Antisocial prevalence of ASPD helps government and NHS

Antisocial personality disorder
(ASPD) is one of few personality disorders included in  the DSM-IV (World Health Organisation, 1992; DSM-IV-TR,
American Psychiatric Association, 1994). Criteria for this disorder includes
irresponsibility, inability to maintain loving relationships, becoming easily
frustrated, passing blame; along with several other attributes which have also
been associated with psychopathy; callousness, lack of remorse and lack of
empathy (American Psychiatric Association, 1994). Although this diagnostic
category is quite broad, covering delinquency in childhood as well as those who
commit the most severe crimes, researchers have deemed it the most reliable of
diagnostic categories due to the differentiation and extension of symptoms
across a life-span (Coid, 2003; Pulkkinen, 2001). ASPD has proven to be costly
for society with those who suffer from ASPD costing public services up to ten
times what the average individual costs; based on mental and physical health
problems and criminal convictions (Scott, Knapp, Henderson & Maughan, 2001;
Odgers et al., 2008). ASPD is strongly, statistically associated with criminal
offending and aggressive, destructive behaviour; with 63% of male remand
prisoners, 49% of male sentenced prisoners and 31% of female prisoners holding
a ASPD diagnosis in England and Wales (Office for National Statistics, 1997). The
World Health Organization (WHO) describes risk factors as “any attribute,
characteristic or exposure of an individual that increases the likelihood of
developing a disease or injury” (“risk factors”, n.d.). It is important to
identify risk factors which could trigger or even cause ASPD in order to
investigate potential solutions particularly in terms of resolving the negative
impacts on society. Developing understanding of the extent to which these
factors impact the prevalence of ASPD helps government and NHS develop
intervention and rehabilitation schemes to work towards prevention of
acquisition. Research has considered both static and dynamic risk factors for
ASPD, for example: brain physiology, genetics, childhood experiences and
maltreatment, peer influence and television consumption. This essay looks to
discuss and evaluate existing research regarding the extent of the impact of static
and dynamic risk factors upon the diagnosis and development of ASPD.

            Brain
physiology is one potential risk factor of ASPD, there is evidence to suggest
that poor functioning in the prefrontal cortex is associated with violent and
anti-social behaviour (Raine, Meloy, Bihrle, Stoddard, LaCasse & Buchsbaum,
1998). Case studies have provided support for the idea that poor functioning or
damage to the prefrontal cortex results in various social problems, for example
lack of ability to make rational decisions, process emotions and respond to
‘meaningful’ stimuli (Damasio, Grabowski, Frank, Galaburda & Damasio, 1994;
Damasio, Tranel & Damasio, 1990). However majority of the case study
evidence comes from individuals who have suffered from an accident or have
lesions on the brain, whereas ASPD is present across a lifespan separate from
brain damage. The symptoms which presented upon experiencing damage to the
prefrontal lobe encouraged researchers to investigate deficits in the
prefrontal cortex of individuals with ASPD.

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            The
prefrontal cortex by nature regulates emotion, arousal, attention and decision
making (Davidson, 1993; Raine, Reynolds, Sheard, 1991). When reviewed in more
detail using magnetic resonance imaging (MRI) individuals with ASPD exhibited
major differences in the volume of gray and white matter in the prefrontal
cortex (Raine, Lencz, Bihrle, LaCasse & Colletti, 2000). Compared to a
control group individuals with ASPD showed an 11% reduction in gray matter
volume; which explains symptoms such as low arousal, lack of conscience and
lack of ability to make rational decisions (Barkataki, Kumari, Das, Taylor
& Sharma, 2006; Laakso, Gunning-Dixon, Vaurio, Repo-Tiihonen, Soirinen
& Tiihonen, 2002; Narayan et al., 2007). Males as a whole have reduced gray
matter in the prefrontal cortex compared to females, which offers a potential
explanation for the sex differences in ASPD; males gray matter volume in the
pre-frontal cortex is reduced compared to females, and an individual with ASPD
has an even lower volume than males (Raine, Yang, Narr & Toga, 2009). Besides
gender differences, this also provides supporting evidence for the argument
that individuals with ASPD have a predetermined genetic vulnerability to
developing the disorder; reduced amount of gray matter in the prefrontal cortex
reduces one’s ability to regulate emotion and make rational decisions therefore
explaining some of the symptoms of ASPD e.g. incapacity to maintain
relationships,  irresponsibility, and
lack of empathy (Gregory, Fftche, Simmons, Kumari, Howard, Hodgins &
Blackwood, 2012). However in many studies which have considered gray matter
volume in regards to ASPD, it is not made clear whether the participants also
suffer from co-morbid disorders such as psychopathy or substance abuse (Yang
& Raine, 2009; Raine, Yang, Narr & Toga, 2009).

