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Running head: MAOA, IMPULSIVITY, AND AGGRESSION 1
Monoamine Oxidase A (MAOA) Genotype Predicts Greater Aggression Through
Impulsive Reactivity to Negative Affect
David S. Chester1*, C. Nathan DeWall1, Karen J. Derefinko1, Steven Estus2,3,
Jessica R. Peters1, Donald R. Lynam4, Yang Jiang3,5
1Department of Psychology, University of Kentucky
2Department of Physiology, University of Kentucky
3Sanders-Brown Center on Aging, University of Kentucky
4Department of Psychological Sciences, Purdue University
5Department of Behavioral Science, University of Kentucky
in press at Behavioural Brain Research
*Correspondence should be addressed to:
David S. Chester
302 Thurston House, Department of Psychology
Virginia Commonwealth University
Richmond, VA, USA 23284
dschester@vcu.edu
MAOA, IMPULSIVITY, AND AGGRESSION 2
Highlights
-Low functioning MAOA genotype was linked to greater past aggression
-Low functioning MAOA genotype was linked to greater negative urgency
-The effect of MAOA genotype on aggression was mediated by greater negative
urgency
MAOA, IMPULSIVITY, AND AGGRESSION 3
Abstract
Low functioning MAOA genotypes have been reliably linked to increased reactive
aggression, yet the psychological mechanisms of this effect remain largely unknown.
The low functioning MAOA genotype’s established link to diminished inhibition and
greater reactivity to conditions of negative affect suggest that negative urgency, the
tendency to act impulsively in the context of negative affect, may fill this mediating role.
Such MAOA carriers may have higher negative urgency, which may in turn predict
greater aggressive responses to provocation. To test these hypotheses, 277 female and
male participants were genotyped for an MAOA SNP yet to be linked to aggression
(rs1465108), and then reported their negative urgency and past aggressive behavior.
We replicated the effect of the low functioning MAOA genotype on heightened
aggression, which was mediated by greater negative urgency. These results suggest
that disrupted serotonergic systems predispose individuals towards aggressive behavior
by increasing impulsive reactivity to negative affect.
Keywords: MAOA, aggression, negative urgency, UPPS model, genetics, impulsivity
MAOA, IMPULSIVITY, AND AGGRESSION 4
1. Introduction
Aggression, the act of harming others against their will, is a ubiquitous and
resilient phenomenon (Anderson & Bushman, 2002). Although numerous situational
factors can increase aggression, substantial evidence suggests that people have a
disposition to behave aggressively, with approximately half of this tendency being
genetically inherited (e.g., Moffitt, 2005). To reduce aggression, it is crucial to determine
the factors that give rise to such dispositional aggression tendencies.
Of the various genetic predictors of aggression, low functioning allelic variants of
the monoamine oxidase A (MAOA) gene have emerged as uniquely potent correlates
with violence (Gallardo-Pujol, Andrés-Pueyo, & Maydeu-Olivares, 2013; Kuepper,
Grant, Wielpuetz, & Hennig, 2013; McDermott, Tingley, Cowden, Frazzetto, & Johnson,
2009; Raine, 2008). However, the psychological mechanisms that explain this genetic
link to aggression remain largely unexamined. To fill this gap, we sought to identify
personality traits that arise from the MAOA gene. Specifically, we sought to implicate
negative urgency, the tendency to act rashly when experiencing negative affect, as a
mechanism through which the MAOA minor allele predicts aggression (e.g., McDermott
et al., 2009).
1.1 MAOA and Aggression
The MAOA gene encodes monoamine oxidase A, an enzyme that breaks down
monoamine neurotransmitters, chiefly serotonin, into their constituent molecular
compounds (Buckholtz & Meyer-Lindenberg, 2008; Raine, 2008). Providing the initial
evidence of a link between this gene and aggression, MAOA knockout mice showed
greater instances of aggression against conspecifics (Cases et al., 1995). Humans with
MAOA, IMPULSIVITY, AND AGGRESSION 5
a low functioning mutation of this gene show greater levels of aggression (Brunner,
Nelen, Breakefield, Ropers, & van Oost, 1993; Meyer-Lindenberg et al., 2006; Raine,
2008), whereas those with a higher functional allelic variant show greater prosociality
(Mertins, Schote, Hoffeld, Griessmair, & Meyer, 2011). This antisocial tendency of low
functioning MAOA genotypic individuals is exacerbated among those with adverse early
life experiences of maltreatment (Caspi et al., 2002; Kim-Cohen et al., 2006).
