Personality disorders are generally believed to be caused by a combination and interaction of genetics and environmental influences. Fire-setting and
cruelty to animals during childhood are also linked to the development of an antisocial personality disorder, along with being more common in males and among incarcerated populations. According to professor
Emily Simonoff of the
Institute of Psychiatry, Psychology and Neuroscience, there are many variables that are consistently connected to ASPD, such as: childhood
hyperactivity and conduct disorder, criminality in adulthood, lower IQ scores, and reading problems. Additionally, children who grow up with a predisposition of ASPD and interact with other delinquent children are likely to later be diagnosed with ASPD.
Genetic Research into genetic associations in antisocial personality disorder suggests that ASPD has some or even a strong genetic basis. The prevalence of ASPD is higher in people related to someone with the disorder.
Twin studies, which are designed to discern between genetic and environmental effects, have reported significant genetic influences on antisocial behavior and conduct disorder. In the specific
genes that may be involved, one gene that has shown particular promise in its correlation with ASPD is the gene that encodes for
monoamine oxidase A (MAO-A), an
enzyme that breaks down monoamine
neurotransmitters such as
serotonin and
norepinephrine. Various studies examining the gene's relationship to behavior have suggested that variants of the gene resulting in less MAO-A being produced (such as the 2R and 3R
alleles of the
promoter region) have associations with aggressive behavior in men. This association is also influenced by negative experiences early in life, with children possessing a low-activity variant (MAOA-L) who have experienced negative circumstances being more likely to develop antisocial behavior than those with the high-activity variant (MAOA-H). Even when environmental interactions (e.g., emotional abuse) are taken out of the equation, a small association between MAOA-L and aggressive and antisocial behavior remains. The gene that encodes for the
serotonin transporter (SLC6A4), a gene that is heavily researched for its associations with other mental disorders, is another gene of interest in antisocial behavior and personality traits. Genetic association studies have suggested that the short "S" allele is associated with impulsive antisocial behavior and ASPD in the inmate population. However, research into psychopathy find that the long "L" allele is associated with the Factor 1 traits of psychopathy, which describes its core affective (e.g. lack of empathy, fearlessness) and interpersonal (e.g. grandiosity, manipulativeness) personality disturbances. This is suggestive of two different forms of the disorder, one associated more with impulsive behavior and emotional dysregulation, and the other with predatory aggression and affective disturbance. Various other gene candidates for ASPD have been identified by a
genome-wide association study published in 2016. Several of these gene candidates are shared with attention-deficit hyperactivity disorder, with which ASPD is often comorbid. The study found that those who carry four
mutations on
chromosome 6 are 50% more likely to develop antisocial personality disorder than those who do not.
Physiological Hormones and neurotransmitters Traumatic events can disrupt the standard development of the
central nervous system, which can generate a release of
hormones that can change normal patterns of development. One of the
neurotransmitters that has been discussed in individuals with ASPD is serotonin, also known as 5-HT. While it has been shown that lower levels of serotonin may be associated with ASPD, there has also been evidence that decreased serotonin function is highly correlated with impulsiveness and aggression across a number of different experimental paradigms. Impulsivity is not only linked with irregularities in 5-HT metabolism but may be the most essential
psychopathological aspect linked with such dysfunction. Correspondingly, the DSM classifies "impulsivity or failure to plan ahead" and "irritability and aggressiveness" as two of seven sub-criteria in category A of the diagnostic criteria of ASPD.
Neurological Antisocial behavior may be related to a number of neurological defects, such as head trauma. Antisocial behavior is associated with decreased
grey matter in the right
lentiform nucleus, left
insular, and
frontopolar cortex. Increased volumes of grey matter have been observed in the right
fusiform gyrus, inferior parietal cortex, right
cingulate gyrus, and post-central cortex. Intellectual and cognitive ability is often found to be impaired or reduced in the ASPD population. Contrary to stereotypes in popular culture of the "psychopathic genius", antisocial personality disorder is associated with reduced overall intelligence and specific reductions in individual aspects of cognitive ability. These deficits also occur in general-population samples of people with antisocial traits and in children with the precursors to antisocial personality disorder. People who exhibit antisocial behavior tend to demonstrate decreased activity in the
prefrontal cortex, and is more apparent in functional neuroimaging as opposed to structural neuroimaging. Some investigators have questioned whether the reduced volume in prefrontal regions is associated with antisocial personality disorder, or whether they result from co-morbid disorders, such as substance use disorder or childhood maltreatment. It is still considered an open question if the anatomical abnormality causes the psychological and behavioral abnormality, or vice versa. Some of the major areas involved are areas of the prefrontal cortex, such as the right frontal and temporal cortices, the ventromedial prefrontal cortex, and the middle and orbitofrontal cortices. Additionally, those with ASPD have shown decreased gray matter volumes in other brain areas such as the amygdala and insula, suggesting possible issues with emotional reactions to certain stimuli. People that exhibit antisocial behavior also tend to demonstrate decreased activity in the prefrontal cortex, as is apparent in functional neuroimaging.