            It
is difficult to pinpoint reduction in gray matter uniquely to ASPD as the
presented symptoms also identify with psychopathy. ASPD is co-morbid with
psychopathy and shares selected symptoms with psychopathy disorders; therefore
it could be argued that the pre-frontal cortex deficits are a risk-factor for
psychopathy rather than ASPD as the two overlap. ASPD is also considered
co-morbid with substance abuse disorders; up to 85% of individuals with ASPD
also fit the criteria for substance abuse (Regier, Farmer, Rae, Locke, Keith,
Judd & Goodwin, 1990). Many studies do not clarify whether the participants
also suffer from substance abuse; as a result it is not clear whether the
reduction in gray matter is a predetermined deficit or if it is a result of substance
abuse disorders (Gregory et al., 2012). Furthermore ASPD is a spectrum disorder
which means symptoms can vary in terms of severity and number of symptoms
experienced, given the broad nature of ASPD, it is difficult to explain through
neuroimaging as it doesn’t account for individual differences in symptom
expression (Gregory et al., 2012).

            Unlike
other disorders, ASPD does not have an established biological marker, which
makes it difficult to make predictions surrounding development and diagnosis
(Rogers, Dion and Lynett, 1992). However a meta-analytic review concluded
genetics to explain 56% of variance in ASPD; and genetic effects are considered
largely gender specific (Eaves, Prom & Silberg, 2010). ASPD has been
established as much more prominent among males compared to females, for example
Robins and Price (1991) conducted a epidemiological catchment area project and
found the prevalence of ASPD among men in the US was six times higher than in
females. One genotype in particular was found to impact the development of
ASPD: monoamine oxidase (MOAO). Recent research has established the MOAO
genotype to have a large impact on whether an individual exhibits ASPD symptoms
(Ferguson, 2010). Having low MOAO activity increases the likelihood of the development
of ASPD when a child has been exposed to maltreatment; whereas if an individual
exhibits high MOAO activity they are less likely to develop ASPD, despite exposure
to maltreatment (Ferguson, 2010). The high activity MOAO genotype is a
recessive in nature and it is only present on the X chromosome; this might
explain why ASPD is more prominent in males, as females are more likely to
inherit the high activity MOAO genotype through their homogenous X chromosomes
(Ferguson, 2010). However the MOAO genotype itself does not cause ASPD, instead
it just places individuals at higher risk of developing it; it relies on
assistance from environmental factors in order for ASPD to manifest itself
which highlights the overlap in static and dynamic risk factors. It also needs
to be taken into account that not every person with ASPD has the MOAO genotype
so this alone can’t be accountable for the development of ASPD (Ducci, Enoch,
Hodgkinson, Xu, Catena, Robin & Goldman, 2007).

            Non-genetic
factors are said to explain 31% of variance in ASPD (Ferguson, 2010). As is
evident from the research into the MOAO genotype, environment plays an
important role in the development and expression of anti-social behaviour.
Having an adverse family environment from a young age is said to strongly
encourage the development of ASPD; for example there is a significant
association between childhood maltreatment, parental engagement, and ASPD (Lee,
Brook, Finch & Brook, 2015; Krastins, Francis, Field & Carr, 2014).
Majority of research into childhood maltreatment as a risk factor for ASPD has
controlled for demographic characteristics, including gender, race, family
social class and socioeconomic status; which implies that the strong
significant relationship between childhood maltreatment and development of ASPD
is highly reliable (Luntz & Widom, 1994; Johnson, Cohen, Brown, Smailes
& Bernstein, 1999; Krastins, Francis, Field & Carr, 2014). ASPD has
been associated with low parental care and high maternal overprotection;
suggesting that either end of the spectrum (over protectiveness or complete
unavailability) increases the likelihood of the prevalence of anti-social
personality traits and development of the disorder (Reti, Samuels, Eaton,
Bienvenu, Costa Jr & Nestadt, 2002). However more recent research has argued
that anti-social parents and more specifically maternal withdrawal are
particularly high predictors of ASPD; anti-social parents have poorer parenting
strategies, the inconsistency and lack of warmth and affection predicts the
extent of ASPD features independently of whether child experiences abuse (Shi,
Bureau, Easterbrooks, Zhao & Lyons-Ruth, 2012; Roberts, Gilman,
Fitzmaurice, Decker & Koenen, 2010; Semiz, Basoglu, Ebrinc & Cetin,
2007).

