The Genetic and Environmental Causes of Antisocial Personality Disorder

Antisocial Personality Disorder (ASPD) is a personality disorder that is characterized by chronic boredom or irritability, as well as the blatant disregard for society’s norms.[1] ASPD is an umbrella term that encompasses individuals with both psychopathic and sociopathic tendencies. A great deal of research has been conducted upon identifying and understanding the phenotypes and symptoms of ASPD, however not much is known about the causes. Researchers are generally in agreement, however, that it is a combination of environmental and genetic influences that preclude the onset of the disorder.[1] Sociopathic tendencies are believed to have a greater influence from environmental factors, whereas symptoms that are more psychopathic in nature are considered to be more heavily influenced by genetics.[2]

1. Psychopathy vs. Sociopathy

The symptoms of ASPD have been documented throughout human history, however it is only in recent times that a name was given to them: psychopathy.[2] Although psychopathy is the popular term to define the symptoms of the disorder, it does not offer a complete picture, as ASPD is an umbrella term than encompasses both psychopathy and sociopathy. Although similar, the two branches of ASPD vary in how they are believed to be caused, as well as the ultimate outcome the disease has on shaping their personalities.[2]

Psychopathy is believed by most researchers to be primarily biological in origin, and it is thought that not all psychopaths turn to criminal behaviour despite the inherent lack of empathy. It is also widely considered that the number of psychopaths in society is small, and that this number stays relatively stable throughout cultures and time periods.[2]

Sociopathy, on the other hand, is believed to have its origins due to environmental and societal causes. Although there is believed to be a genetic link with sociopaths as well, it is more the adverse conditions that they may have been subject to in their early childhood, including poverty and abuse, that eventually results in sociopathic behaviour. Unlike psychopaths, the number of sociopaths in society fluctuates, and they tend to come from lower class households as well as disadvantaged minority groups. It has also been studied that sociopaths inevitably turn to a life of crime.[2]

1.1 Environmental Influences

There is no doubt that environmental influences play a key role in ASPD. One of the criteria of diagnosing ASPD is that the person in question must have displayed some antisocial tendencies before the age of 15.[2] Due to this, it can be concluded that a person’s early childhood life has a great impact on the subsequent development of ASPD.

A chaotic family life with an absence of supervision from parents or other adult role models contributes greatly to this personality disorder, as well as in communities where there is little reward for positive behaviour, or where negative behaviour is actually praised.[1] A study was performed by Alloway et al. in the United Kingdom, where they examined the contribution of cognitive, behavioural and environmental influences on antisocial adolescents that had been expelled from school. Using a geodemographic database, they determined that 53% of the adolescents that were surveyed came from the socio-economic status described as “hard-pressed”. This socio-economic status encompasses the poorest areas of the United Kingdom, where unemployment is much higher than other areas of the country and education levels are much lower.[3]

1.2 Gene-Environment Interactions

Despite it being widely accepted that both genetic and environmental factors influence the onset of ASPD, not much is known about how this development occurs. In a study conducted by Tuvblad et al., 2600 male and female twins from the Swedish Twin Registry were examined.[4]

The antisocial behaviour of the twins was measured on four occasions, when the twins were at the ages of 8-9, 13-14, 16-17, and 19-20 years old.[4] The stability of their antisocial behaviour over time was measured by a common latent persistent antisocial behaviour factor. 67% of the variance in this latency factor was explained by common genetic influences, 26% by shared environments, and the remaining 7% by differing environments.[4]

This study, along with other longitudinal design studies suggests that in a smaller sample size of 1500 twins or less, the stability of the antisocial behaviour was seen to be influenced largely by genetic factors. However in sample sizes larger than 1500 twins, genetics and the environment were both observed to play major roles in the onset of ASPD symptoms.[4]

2. Genetic Influences

The general consensus in the scientific community is that the root cause of ASPD is due to genetic influences. Many studies have shown that genetic predispositions play a significant role in the normal variations in aggressive behaviour amongst adults.[5] This is especially the case in more impulsive forms. A lot of adoption studies that had been performed early on in the US and Scandinavia shows that the risk for adult criminal offending ran in families, and that this risk is due to genetic factors.[5]

The exact genetic cause of ASPD is still unknown, however various family, twin and adoption studies have shown that heredity plays a key role in the onset of the disorder. Researchers have examined a variety of possible gene candidates to try and determine the genetic origin of ASPD.[6]

2.1 The SLC6A4 Gene

The serotonin transport gene SLC6A4 regulates key serotonergic activity within the brain, and in the last decade, has been the subject of several studies linking it to the symptoms of ASPD.[7] In the past, it has been documented that the aggression, violence and impulsivity that are associated with ASPD can be linked to a decrease in serotonin activity. Past research has shown that there is indeed a serotonergic reduction in highly impulsive aggressors and people exhibiting antisocial behaviours.