Cavum septi pellucidi (CSP) is a marker for
limbic neural maldevelopment, and its presence has been loosely associated with certain mental disorders, such as
schizophrenia and
post-traumatic stress disorder. One study found that those with CSP had significantly higher levels of antisocial personality, psychopathy, arrests and convictions compared with controls.
Parenting styles Some hypothesize that
parenting styles can affect how children experience and develop in their youth, and can have an impact on a child's diagnosis of ASPD.
Childhood trauma ASPD is highly comorbid with emotional and physical abuse in childhood. Physical neglect also correlates significantly with ASPD. The way a child bonds with its parents early in life is important. Poor parental bonding due to abuse or neglect puts children at greater risk for developing antisocial personality disorder. There is also a significant correlation with parental overprotection and people who develop ASPD. Those with ASPD may have experienced any of the following forms of
childhood trauma or abuse: physical or sexual abuse, neglect, coercion, abandonment or separation from caregivers, violence in a community, acts of terror, bullying, or life-threatening incidents. Some symptoms can mimic other forms of mental illness, such as: • post-traumatic stress disorder (symptoms of upsetting/terrifying memories of traumatic events) •
reactive attachment disorder (little to no response regarding emotional triggers) •
disinhibited social engagement disorder (roaming off with people you don't know without caregivers being informed) •
dissociative identity disorder (disconnection from self or environment) The comorbidity rate of the previously listed disorders with ASPD tends to be much higher.
Cultural influences The sociocultural perspective of clinical psychology views disorders as influenced by cultural aspects; since cultural norms differ significantly, mental disorders (such as ASPD) are viewed differently.
Robert D. Hare suggested that the rise in ASPD that has been reported in the United States may be linked to changes in cultural norms, serving to validate the behavioral tendencies of many individuals with ASPD. While the rise reported may be in part a byproduct of the widening use (and abuse) of diagnostic techniques, given
Eric Berne's division between individuals with active and latent ASPD – the latter keeping themselves in check by attachment to an
external source of control like the law, traditional standards, or religion – it has been suggested that the erosion of collective standards may serve to release the individual with latent ASPD from their previously prosocial behavior. Controversial
clinical psychiatrist Pierre-Édouard Carbonneau suggested that the problem with legal forced admittance is the rate of failure when diagnosing ASPD. He contends that the possibility of diagnosing and coercing a patient into prescribing medication to someone without ASPD, but is diagnosed with ASPD, could be potentially disastrous. But the possibility of not diagnosing ASPD and seeing a patient go untreated because of a lack of sufficient evidence of cultural or environmental influences is something a psychiatrist must ignore; and in his words, "play it safe".
Conduct disorder While antisocial personality disorder is a mental disorder diagnosed in adulthood, it has its precedent in childhood. The DSM-5's criteria for ASPD require that the individual have conduct problems evident by the age of 15. About 25–40% of youths with conduct disorder will be diagnosed with ASPD in adulthood. Conduct disorder (CD) is a disorder diagnosed in childhood that parallels the characteristics found in ASPD. It is characterized by a repetitive and persistent pattern of behavior in which the basic rights of others or major age-appropriate norms are violated by the child. Children with the disorder often display impulsive and aggressive behavior, may be callous and deceitful, may repeatedly engage in petty crime (such as stealing or vandalism), or get into fights with other children and adults. CD is distinct from
oppositional defiant disorder (ODD) in that children with ODD do not commit aggressive or antisocial acts against other people, animals, or property, though many children diagnosed with ODD are subsequently re-diagnosed with CD. Two developmental courses for CD have been identified based on the age at which the symptoms become present. The first course is known as the "childhood-onset type" and occurs when conduct disorder symptoms are present before the age of 10. This course is often linked to a more persistent life course and more pervasive behaviors, and children in this group express greater levels of ADHD symptoms, neuropsychological deficits, more academic problems, increased family dysfunction, and higher likelihood of aggression and violence. The second course is known as the "adolescent-onset type" and occurs when conduct disorder develops after the age of 10 years. Compared to the childhood-onset type, less impairment in various cognitive and emotional functions are present, and the adolescent-onset variety may remit by adulthood. In addition to this differentiation, the DSM-5 provides a specifier for a callous and unemotional interpersonal style, which reflects characteristics seen in psychopathy and are believed to be a childhood precursor to this disorder. Compared to the adolescent-onset subtype, the childhood-onset subtype tends to have a worse treatment outcome, especially if callous and unemotional traits are present. ==Diagnosis==