            It
has been argued that environmental influences separate from family life also impact
the development of ASPD; Kasen, Cohen and Brooks (1998) concluded that having a
higher proportion of deviant friends during childhood and adolescence increased
the likelihood of being diagnosed with ASPD. The study controlled for age,
gender, school performance, earlier behavioural problems, and socioeconomic
status and still found the relationship between deviant friends and ASPD
diagnosis to be significant. Similarly longitudinal research by Fergusson and
Horwood (1999) found that being part of a friendship group with deviant
individuals in adolescence was a predictor of deviancy and the development of ASPD.
This study used a randomly selected and representative sample and accounted for
adjustments of school effects, IQ, socioeconomic status and childhood conduct
problems; so the established relationship was entirely independent. Challenging
research has argued that it is potentially the predisposed genetic vulnerability
and/or parent absenteeism which encourages deviant personality traits such as
loss of control and impulsivity; which in turn makes individuals more attracted
to delinquent personality styles among peers (Beaver, Schutt, Eagle, Boutwell,
Ratchford, Roberts & Barnes, 2009). This makes it difficult to establish
whether having deviant peers predicts the development of ASPD or if
pre-existing attachment issues predict friendships with deviant individuals;
which would mean being part of a group of deviant individuals is a symptom of
pre-existing issues and only further encourages development of ASPD.

            Research
investigating the impact of the media upon antisocial behaviour implies individuals
who spend more time watching TV during childhood are significantly more likely
to receive a diagnosis of ASPD and/or have a criminal conviction  (Johnson, Cohen, Smailes, Kasen & Brook,
2002; Robertson, McAnally & Hancox, 2013). These studies controlled for
sex, IQ, socioeconomic status, previous anti-social  behaviour, parental control, childhood
neglect, parental education and other psychiatric disorders; so provide a strong,
 reliable relationship between television
consumption and ASPD diagnosis. However these studies did not consider the
content of the TV watched and whether that impacted these results, so it is
hard to unveil which programmes have the most detrimental effects or propose
the biggest risk of developing ASPD (Robertson, McAnally & Hancox, 2013).
It has been argued that the causation could be reversed, those who are
genetically predisposed to ASPD may watch more TV as a result of being
withdrawn and having such disregard for social norms rather than television
causing the development of ASPD (Glenn, Johnson & Raine, 2013).

            To
conclude, it is apparent that both static and dynamic risk factors play
important roles in mediating ASPD. Research is clear in that there are
biological discrepancies between the brain of an individual with ASPD in
comparison to the average person, however it is yet to be established whether
these discrepancies are the result of co-morbid disorders such as substance
abuse and psychopathy (Raine et al., 1998; Gregory et al., 2012; Yang &
Raine, 2009; Raine, Yang, Narr & Toga, 2009). Majority of research uses
prisoners or patients of psychiatric hospitals as participants to investigate
ASPD, which means it is not representative of the general population nor does
it account for individuals who have a less severe diagnosis of ASPD (De Brito
& Hodgins, 2009; Robins & Price, 1991; Regier et al., 1990). Additionally
it can be argued that there is conclusive interaction between static and
dynamic risk factors; for example the presence of the high activity MOAO
genotype has the ability to deter development of antisocial behaviour despite
exposure to maltreatment in childhood (Ferguson, 2010; Ducci et al., 2008).
Separate from biology, environment also has a significant impact on ASPD
development, an adverse family environment during upbringing, deviant peers in
adolescence and television consumption all have been established as having a
significant positive relationship with the development of ASPD (Lee, Brook,
Finch & Brook, 2015; Shi, Bureau, Easterbrooks, Zhao & Lyons-Ruth,
2012; Kasen, Cohen & Brooks, 1998; Fergusson & Howard, 1996; Robertson,
McAnally & Hancox, 2013). However childhood experiences only account for
13% of the variance in ASPD and again substance abuse disorders were not
controlled for (Krastins, Francis, Field & Carr, 2014). Future research
should look to explore risk factors of ASPD whilst controlling for co-morbidity
of other disorders such as substance abuse so that it is clear that these
factors are influencing ASPD directly.