SLC6A4 gene
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The location of the SLC6A4 gene on chromosome 17.

The SLC6A4 gene plays a major role in controlling serotonin availability in the synapse by regulating its uptake. Many polymorphisms of this gene have been identified, including two variable number of tandem repeat (VNTR) polymorphisms within the promoter regions.[7]

A study in 2010 performed by Garcia et al. examined the role of the 5-HTTLPR and 5-HTTVNTR polymorphisms of the SLC6A4 gene.
The 5-HTTLPR polymorphism is a VNTR, having a repeat unit of 22 nucleotides. It has four different alleles, two of which are common: the short (S) and long (L) alleles. The S allele of 5-HTTLPR has no repeats and the L allele has two repeats.[7] Past experiments have shown that the S allele of this polymorphism has been associated with antisocial behaviours as well as substance dependence in individuals. It was also observed that males with the S allele were more prone to aggression and conduct disorder than those with the L allele.[7]

The second polymorphism that has been implicated in ASPD is the 5-HTTVNR polymorphism, and it has been studied significantly less compared to the 5-HTTLPR polymorphism. This VNTR has a repeat unit of 17 nucleotides, and it has four different alleles as well, two of which are common: the 10 repeat units allele and the 12 repeat units allele. A lack of the 10 allele and a prevalence of the 12 allele has been implicated in the high aggression phenotype in children.[7]

In their study, Garcia et al. found that inmates that presented the 5-HTTLPR S/S + S/L genotype and the 5-HTTVNTR 12/12 genotype has a much greater risk of being classified as displaying symptoms of ASPD.[7] These results were compared to inmates that presented the 5-HTTLPR L/L and 5-HTTVNTR 10/10 + 10/12 genotypes, and as such had a much less risk of being categorized into the ASPD group.

After studying and analyzing the genotypes of the inmates, it was determined that those that scored high on Aluja’s Antisocial Personality Disorder Scale also showed much greater instances of certain polymorphisms of SLC6A4 over others.[7] Alongside finding a link between a gene and symptoms of ASPD, this study was also incredibly important because it did not have an under-representation of extremely high ASPD patients within the group that was studied.

2.2 Epistatic Interactions

Most of the genes that are considered to be implicated in the onset of ASPD are those that have main serotonin pathway effects. In a study conducted by Arias et al., 10 candidate genes were evaluated: SLC6A4, HTR1A, HTR2C, HTR1B, HTR2A, SLC18A2, SNAP 25, tryptophan hydroxylase (TPH1), and catechol-O-methyltransferase (COMT).[8] The researchers examined the genetic associations and interactions between the 11 loci of these 10 genes to determine whether there was a variation that could be a cause of ASPD.

Through analyzing these genes, an association was found with the COMT gene, a gene that plays a major role in dopamine inactivation. There are two alleles of the COMT gene; a low activity variant (L) that codes for Methionine at locations 108/158, and a high activity variant (H) that codes for Valine at the same locations. Arias et al.’s study found that there is an association between the L allele of the COMT gene, and symptoms of ASPD.[8]

COMT gene
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The location of the COMT gene on chromosome 22.

It was also observed that there was a significant interaction amongst the genetic variant of the COMT gene, the 5-HTR2A gene and the TPH1 gene. This three-way interaction was determined by the researchers to be their best model of epistasis, as the susceptibility of ASPD was greatly increased due to these interactions between variants of a serotonin receptor gene as well as the low enzyme activity of the COMT allele.[8]

The research performed by Arias et al. proved incredibly important in finding the genetic influences for ASPD by suggesting that it may not be one gene that is the root, but instead interactions between multiple alleles and polymorphic variants that are working together and thus causing the onset of the disorder.