Crucially, this aggressive tendency among low functioning MAOA genotypic
people is most pronounced and perhaps specific to situations characterized by
interpersonal exclusion or provocation (Gallardo-Pujol et al., 2013; Kuepper et al., 2013;
McDermott et al., 2009). Thus, the MAOA gene, also known from earlier research as
“warrior gene”, may not be associated with aggression per se but with reactive,
retaliatory aggression to provocative situations. This specificity fits well with the gene-
environment interactionist approach to behavioral genetics (e.g., McDermott et al.,
2009) as well as contemporary meta-theories of aggression such as the General
Aggression Model (Anderson & Bushman, 2002; DeWall, Anderson, & Bushman, 2011)
and I3 Theory (Finkel, in press; Slotter & Finkel, 2011). However, it remains largely
unknown what psychological dispositions contribute to this link between low functioning
MAOA genotype and retaliatory aggression. A psychological phenotype marked by
heightened reactivity to provocative situations may partially account for the relationship
between low functioning MAOA and greater aggression.
1.2 Mechanisms Underlying the MAOA-Aggression Link
Reactive aggression often results from a combination of the discrete elements of
provocation, heightened emotional reactivity to a provocative event, and impaired
MAOA, IMPULSIVITY, AND AGGRESSION 6
inhibition (e.g., Chester et al., 2014; see Denson, DeWall, & Finkel, 2012). Crucially,
these factors interact with one another to further exacerbate one another. Individuals
with the low functioning MAOA genotype possess a neural makeup that would establish
just such a perfect storm of heightened emotional reactivity and impaired inhibition. Low
functioning MAOA genotypes show reduced levels of monoamine oxidase A which
results in greater, dysregulated levels of circulating central serotonin (for a more
detailed account see Buckholtz & Meyer-Lindenberg, 2008). These heightened
serotonin levels predispose neural regions that produce and regulate affective
responses to social stimuli to behave in a dysregulated and labile manner (Buckholtz &
Meyer-Lindenberg, 2008).
A seminal neuroimaging study demonstrated that the low expression MAOA
allelic variant was associated with hyper-reactivity of the amygdala and hypo-reactivity
of the dorsal lateral prefrontal cortex (DLPFC) during an emotionally arousing task
(Meyer-Lindenberg et al., 2006). This association between low functioning MAOA
genotype and hyper reactivity of the amygdala to negatively valenced affective stimuli
was recently replicated, using an ecologically valid provocation paradigm, and shown to
predict greater subsequent effort required to control anger (Denson, Dobson-Stone,
Ronay, von Hippel, & Schira, 2014). This effect of MAOA genotype on anger control
also held for the dorsal anterior cingulate cortex (dACC), a neural region implicated in
responding to events characterized by negative affect (Denson et al., 2014). Further,
the association between low functioning MAOA genotype and aggression was mediated
by greater reactivity of the dACC during an instance of social rejection (Eisenberger,
Way, Taylor, Welch, & Lieberman, 2007). Combining these findings with the behavioral
MAOA, IMPULSIVITY, AND AGGRESSION 7
literature on the MAOA-aggression link suggests that the disruption of the serotonergic
system that is associated with the low functioning allelic variants of the MAOA gene
predisposes individuals to experience greater negative affect in response to
interpersonal threat.
According to balance theory, the LPFC maintains a self-regulatory balance by
inhibiting activity in the amygdala and other regions such as the dACC (Heatherton &
Wagner, 2011). But when this balance is tipped in favor of the amygdala, possibly by
genetic influences from the MAOA gene, self-regulation fails and increases aggression.
This unbalanced combination of greater amygdala and blunted LPFC activity during
negative affect is prevalent in highly aggressive populations (Coccaro, McCloskey,
Fitzgerald, & Phan, 2007). Specifically, this maladaptive neural mechanism may
underpin a unique facet of impulsivity called negative urgency, which is characterized by
both deficits in inhibition and negative behavioral outcomes such as aggression (Cyders
& Smith, 2008).
1.3 Negative Urgency as a Mechanism
Negative urgency refers to the tendency to react impulsively to experiences of
negative affect (Cyders & Smith, 2008; Whiteside & Lynam, 2001). Negative urgency is
one of four facets of impulsivity that also include the lack of perseverance, the lack of
premeditation, and sensation-seeking (Whitesyde & Lynam, 2001). We focus on
negative urgency for two key reasons. First, this facet of impulsivity is predictive of
aggressive responses to provocation and threat (not aggression per se) above and
beyond other features of impulsivity (Anestis, Anestis, Selby, & Joiner, 2009; Cyders &
Smith, 2008; Derefinko, DeWall, Metze, Walsh, & Lynam, 2011; Settles et al., 2012).
