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 includesirresponsibility, inability to maintain loving relationships, becoming easilyfrustrated, passing blame; along with several other attributes which have alsobeen associated with psychopathy; callousness, lack of remorse and lack ofempathy (American Psychiatric Association, 1994). Although this diagnosticcategory is quite broad, covering delinquency in childhood as well as those whocommit the most severe crimes, researchers have deemed it the most reliable ofdiagnostic categories due to the differentiation and extension of symptomsacross a life-span (Coid, 2003; Pulkkinen, 2001). ASPD has proven to be costlyfor society with those who suffer from ASPD costing public services up to tentimes what the average individual costs; based on mental and physical healthproblems and criminal convictions (Scott, Knapp, Henderson & Maughan, 2001;Odgers et al.

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, 2008). ASPD is strongly, statistically associated with criminaloffending and aggressive, destructive behaviour; with 63% of male remandprisoners, 49% of male sentenced prisoners and 31% of female prisoners holdinga ASPD diagnosis in England and Wales (Office for National Statistics, 1997). TheWorld Health Organization (WHO) describes risk factors as “any attribute,characteristic or exposure of an individual that increases the likelihood ofdeveloping a disease or injury” (“risk factors”, n.d.). It is important toidentify risk factors which could trigger or even cause ASPD in order toinvestigate potential solutions particularly in terms of resolving the negativeimpacts on society. Developing understanding of the extent to which thesefactors impact the prevalence of ASPD helps government and NHS developintervention and rehabilitation schemes to work towards prevention ofacquisition. Research has considered both static and dynamic risk factors forASPD, for example: brain physiology, genetics, childhood experiences andmaltreatment, peer influence and television consumption.

This essay looks todiscuss and evaluate existing research regarding the extent of the impact of staticand dynamic risk factors upon the diagnosis and development of ASPD.            Brainphysiology is one potential risk factor of ASPD, there is evidence to suggestthat poor functioning in the prefrontal cortex is associated with violent andanti-social behaviour (Raine, Meloy, Bihrle, Stoddard, LaCasse & Buchsbaum,1998). Case studies have provided support for the idea that poor functioning ordamage to the prefrontal cortex results in various social problems, for examplelack 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 studyevidence comes from individuals who have suffered from an accident or havelesions on the brain, whereas ASPD is present across a lifespan separate frombrain damage.

The symptoms which presented upon experiencing damage to theprefrontal lobe encouraged researchers to investigate deficits in theprefrontal cortex of individuals with ASPD.            Theprefrontal cortex by nature regulates emotion, arousal, attention and decisionmaking (Davidson, 1993; Raine, Reynolds, Sheard, 1991). When reviewed in moredetail using magnetic resonance imaging (MRI) individuals with ASPD exhibitedmajor differences in the volume of gray and white matter in the prefrontalcortex (Raine, Lencz, Bihrle, LaCasse & Colletti, 2000).

Compared to acontrol group individuals with ASPD showed an 11% reduction in gray mattervolume; which explains symptoms such as low arousal, lack of conscience andlack 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 graymatter in the prefrontal cortex compared to females, which offers a potentialexplanation for the sex differences in ASPD; males gray matter volume in thepre-frontal cortex is reduced compared to females, and an individual with ASPDhas an even lower volume than males (Raine, Yang, Narr & Toga, 2009). Besidesgender differences, this also provides supporting evidence for the argumentthat individuals with ASPD have a predetermined genetic vulnerability todeveloping the disorder; reduced amount of gray matter in the prefrontal cortexreduces one’s ability to regulate emotion and make rational decisions thereforeexplaining some of the symptoms of ASPD e.g. incapacity to maintainrelationships,  irresponsibility, andlack of empathy (Gregory, Fftche, Simmons, Kumari, Howard, Hodgins , 2012). However in many studies which have considered gray mattervolume in regards to ASPD, it is not made clear whether the participants alsosuffer from co-morbid disorders such as psychopathy or substance abuse (Yang& Raine, 2009; Raine, Yang, Narr & Toga, 2009).