Previous research has also shown that epistatic interactions between the 5-HTR2A variant and the low enzyme activity variant of COMT coregulate the dopamine system, and as such, may influence the dopamine reward pathways and be implicated in modulating serotonin levels. As such, this involvement of the dopamine system can suggest that comorbidity can be seen between addiction disorders and ASPD.[8]

2.3 Comorbidity

Comorbidity between addiction and ASPD is very commonly seen, and as a result, researchers have tried to single out candidate genes that may explain both addictive and antisocial behaviours. Both adoption and twin studies have found evidence of genetic as well as environmental influences in ASPD and substance abuse disorders. As such, it is believed that comorbidity between ASPD and substance abuse disorders may be the result of shared genetic influences and shared environmental influences.[9]

In a study performed by Li at al., 627 different single nucleotide polymorphisms (SNPs) were examined in 179 candidate genes for addiction. The subjects that were analyzed included people with either just substance abuse disorder, or with both ASPD and substance abuse disorder.[6]

Their research revealed one SNP that was significantly associated with ASPD in both African American and European populations. The SNP was found in the COL25A1 gene which encodes the collagen-like Alzheimer amyloid plaque component precursor; a type II transmembrane protein that is specifically expressed in neurons. This gene has also been found to promote an Alzheimer’s-like pathology in vivo.[6]

COL25A1 gene
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The location of the COL25A1 gene on chromosome 4.

Due to their findings showing the association of this SNP, it was concluded that the COL25A1 gene may play a key role in the causation of ASPD, especially with an associated comorbidity of substance abuse disorder.[6]

3. Associated Causes

Apart from possible genetic causes of ASPD, patients exhibit certain variations in brain structure that may or may not be a contributing factor to the onset of the disease. Changes in the frontal lobe of the brain have been observed in patients exhibiting ASPD, as well as a change in the volume of the areas that govern violent behaviour.[1] This may be one reason as to why people with ASPD seem unable to control their violent urges and impulses. People with ASPD also show a flat response to stress, and have less anxiety than the average person. Scientists are unsure whether or not these physiological variations in people with ASPD are direct causes of the disorder, or simply as a result of life experiences. [1]

Bibliography
1. Harvard Health Publications (2011) “Antisocial Personality Disorder” Belvoir Media Group, LLC.
2. Walsh A, Wu H. (2013) “Differentiating antisocial personality disorder, psychopathy, and sociopathy: evolutionary, genetic, neurological, and sociological considerations” Criminal Justice Studies 21(2):135-52.
3. Alloway TM, Lawrence A, Rodger S. (2008) “Antisocial Behavior: Exploring Behavioral, Cognitive, and Environmental Influences on Expulsion” Appl. Cognit. Psychol. 27:520–526.
4. Tuvblad C, Narusyte J, Grann M, Sarnecki J, Lichtenstein P. (2011) “The Genetic and Environmental Etiology of Antisocial Behavior from Childhood to Emerging Adulthood” Behav. Genet. 41:629–640.
5. Baker LA, Jacobson KC, Raine A, Lozano DI, Bezdjian S. (2007) “Genetic and Environmental Bases of Childhood Antisocial Behavior: A Multi-Informant Twin Study” Journal of Abnormal Psychology 116(2):219-235.
6. Li D, Zhao H, Kranzler HR, Oslin D, Anton RF, Farrer LA, Gelernter J. (2012) “Association of COL25A1 with Comorbid Antisocial Personality Disorder and Substance Dependence” Biol Psychiatry 71:733-740.
7. Garcia LF, Aluja A, Fibla J, Cuevas L, Garcia, O. (2010) “Incremental effect for antisocial personality disorder genetic risk combining 5-HTTLPR and 5-HTTVNTR polymorphisms” Psychiatry Research 177:161-166.
8. Arias JMC, Acosta CAP, Valencia JG. (2011) “Exploring epistasis in candidate genes for antisocial personality disorder” Psychiatr Genet 21:115–124.
9. van den Bree MBM, Svikis DS, Pickens RW. (1998) “Genetic influences in antisocial personality and drug use disorders” Drug and Alcohol Dependence 49:177–187.
10. Ferguson CJ. (2010) “Genetic Contributions to Antisocial Personality and Behavior: A Meta-Analytic Review From an Evolutionary Perspective” The Journal of Social Psychology 150(2):160-180.

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