MAOA, IMPULSIVITY, AND AGGRESSION 8
Second, negative urgency has been previously linked to a low functioning serotonergic
genotype using the 5HTTLPR gene (Carver, Johnson, Joorman, Kim, & Nam, 2011;
Carver, LeMoult, Johnson, & Joormann, 2014). This evidence, combined with the effect
of MAOA on tipping the balance of the self-regulatory neural network that likely elicits
negative urgency suggests that negative urgency (Eisenberger et al., 2007; Meyer-
Lindenberg et al., 2006) might relate to having a low functioning MAOA genotype.
Further, this expression of a low functioning MAOA genotype as greater negative
urgency may help explain why MAOA most often relates to aggression under conditions
of negative affect (e.g., McDermott et al., 2009).
1.4 Current Study
The current study sought to replicate and examine a psychological phenotype
that may help explain why the low functioning genotype of the MAOA gene often relates
to greater aggression. Further, the study sought to test the novel hypothesis that the
positive association between low functioning MAOA genotype and greater aggression
would be mediated by heightened negative urgency. Finally, we aimed to genotype
individuals on a single nucleotide polymorphism (SNP; rs1465108; Figure 1) of the
MAOA gene that has yet to be linked to aggression. The functionality of this SNP has
yet to be fully established, a fruitful avenue for future MAOA research.\
Figure 1. Spatial schematic of the MAOA gene’s VNTR promoter region and
adjacent SNPs, including the SNP genotyped in this study (i.e., rs1465108).
Single-digit numbers represent the location of exons.
MAOA, IMPULSIVITY, AND AGGRESSION 9
To achieve these aims, undergraduate students were genotyped on the
rs1465108 SNP and reported their levels of negative urgency, relevant personality
traits, and aggressive behavior. To disentangle the effects of negative urgency from
those of closely-related personality constructs, participants also reported their general
levels of negative affect (i.e., neuroticism), other facets of impulsivity and personality,
and dispositional self-control, which were accounted for in all analyses. These
hypotheses were tested among both females and males as previous research has
observed associations between MAOA genotype and aggression across both groups
(e.g., Kuepper et al., 2013).
2. Materials and Methods
2.1 Participants
Participants were originally 376 female and male undergraduates recruited from
introductory psychology courses and received both course credit and monetary
incentives for participation. “High risk” participants were over-recruited to ensure
MAOA, IMPULSIVITY, AND AGGRESSION 10
sufficient variability in conduct problems (e.g., aggression). Participants were
determined to be “high risk” if they fell within the upper quartile of a 12-item composite
measure of conduct problems administered in a screening session prior to recruitment.
Due to the relatively small numbers of racial minorities in this sample and the variance
in MAOA allelic frequency among these groups, racial minorities were excluded from
the sample to avoid population stratification. Participants were 277 Caucasian
undergraduates (50.9% female; Age: M = 18.88, SD = 0.47) of whom approximately
25% were categorized as “high risk”.
2.2 Measures
2.2.1. Aggression composite score. Items from two different measures were
aggregated to form a composite measure of aggression. Items included those from the
screening measure that assessed aggression (e.g., Before the age of 18, did you ever
pick on smaller peers or threaten or tease those who were too scared to fight you?;
Before the age of 18, did you ever take part in a fight where a group of your friends
were against another group?), and three additional aggression items from the Crime
and Analogous Behavior Scale (CAB; Lynam, Whiteside, & Jones, 1999), including:
Ever been in a physical fight?; Ever hurt someone intentionally to the extent that they
needed bandages or a doctor?; and Ever attacked someone with intent of seriously
hurting or killing them? All five items from the aggression composite were scored ‘yes’
or ‘no’ (1 and 0, respectively). Values were then summed across the five items to create
an aggression index that could range from 0 to 5.