            Itis difficult to pinpoint reduction in gray matter uniquely to ASPD as thepresented symptoms also identify with psychopathy. ASPD is co-morbid withpsychopathy and shares selected symptoms with psychopathy disorders; thereforeit could be argued that the pre-frontal cortex deficits are a risk-factor forpsychopathy rather than ASPD as the two overlap. ASPD is also consideredco-morbid with substance abuse disorders; up to 85% of individuals with ASPDalso fit the criteria for substance abuse (Regier, Farmer, Rae, Locke, Keith,Judd & Goodwin, 1990). Many studies do not clarify whether the participantsalso suffer from substance abuse; as a result it is not clear whether thereduction in gray matter is a predetermined deficit or if it is a result of substanceabuse disorders (Gregory et al., 2012).

Furthermore ASPD is a spectrum disorderwhich means symptoms can vary in terms of severity and number of symptomsexperienced, given the broad nature of ASPD, it is difficult to explain throughneuroimaging as it doesn’t account for individual differences in symptomexpression (Gregory et al., 2012).             Unlikeother disorders, ASPD does not have an established biological marker, whichmakes it difficult to make predictions surrounding development and diagnosis(Rogers, Dion and Lynett, 1992). However a meta-analytic review concludedgenetics to explain 56% of variance in ASPD; and genetic effects are consideredlargely gender specific (Eaves, Prom & Silberg, 2010). ASPD has beenestablished as much more prominent among males compared to females, for exampleRobins and Price (1991) conducted a epidemiological catchment area project andfound the prevalence of ASPD among men in the US was six times higher than infemales.

One genotype in particular was found to impact the development ofASPD: monoamine oxidase (MOAO). Recent research has established the MOAOgenotype to have a large impact on whether an individual exhibits ASPD symptoms(Ferguson, 2010). Having low MOAO activity increases the likelihood of the developmentof ASPD when a child has been exposed to maltreatment; whereas if an individualexhibits high MOAO activity they are less likely to develop ASPD, despite exposureto maltreatment (Ferguson, 2010). The high activity MOAO genotype is arecessive in nature and it is only present on the X chromosome; this mightexplain why ASPD is more prominent in males, as females are more likely toinherit the high activity MOAO genotype through their homogenous X chromosomes(Ferguson, 2010).

However the MOAO genotype itself does not cause ASPD, insteadit just places individuals at higher risk of developing it; it relies onassistance from environmental factors in order for ASPD to manifest itselfwhich highlights the overlap in static and dynamic risk factors. It also needsto be taken into account that not every person with ASPD has the MOAO genotypeso this alone can’t be accountable for the development of ASPD (Ducci, Enoch,Hodgkinson, Xu, Catena, Robin & Goldman, 2007).            Non-geneticfactors are said to explain 31% of variance in ASPD (Ferguson, 2010). As isevident from the research into the MOAO genotype, environment plays animportant role in the development and expression of anti-social behaviour.Having an adverse family environment from a young age is said to stronglyencourage the development of ASPD; for example there is a significantassociation 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 hascontrolled for demographic characteristics, including gender, race, familysocial class and socioeconomic status; which implies that the strongsignificant relationship between childhood maltreatment and development of ASPDis highly reliable (Luntz & Widom, 1994; Johnson, Cohen, Brown, Smailes& Bernstein, 1999; Krastins, Francis, Field & Carr, 2014). ASPD hasbeen associated with low parental care and high maternal overprotection;suggesting that either end of the spectrum (over protectiveness or completeunavailability) increases the likelihood of the prevalence of anti-socialpersonality traits and development of the disorder (Reti, Samuels, Eaton,Bienvenu, Costa Jr & Nestadt, 2002).

