On emotional information and behavioural regulation. The reduced functional

On biological level, this extension could be
attributed to genetic and neurological factors. Consistently, around 40-50%
genetic overlap between CU traits and antisocial behaviour was found (Viding &
Larsson, 2010; Larsson et al., 2008). The strong
genetic basis does not only make individuals with CU traits more vulnerable to antisocial
behaviour, but also contributes to their stability towards adulthood
psychopathy. A 7-year longitudinal study between 17 and 24 years
old found 58% and 62% of the stability in fearless dominance and impulsive-antisocial dimensions were
due to genetic influences (Blonigen et al., 2006). Although the molecular
genetics of psychopathy is still in infancy, the similar brain abnormalities in
CU and psychopathic traits may be one of its
influences. Neurological evidence regarding CU traits and psychopathy is
robust, but the contributions of aberrant
limbic-prefrontal circuit to deficits in encoding emotional associations for
behavioural regulation are decently recognized. Amygdala malfunction plays a
critical role in emotional deficits. Structurally, both CU traits and
psychopathy were consistently found to be associated with volume reduction in amygdala (Cohn et al., 2016; Yang et al., 2009). Functionally, hypoactive amygdala is associated with insensitivity
towards pre-attentively masked fear (Viding et al., 2012; Jones et al.,
2009; Marsh et al., 2008), and higher evaluated acceptability of causing
others’ distress (Cardinale et al., 2017; Marsh & Cardinale, 2014) in CU traits and psychopathy. Amygdala has reciprocal connections
with frontal cortex for incorporation of emotional information and behavioural
regulation. The reduced functional connectivity within the limbic-prefrontal
circuit in CU traits (Yoder et al., 2016) and psychopathy (Motzkin et
al., 2011) leads to impairments in both emotionality and behavioural
regulation. Although neurological findings on abnormalities
in frontal cortex are inconsistent, some studies suggested smaller bilateral
orbitofrontal cortex (OFC) in juvenile delinquents with high CU traits (Sebastian
et al., 2016) and 22.3% prefrontal gray matter
reduction in psychopaths (Yang et al., 2005). Studies with psychopaths have further located the reward-dominant
cognitive style to hyperactive nucleus accumbens during reward
anticipation (Hosking et al., 2017; Buckholtz et al., 2010). Importantly, with
weaker connectivity within the circuit, it seems that
cortical regions are failed to update both positive and negative valence in CU
traits and psychopathy. During reward anticipation, CU traits and psychopathy
are negatively related to prefrontal cortex activity (Murray et al.,
2017; Veroude et al, 2016; Hosking et al., 2017); and
psychopaths shown diminished left amygdala and OFC activation during punishment
anticipation (Birbaumer et al., 2005). As mentioned, psychopaths have inverted sense of reward. It is possible
that individuals with CU or psychopathic traits are not only incapable in
learning from social punishment, but they are also prone to seek rewards from
aggression due to reward insensitivity.

 

CU
traits do not necessarily develop into psychopathy, but witnessing violence
could increase the risk. Studies reported significant number of youths who
showed decreases in level of CU traits over years (Frick & White, 2008;
Andershed, 2010), and social-learning-based parent training has found to be
relatively effective in improving CU traits (Hawes et al., 2014). This means
that despite stability contributed by biological and psychological factors,
environmental influences do seem to play a role in CU traits’ developmental
trajectories. There are several studies suggested that witnessing violence
would possibly maintain or increase CU traits and violent delinquency. Juvenile
delinquents in detention centre with high levels of CU and psychopathic traits
reported more lifetime violence exposure (Kimonis et al., 2008; Schraft et al.,
2013). Witnessing violence, but not direct victimization, mediated the positive
relationship between CU traits and violent delinquency (Howard et al., 2012). Recently,
study with adult psychopaths found positive relationship between witnessing
violence and levels of psychopathy, and even stronger association with
affective features of psychopathy (Dargis & Koenigs, 2017). Together, these
findings have suggested witnessing violence as a perpetuating factor of CU
traits and associated aggressive behaviour. Beyond that, its strong
relationship with affective features of psychopathy indicates potential
associations between CU traits, witnessing violence and adulthood psychopathy. The
findings were further generalized to community samples. In a 5-year
longitudinal study, witnessing violence was again found to be the mediator
between CU traits and violent delinquency (Oberth et al., 2017). Another
longitudinal study with high-risk 6th graders further suggested a
bidirectional relationship between physical aggression and witnessing violence
(Farrell et al., 2014). This is possible that the “fearlessness” and
“reward-dominant” temperaments drive individuals with CU traits to expose to
violence, and insensitivity to aversive social feedback makes them more likely
to model aggressive behaviour despite causing others’ suffers. The social
learning of “violence” is not only behaviourally, but also biologically-based:
studies have suggested that chronic exposure to violence could lead to moral
and emotional desensitization. In was found that even short-term repeated
exposure to violent clips could lead to diminished activity in OFC, as well as
reduced amygdala-OFC function connectivity (Kelly et al., 2007). Considering
long-term effects, amygdala activation responding to violent words was negatively
correlated to high levels, but positively correlated to low levels of media
violence exposure in adolescents with behavioural problems (Kalnin et al.,
2011). However, the relationship was reversed in control groups. This means
that individuals with conduct problems may be biologically more vulnerable to
violence modelling. Although Baskin-Sommers and colleagues (2015) did not
identify subgroups with changing levels of CU traits over 5-year period in male
offenders between 14 and 18 years old, it is possibly due to the relatively old
juvenile samples they used. Witnessing violence has a convincing role in
perpetuating or modulating CU traits development towards psychopathy, but its
importance decreases over time as the traits become relatively stable.

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In conclusion, the
reciprocal relationship between CU traits and violence could account for
psychological, biological and environmental precursors to psychopathy. Youths
with CU traits are more likely to expose to and engage in violence.