2.2.2 UPPS-P Impulsivity Scale. The UPPS-P (Lynam, Smith, Whiteside, &
Cyders, 2006; Whiteside & Lynam, 2001) includes 59 items, scored on a 4-point Likert-
MAOA, IMPULSIVITY, AND AGGRESSION 11
style scale, assessing five distinct personality pathways to impulsive behavior: negative
urgency (the tendency to behave rashly when distressed), lack of premeditation (failure
to think about consequences of behavior before acting), lack of perseverance (failure to
persist in tasks or obligations), sensation seeking (preference for stimulation and
excitement), and positive urgency (tendency to act rashly when feeling positive
emotion). Internal consistency is good to excellent for all of the subscales in previous
research (Cyders & Smith, 2010; Whiteside, Lynam, & Miller, 2005) and in the present
study, α = .82-.93. Because of the high intercorrelation between negative and positive
urgency, r(275) = .75, p < .001, the lack of any research on positive urgency and MAOA
genotype, and the fact that negative, rather than positive, urgency has been shown to
relate to greater aggressive reactivity to provocation (e.g., Derefinko et al., 2011)
positive urgency scores were not included in any subsequent analyses.
2.2.3 Revised NEO Personality Inventory. The NEO-PI-R (Costa & McCrae,
1992) is a self-report questionnaire assessing general personality dimensions based on
the Five Factor Model of personality. The NEO-PI-R consists of 240 items, which are
rated on a 5-point scale, anchored by 1 (strongly disagree) and 5 (strongly agree). The
inventory provides scores for each of the five personality domains (Agreeableness,
Conscientiousness, Extraversion, Neuroticism, and Openness to Experience), with 48
questions per domain, as well as six facet scores per domain. An extensive research
base supports the reliability and validity of the NEO-PI-R (Costa & McCrae, 1992;
2010). The Agreeableness, Conscientiousness, Extraversion, Neuroticism, and
Openness to Experience domain scores demonstrated excellent internal consistency in
the present sample, α = .87-.92.
MAOA, IMPULSIVITY, AND AGGRESSION 12
2.2.4 Self-Control Scale. The Self-Control Scale is a 36-item self-report
questionnaire developed by Tangney, Baumeister, & Boone (2004) to assess individual
differences in multiple aspects of self-control. Items are rated on a 5-point scale, from
‘Not At All Like Me’ to ‘Very Much Like Me’. The total score demonstrated good internal
consistency in the present sample (α = .90). The construct of trait self-control is different
than conscientiousness as this trait reflects the dispositional ability and tendency to
effortfully inhibit prepotent impulses and action tendencies (Hoffman, Friese, & Strack,
2009).
2.3 Procedure
This study represents data from the first year of a 3-year longitudinal data
collection in which data were collected annually. With the exception of the trait self-
control data which was acquired in the second year, all data were obtained from the first
year precluding any longitudinal analyses. All study procedures were reviewed and
approved by the University of Kentucky’s IRB and a federal Certificate of Confidentiality
was acquired. After providing informed consent, participants were asked to voluntarily
provide a saliva sample for genotyping. Then, participants completed a battery of
computerized questionnaires which included the aggression items, UPPS-P impulsivity
scale, and NEO-PI-R personality scale. Participants returned for the second year in
which they completed another battery of computerized questionnaires which included
the Self-Control Scale.
Saliva samples were collected from the participants who signed additional
consent forms for genotyping at the time of the experiment. The subjects were de-
identified for genetic analysis. DNA was extracted from saliva samples in the genetic
MAOA, IMPULSIVITY, AND AGGRESSION 13
laboratory at the University of Kentucky’s College of Medicine. The de-identified DNA
samples were sent to Yale University’s Center for Genetics for genotyping.
2.3.1 Genotyping. DNA was purified from Oragene saliva collection kits
according to the manufacturer’s directions (DNA Genotek). DNA was quantified by UV
absorbance at 260 nm, diluted to 10 ng/µl and MAOA rs1465108 and MAOB SNPs
were genotyped by Sequenom MassARRAY iPLEX technology (W.M. Keck Foundation
Biotechnology Resource Laboratory at Yale University; http://ycga.yale.edu/). This
MAOA SNP, located at the position 43294463 MFA 0.338, has previously been linked to
antisocial personality disorder in adult females (Ducci et al., 2008), inattention-
hyporeactivity levels among children (Karmakar et al., 2014), autism spectrum disorder
(Verma et al., 2014), and the efficacy of antidepressants (Peters, Slager, McGrath,
Knowles, & Hamilton, 2004). This SNP has yet to be linked to aggression, though its
inclusion in the MAOA gene suggests it may exhibit just such an association. Because
the MAOA gene is X-linked, heterozygous genotypes (i.e., GA) were only possible
among females.