However more recent research has arguedthat anti-social parents and more specifically maternal withdrawal areparticularly high predictors of ASPD; anti-social parents have poorer parentingstrategies, the inconsistency and lack of warmth and affection predicts theextent 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).            Ithas been argued that environmental influences separate from family life also impactthe development of ASPD; Kasen, Cohen and Brooks (1998) concluded that having ahigher proportion of deviant friends during childhood and adolescence increasedthe likelihood of being diagnosed with ASPD. The study controlled for age,gender, school performance, earlier behavioural problems, and socioeconomicstatus and still found the relationship between deviant friends and ASPDdiagnosis to be significant. Similarly longitudinal research by Fergusson andHorwood (1999) found that being part of a friendship group with deviantindividuals in adolescence was a predictor of deviancy and the development of ASPD.This study used a randomly selected and representative sample and accounted foradjustments of school effects, IQ, socioeconomic status and childhood conductproblems; so the established relationship was entirely independent. Challengingresearch has argued that it is potentially the predisposed genetic vulnerabilityand/or parent absenteeism which encourages deviant personality traits such asloss of control and impulsivity; which in turn makes individuals more attractedto delinquent personality styles among peers (Beaver, Schutt, Eagle, Boutwell,Ratchford, Roberts & Barnes, 2009). This makes it difficult to establishwhether having deviant peers predicts the development of ASPD or ifpre-existing attachment issues predict friendships with deviant individuals;which would mean being part of a group of deviant individuals is a symptom ofpre-existing issues and only further encourages development of ASPD.            Researchinvestigating the impact of the media upon antisocial behaviour implies individualswho spend more time watching TV during childhood are significantly more likelyto receive a diagnosis of ASPD and/or have a criminal conviction  (Johnson, Cohen, Smailes, Kasen & Brook,2002; Robertson, McAnally & Hancox, 2013).

These studies controlled forsex, IQ, socioeconomic status, previous anti-social  behaviour, parental control, childhoodneglect, parental education and other psychiatric disorders; so provide a strong, reliable relationship between televisionconsumption and ASPD diagnosis. However these studies did not consider thecontent of the TV watched and whether that impacted these results, so it ishard to unveil which programmes have the most detrimental effects or proposethe biggest risk of developing ASPD (Robertson, McAnally & Hancox, 2013).It has been argued that the causation could be reversed, those who aregenetically predisposed to ASPD may watch more TV as a result of beingwithdrawn and having such disregard for social norms rather than televisioncausing the development of ASPD (Glenn, Johnson & Raine, 2013).

            Toconclude, it is apparent that both static and dynamic risk factors playimportant roles in mediating ASPD. Research is clear in that there arebiological discrepancies between the brain of an individual with ASPD incomparison to the average person, however it is yet to be established whetherthese discrepancies are the result of co-morbid disorders such as substanceabuse and psychopathy (Raine et al., 1998; Gregory et al.

, 2012; Yang , 2009; Raine, Yang, Narr & Toga, 2009). Majority of research usesprisoners or patients of psychiatric hospitals as participants to investigateASPD, which means it is not representative of the general population nor doesit account for individuals who have a less severe diagnosis of ASPD (De Brito& Hodgins, 2009; Robins & Price, 1991; Regier et al., 1990). Additionallyit can be argued that there is conclusive interaction between static anddynamic risk factors; for example the presence of the high activity MOAOgenotype has the ability to deter development of antisocial behaviour despiteexposure to maltreatment in childhood (Ferguson, 2010; Ducci et al., 2008).Separate from biology, environment also has a significant impact on ASPDdevelopment, an adverse family environment during upbringing, deviant peers inadolescence and television consumption all have been established as having asignificant 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 for13% of the variance in ASPD and again substance abuse disorders were notcontrolled for (Krastins, Francis, Field & Carr, 2014).

Future researchshould look to explore risk factors of ASPD whilst controlling for co-morbidityof other disorders such as substance abuse so that it is clear that thesefactors are influencing ASPD directly.