theory relates to more impulsive and sudden acts of violence rather than
premeditated and planned acts of violence against another
In the US, one can pay for DNA testing to establish the presence of the warrior gene. Quite why men
would want to pay for such a test highlights the potential misconception that the presence of MAOA-
L means any violent aggression is entirely genetic and out-with their control, essentially removing
any blame or responsibility from the individual themselves.
- Evidence suggests that having the warrior gene alone is not enough to cause any violent
behaviour. It’s a genetic predisposition that can be triggered by external factors
o When discussing the warrior gene, while the nature clearly plays a part, it is the
nurture that is vital in impacting how an individual is going to turn out (violent
behaviour and crime)
A positive upbringing away from violence and abuse, even with genetics
predisposing a person to potential violent behaviour, can mean a much more
balanced well-adjusted adult
- The fundamental question is whether that individual was in full control of their actions at the
time of the offense
o For a person to be found guilty and convicted it must be shown that they were fully
aware of what they were doing
o The intro of behavioural genetics complicates this standard, bringing in extra factors
with regards to an individual’s level of control under different circumstances and as a
consequence, their level of criminal responsibility
The case that caused the most controversy in using such genetic arguments
in court is that of Bayout in 2009 (case). A primary concern about this
decision was that while he had the warrior gene, he did not have the
maltreatment history in his childhood
,Baum (2013) – The MAOA Genetic Predisposition to Impulsive Violence: Is It Relevant to Criminal
Trials?
Reviews in context recent work on the MAOA gene-environment interaction in predisposing
individuals to violence and addresses the relevance of such findings to murder trials.
- The MAOA genetic variants impact future violence and aggression only when combined with
the adverse environmental stimuli of childhood maltreatment
o Thus nature and nurture interact to determine the individual’s risk
This paper refers to impulsive, reactive violence caused by a stimulus: anger, frustration, or other
provocation. Although reactive violence can sometimes be adaptive, as in defending oneself, a
reaction that is disproportional to the provocation, or in response to perceived and not actual
provocation, can become pathological.
When it does, this impulsive violence takes major tolls from society.
- Most of the homicides represent causalities of impulsive aggression; while some of the most
chilling cases in criminology deal with individuals who commit acts of premeditated violence,
these cases are the extreme minority (and will not be discussed in this paper)
Genetic predispositions to complex physical conditions gained credibility and public trust with their
success in cardiovascular decrease, establishing terminology and a way of thinking about risk that
was an essential step towards current molecular genetics research on predispositions to violence.
Research found a gene x environment interaction for crime: Gene variant coding for MAOA x an
adverse environment
- Gene variant coding for MAOA confers susceptibility to the negative influence of adverse
environmental stimuli like childhood maltreatment to predispose to future violence
- The other variant (high-MAOA) confers resilience
MAOA: involved primarily in degradation of 5-HT and to a lesser extent, NE and DA.
- The MAOA gene exists in several common variants. 3 or 4 repeats are most common
o ~30% of the gene copies in the population contain 3 repeats, while ~65% contain 4
o Caspi et al. tested the hypothesis that the low-expressing variant would correlate
with antisocial behaviour. They tracked a birth cohort of male children at regular
intervals as they grew to 26 years of age
When the children were grouped by the low (3 repeats, MAOA-low) or high
(4 repeats, MAOA-high) activity polymorphisms in the MAOA gene, there
was no significant correlation between genotype and antisocial behaviour
However, there was a significant positive correlation between maltreatment
& later antisocial behaviour
Boys who had been maltreated AND possessed MAOA-low were
significantly more likely to exhibit later antisocial behaviour than
were maltreated boys with MAOA-high
The boys who were maltreated were not more likely than non-
maltreated boys to possess MAOA-low, which suggests that
genotype did not predispose the boys to receive maltreatment, but
rather their resilience to it
This gene x environment interaction was still seen after correction for
SES + several other environmental variables
The MAOA-low variant seemed to confer sensitivity to maltreatment while
the high MAOA conferred a sort of protection
, Important shortcoming in the current literature : exactly what is an adverse
environment needs to be better defined and might be the leading reason for
discrepancies between trials
However, the G x E interaction held up to the meta-analysis even
with the agglomeration of loosely defined “adverse environments”
- The MAOA gene promoter contains glucocorticoid (stress hormones)/testosterone response
elements that govern the gene’s transcription, which could further tie MAOA to male violence
o Glucocorticoid binding leads to a larger increase in transcription than does
testosterone binding, which suggests that an elevated level of testosterone would
compete for binding and actually decrease the net rate of transcription
High testosterone levels correlate with antisocial personality disorder &
aggression only in males who also possessed the MAOA low genotype
No significant correlation between MAOA high males producing high
testosterone and ASPD or aggression
- Low MAOA males: increased functional connectivity between the ventromedial PFC, a region
implicated in impulse repression, & the amygdala, a region implicated in emotional salience
o Increased activation of the emotional amygdala + decreased activation of the
inhibitory input from the cortex
o This connectivity seems to be mediated through the perigenual anterior cingulate, a
region that contains the highest concentration of the 5-HT 2A receptor
Inhibition of the 5-HT2A receptor decreases impulsivity + aggression, while
activation increases aggression
The hypothesis follows: MAOA low variant under normal conditions leads to a slight biasing of the
development of neural systems that in turn contribute to a hyperactive amygdala + underactive
vmPFC in response to emotional stimuli. This aberrant activation pattern may then contribute to
exaggerated emotional salience with decreased impulse control (hypoactive vmPFC in turn results
into an even more hyperreactive amygdala). This creates the risk of provocative stimuli seeming even
more provocative and contributing to increased likelihood and intensity of response. Though more
empirical research is needed, it’s hypothesized that the addition of an adverse environment
supercharges the mechanism, thereby leading to even greater effects.
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