3. Results
3.1 Descriptives
Genotyping results on the rs1465108 SNP of the MAOA gene indicated that of
the 277 participants, 58.5% were of the GG genotypes, 22.0% were of the GA genotype
(all female), and 19.5% were of the AA genotype. The rs1465108 SNP was within
Hardy-Weinberg equilibrium, Χ2 = 1.86, p > .05. To assess the specificity of the MAOA
gene, we also genotyped participants on the rs295791 SNP of the MAOB gene, which
indicated that all participants were of the CC genotype. Because there was no variability
MAOA, IMPULSIVITY, AND AGGRESSION 14
in the MAOB genotype, no effects on aggression were tested. Across all MAOA
genotypes, aggression levels (which could range from 0 to 5) showed substantial
variability, M = 0.87, SD = 1.13, observed range = 0 - 5. To reflect genotypes that were
associated with low functioning MAOA, a dummy code was created in which GG
genotypes were coded as 0 and GA and AA genotypes were coded as 1. Thus, higher
values represented the presence of the MAOA minor allele (i.e., the A allele).
3.2 Mediation Model
A bias-corrected, bootstrapped mediation model (Preacher & Hayes, 2008) was
fit to the data using 1,000 bootstrap samples in which the dummy code for the MAOA
minor allele was the independent variable, negative urgency was the mediator, and the
aggression index was the dependent variable. Gender, personality traits relevant to
aggression (i.e., agreeableness, conscientiousness, extraversion, openness to
experience, neuroticism, self-control), and the other three facets of impulsivity (i.e., lack
of perseverance, lack of premeditation, sensation seeking) were included as covariates
of no interest. Of the 277 participants, five participants were missing NEO-PI-R data and
two participants were missing trait self-control data. Thus the mediation model was run
on the remaining 270 participants.
The mediation model explained a significant portion of variance in aggression,
F(12,257) = 8.48, p < .001, adjusted R2 = .25. Replicating previous research, the MAOA
minor allele was marginally associated with greater aggression, B = .25, t(258) = 1.92, p
= .056. Supporting our mediation hypotheses, low functioning MAOA genotype exhibited
an indirect effect on aggression through greater levels of negative urgency (95%
confidence interval: .007, .135; Figure 2); this indirect effect account for an estimated
MAOA, IMPULSIVITY, AND AGGRESSION 15
24% of the total effect of the genotype on aggression. Specifically, MAOA minor allele
was associated with greater negative urgency, B = .11, t(258) = 2.14, p = .033, which
was in turn associated with greater aggression, B = .48, t(258) = 3.05, p = .003.
Controlling for this indirect effect substantially reduced the effect of MAOA minor allele
on aggression, B = .19, t(258) = 1.53, p = .127, providing additional evidence for
mediation. Among the control variables, being female was significantly associated with
lesser aggression, B = -.54, t(258) = -3.68, p < .001, as was agreeableness, B = -.48,
t(258) = -2.79, p = .006. All other control variables failed to reach significance, Bs <
0.32, ps > .07. Using the mediation model described above, no other facet of impulsivity
significantly mediated the effect of low functioning MAOA genotype on aggressive
behavior.
Figure 2. Bootstrapped mediation model whereby greater negative urgency
mediated the positive association between MAOA minor allele and aggression.
Non-parenthesized values represent partial, unstandardized regression
coefficients. Parenthesized values represent standard errors of the regression
coefficients. Bracketed values represent the direct effect after controlling for the
indirect path. †p < .06, *p < .05, **p < .005.
MAOA, IMPULSIVITY, AND AGGRESSION 16
4. Discussion
Aggression costs humankind lives, resources, and suffering. Genetic markers
can predispose certain people to behave aggressively, but the psychological
phenotypes underlying this association remain underexplored. This study fills this gap in
the literature by identifying a psychological mechanism through which the low
functioning MAOA allele exerts its influence on aggression.
Consistent with previous research on the MAOA-aggression link, the positive
association between the low functioning, MAOA genotype and aggression (e.g.,
Eisenberger et al., 2007; Gallardo-Pujol et al., 2013; Kuepper et al., 2013; McDermott et
al., 2009). We were also able to substantiate the link between low functioning MAOA
allelic variants on a new SNP that has never before been linked to aggression.
Demonstrating this effect across SNPs on the MAOA gene emphasizes the aggression-
promoting effect of this location on the genotypic map.
Most notably, our findings built upon this established correlation by
demonstrating statistical mediation of the effect of the MAOA minor allele on aggressive
behavior via heightened negative urgency, while controlling for potential confounds.
