While the cause of<unk>  is complicated by an intricate interplay of biological and environmental factors, identifying underlying mechanisms is crucial for obtaining accurate assessment and implementing effective treatment. These mechanisms serve as the fundamental building blocks on which evidence-based treatments are developed. Despite the complexities, several domains have been implicated in the development of<unk>  including cognitive variables, neurological factors, intraindividual factors, familial and peer influences, and wider contextual factors. These factors may also vary based on the age of onset, with different variables related to early (e.g., neurodevelopmental basis) and adolescent (e.g., social/peer relationships) onset. Risks The development of<unk>  is not immutable or predetermined. A number of interactive risk and protective factors exist that can influence and change outcomes, and in most cases<unk>  develops due to an interaction and gradual accumulation of risk factors. In addition to the risk factors identified under cause, several other variables place youth at increased risk for developing the disorder, including child physical abuse, in-utero alcohol exposure, and maternal smoking during pregnancy. Protective factors have also been identified, and most notably include high IQ, being female, positive social orientations, good coping skills, and supportive family and community relationships. However, a correlation between a particular risk factor and a later developmental outcome (such as<unk>  cannot be taken as definitive evidence for a causal link. Co-variation between two variables can arise, for instance, if they represent age-specific expressions of similar underlying genetic factors. There have been studies that found that, although smoking during pregnancy does contribute to increased levels of antisocial behaviour, in mother-fetus pairs that were not genetically related (by virtue of in-vitro fertilisation), no link between smoking during pregnancy and later<unk>  problems was found. Thus, the distinction between causality and correlation is an important consideration. Learning disabilities While language impairments are most common, approximately 20-25% of youth with<unk>  have some type of learning disability. Although the relationship between the disorders is complex, it seems as if learning disabilities result from a combination of ADHD, a history of academic difficulty and failure, and long-standing socialization difficulties with family and peers. However, confounding variables, such as language deficits, SES disadvantage, or neurodevelopmental delay also need to be considered in this relationship, as they could help explain some of the association between<unk>  and learning problems. Cognitive factors In terms of cognitive function, intelligence and cognitive deficits are common amongst youths with<unk> , particularly those with early-onset and have intelligence quotients (IQ) one standard deviation below the mean and severe deficits in verbal reasoning and executive function. Executive function difficulties may manifest in terms of one's ability to shift between tasks, plan as well as organize, and also inhibit a prepotent response. These findings hold true even after taking into account other variables such as socioeconomic status (SES), and education. However, IQ and executive function deficits are only one piece of the puzzle, and the magnitude of their influence is increased during transactional processes with environmental factors. Brain differences Beyond difficulties in executive function, neurological research on youth with<unk>  also demonstrate differences in brain anatomy and function that reflect the behaviors and mental anomalies associated in<unk> . Compared to normal controls, youths with early and adolescent onset of<unk>  displayed reduced responses in brain regions associated with social behavior (i.e., amygdala, ventromedial prefrontal cortex, insula, and orbitofrontal cortex). In addition, youths with<unk>  also demonstrated less responsiveness in the orbitofrontal regions of the brain during a stimulus-reinforcement and reward task. This provides a neural explanation for why youths with<unk>  may be more likely to repeat poor decision making patterns. Lastly, youths with<unk>  display a reduction in grey matter volume in the amygdala, which may account for the fear conditioning deficits. This reduction has been linked to difficulty processing social emotional stimuli, regardless of the age of onset. Aside from the differences in neuroanatomy and activation patterns between youth with<unk>  and controls, neurochemical profiles also vary between groups. Individuals with<unk>  are characterized as having reduced serotonin and cortisol levels (e.g., reduced hypothalamic-pituitary-adrenal (HPA) axis), as well as reduced autonomic nervous system (ANS) functioning. These reductions are associated with the inability to regulate mood and impulsive behaviors, weakened signals of anxiety and fear, and decreased self-esteem. Taken together, these findings may account for some of the variance in the psychological and behavioral patterns of youth with<unk> . Intra-individual factors Aside from findings related to neurological and neurochemical profiles of youth with<unk> , intraindividual factors such as genetics may also be relevant. Having a sibling or parent with<unk>  increases the likelihood of having the disorder, with a heritability rate of .53. There also tends to be a stronger genetic link for individuals with childhood-onset compared to adolescent onset. In addition, youth with<unk>  also exhibit polymorphism in the monoamine oxidase A gene, low resting heart rates, and increased testosterone. Family and peer influences Elements of the family and social environment may also play a role in the development and maintenance of<unk> . For instance, antisocial behavior suggestive of<unk>  is associated with single parent status, parental divorce, large family size, and the young age of mothers. However, these factors are difficult to tease apart from other demographic variables that are known to be linked with<unk> , including poverty and low socioeconomic status. Family functioning and parent-child interactions also play a substantial role in childhood aggression and<unk> , with low levels of parental involvement, inadequate supervision, and unpredictable discipline practices reinforcing youth's defiant behaviors. Peer influences have also been related to the development of antisocial behavior in youth, particularly peer rejection in childhood and association with deviant peers. Peer rejection is not only a marker of a number of externalizing disorders, but also a contributing factor for the continuity of the disorders over time. Hinshaw and Lee (2003) also explain that association with deviant peers has been thought to influence the development of<unk>  in two ways: 1) a “selection” process whereby youth with aggressive characteristics choose deviant friends, and 2) a “facilitation” process whereby deviant peer networks bolster patterns of antisocial behavior. In a separate study by Bonin and colleagues, parenting programs were shown to positively affect child behavior and reduce costs to the public sector. Wider contextual factors In addition to the individual and social factors associated with<unk> , research has highlighted the importance of environment and context in youth with antisocial behavior. However, it is important to note that these are not static factors, but rather transactional in nature (e.g., individuals are influenced by and also influence their environment). For instance, neighborhood safety and exposure to violence have been studied in conjunction with<unk> , but it is not simply the case that youth with aggressive tendencies reside in violent neighborhoods. Transactional models propose that youth may resort to violence more often as a result of exposure to community violence, but their predisposition towards violence also contributes to neighborhood climate.
Conduct disorder
Attention deficit hyperactivity disorder
Tourette syndrome
Antisocial personality disorder  Antisocial personality disorder  1
Oppositional defiant disorder
Obsessive–compulsive disorder
High-functioning autism
Klismaphilia