Genetic factors influence on the development of psychopathy
Recently, different researcher from various field including university professors, psychologists, patients’ clinicians, collaborated to research how genetic factors influences the psychopathy development. The research estimated the differences in callous–unemotional (CU) traits justified for by effects of genetics ranged from forty-two to sixty -eight percent among the psychopaths.
Additionally, although a large proportion of the correlation between CU traits and conduct problems has been reported to be due to shared genetic effects, studies have consistently found unique genetic influences to both constructs as well supporting at least partially distinct etiological foundations [44, 46–48]. In a study of 7-year-old twins, the genetic influences on childhood-onset conduct problems were teacher-reported CU traits (81%) higher than normal group (30%) [49]. The research team also found that the level of genetic influence on conduct problems in those with increased levels of CU traits was not related to the severity of conduct problems and it was not related to ADHD symptoms when the children were 9 years of age [50].
Specifically, one twin study in a sample of boys aged 10–13 reported that left posterior cingulate and right dorsal anterior cingulate gray matter concentrations showed significant heritability (0.46 and 0.37) and that common genes explained the phenotypic relationship between these regions and psychopathic traits and these data suggest that the genetic contribution to CU traits might manifest through an impact on anterior and posterior cingulate cortex development [51].
Several studies have investigated potential genetic polymorphisms associated with CU traits. Especially, Viding et al. documented several potential autosomal single-nucleotide polymorphisms that could play a role in the development of CU traits [52]. Furthermore, Hirata et al. explored the role of COMT gene variants in child aggression and in CU traits and they reported CU traits among children and adolescents were associated with two catechol O-methyltransferase (COMT) polymorphisms [53]. COMT is an enzyme that metabolizes catecholamines including dopamine and norepinephrine, and its activity is mainly located in the frontal areas of the brain, including regions important in regulating aggressive behavior. Male mice lacking COMT displayed increased aggression [54]. Fowler et al. also found evidence to suggest that COMT polymorphisms may be related to CU traits. Additionally, they explored also MAO-A and 5-HTT genes among adolescents (ages 12–19) with childhood ADHD, they demonstrated that the high activity COMT Val/Val genotype, a low activity monoamine oxidase-a receptor (MAO-A) allele, and who were homozygous for the low activity serotonin transporter (5-HTT) allele significantly higher associated with CU traits [55]. In another study of 162 children and adolescents (ages 6–16), CU traits were associated with two polymorphisms on the oxytocin receptor (OSTR) gene [56]. Finally, in a recent study, Hirata et al. explore the role of prolactin and prolactin receptor gene (PRLR) variants in child aggression and CU traits. They found that one of the three single-nucleotide polymorphisms (SNPs) of the PRLR gene (rs187490) was significantly associated with CU traits and participants who carrying the GG genotype having higher CU scores than A-allele carriers [57].
Another promising candidate is FKBP5, which codes for a protein, FK506 binding protein, and regulates the affinity of the glucocorticoid receptor for cortisol [58]. The most prominent polymorphism in this gene (rs1360780) has been linked to increased aggression. Specifically, an interaction effect of FKBP5 diplotypes and childhood trauma was found on lifetime aggressive behavior in 411 male prisoners; carriers of the diplotype linked to increased FKBP5 expression were found to exhibit increased aggression and violent behavior in jail following childhood abuse [59]. This finding has been replicated on a brain imaging by two studies showing that FKBP5 variants interacted with childhood adversity to predict threat-induced activity in the amygdala [60, 61].
A small number of candidate genes (e.g., COMT, MAOA, OSTR, PRLR) are associated with CU traits across independent studies; however, failures to replicate also exist. Studies of gene-environment interplay show that CU traits genetic predispositions also contribute to selection into higher risk environments and that environmental factors can alter the differentially methylated CU trait candidate genes. The field’s understanding of CU traits etiology will benefit from larger, adequately powered studies in gene identification efforts; the incorporation of polygenic approaches in gene-environment interplay studies; attention to the mechanisms of risk from genes to brain to behavior; and the use of genetically informative data to test quasi-causal hypotheses about purported risk factors.
In the future, genetic findings can predict whether aggression will occur in children and it will persist into adulthood, and it may be possible to provide preventive interventions or more targeted treatments for those at high risk. Overall, with further genetic researches may lead to new avenues of risk prediction, prevention, and treatment of aggressive behaviors.
Callous–unemotional (CU) traits include lack of guilt and empathy, as well as shallow affect. Adults with a combination of CU traits and antisocial behavior (AB) are labeled psychopaths within the criminal justice system (Hare & Neumann, 2006)