These findings suggest a unique psychological phenotype, impulsivity under conditions
of negative affect, which helps explain how the low functioning MAOA genotype
influences aggression. This finding meshes well with previous research on the MAOA
gene showing that it predicts greater retaliatory aggression after exclusion or
provocation (Gallardo-Pujol et al., 2013; Kuepper et al., 2013; McDermott et al., 2009),
both of which can be readily construed as an induction of negative affect (Anderson &
Bushman, 2002; Williams, 2009). This empirical emphasis on context specificity fits
MAOA, IMPULSIVITY, AND AGGRESSION 17
within the gene-by-environment interactionist approaches to behavioral genetics that
has yielded great gains and promises to yield much more. Our findings add to a growing
body of literature that demonstrates that the MAOA gene increases the likelihood of
aggression only elicited under conditions of negative affect such as provocation or
social rejection (McDermott et al., 2009).
Our findings also continue to implicate negative urgency as a personality trait and
facet of impulsivity that is uniquely potent in the domain of violence (e.g., Derefinko et
al., 2011). More so, our ability to implicate negative urgency as a mechanism of the
MAOA-aggression link and not other facets of impulsivity (e.g., sensation seeking)
supports the UPPS model of impulsivity, in which impulsivity is comprised of distinct
facets which differentially predict such negative outcomes as aggression (Cyders &
Smith, 2008; Whiteside & Lynam, 2001). This multifaceted view of impulsivity’s
relationship with aggression informs potential interventions for aggressive behavior,
suggesting that targeting reactivity in the context of negative affect and not impulsivity
more generally, may be useful to reduce violence and other problematic behavioral
tendencies.
4.1 Limitations and Future Directions
Our findings were limited in several ways that suggest future avenues for
research. Due to differences in allelic frequencies between racial groups, our findings
are limited to the individuals with Caucasian ancestry and future research should
assess whether these effects hold across racial categories. Second, aggressive
behavior was reported and not observed or measured objectively, thus reports may
have been prone to biases in participants’ recollection. Future research may assess
MAOA, IMPULSIVITY, AND AGGRESSION 18
these effects using valid aggression measurements such as the Taylor Aggression
Paradigm (Anderson & Bushman, 1997) or the voodoo doll task (DeWall et al., 2013). In
addition, future neuroimaging measurements will serve as intermediate phenotypes of
affect-related brain circuits between genetics and behavior (Parasuraman & Jiang,
2012). Third, we were unable to tease apart aggressive behavior that was due to
provocation and that which was not because our measure did not specify this
distinction. Because provocation is the most reliable predictor of aggression (Anderson
& Bushman, 2002), it is safe to assume that much of the aggression reported by our
participants was retaliatory in nature. Fourth, the direct effect of MAOA genotype on
aggressive behavior was only marginally statistically significant. However, the direct
path of mediation models are often statistically underpowered compared to the indirect
effect (Kenny & Judd, 2013). Thus our marginally significant direct effect may be due to
the nature of the mediation test and less a reflection of the actual nature of the
association between MAOA genotype and aggression.
5. Conclusions
Aggression plagues mankind and is a hallmark of many psychopathologies.
Genetic influences on aggressive behavior may cause some to lose hope of ever
reducing violence, yet understanding how genes such as the MAOA gene express
themselves as personality phenotypes allow the opportunity to gain traction on these
effects. We showed that the association between the low functioning variant of the
MAOA gene and aggression likely occurs through increases in impulsivity that is
specific to conditions of negative affect. By understanding the nuanced conditions
MAOA, IMPULSIVITY, AND AGGRESSION 19
through which genes code for aggressive personalities, we may be able to impede the
tide of aggressive acts.
MAOA, IMPULSIVITY, AND AGGRESSION 20
Acknowledgments
This research was supported by funding from the National Institutes of Health
(grant P50-DA05312) to University of Kentucky’s Center for Drug Abuse Research
Translation and from the University of Kentucky’s Department of Behavioral Science.
The authors also gratefully acknowledge research support from the National Institutes
on Drug Abuse (DA007304 and T32DA035200) and National Center for Advancing
Translational Sciences (UL1TR000117) of the National Institutes of Health. The content
is solely the responsibility of the authors and does not necessarily reflect the official
views of the National Institutes of Health. We also thank Richard Milich for his
assistance in developing the study and in data collection, and Ke Xu for comments in an
earlier version of the manuscript.
MAOA, IMPULSIVITY, AND AGGRESSION 21
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