Presently, dimensionality is not typically thought of as a characteristic of psychology. Psychology today is largely categorical resulting in both reductionism and overgeneralization. For example, throughout the literature regarding oppositional defiant disorder, conduct disorder and related syndromes, the term disruptive behavior disorders comes up frequently in place of specific disorders. The group of disorders captured by the term disruptive behavior disorders—from now on to be referred to as DBDs—in this paper refers to the spectrum of externalizing disorders including but not limited to: oppositional defiant disorder, conduct disorder and attention deficit/hyperactivity disorder. The use of DBD begins to suggest that conduct problem disorders may not be so different from each other and some evidence suggests that they are not. In addition to often being lumped together, conduct problem disorders are also often part of a well established developmental pathway, starting with oppositional defiant disorder in early childhood, then on to conduct disorder in adolescence, and finally—if left untreated—to anti-social personality disorder in adulthood. This pathway also suggests the underlying mechanisms of these disorders may be similar, if not the same.
In this paper, the symptoms of oppositional defiant disorder (ODD), conduct disorder (CD) and anti-social personality disorder (ASPD) will be briefly compared, and similarities and differences will be summarized. Based on their symptoms alone, it can be observed that conduct problem disorders are largely similar and differ mostly in severity and age of onset—though it can be argued that ODD and CD are quite different, this will be discussed later. This paper’s main focus will be to present and discuss the genetic, temperamental and relevant environmental evidence that supports the development of a conduct problem spectrum model and move towards a dimensional approach.
Symptoms and Presentations
Oppositional defiant disorder is characterized by a pattern of various oppositional behaviors including: angry/irritable mood, argumentative/defiant behavior and vindictiveness; the severity for ODD is based on the number of contexts in which the disruptive behavior is exhibited (American Psychiatric Association, 2013). Given that ODD can be applied to a wide range of behaviors, ODD refers to a “heterogenous group of individuals” (McKinney & Renk, 2007). More severe cases of ODD can become increasing difficult to distinguish from CD.
Conduct disorder is characterized by a pattern of behavior that violates the rules and right of others, exhibited by behaviors such as aggression to others or animals, destruction of property, deceitfulness, theft and violations of rules—often referring to laws but also social rules (American Psychiatric Association, 2013). Anti-social personality disorder is also characterized by the same kind of violations of the rights of others as CD, furthermore, CD must be present before age 15 in order to diagnose ASPD, the individual must also be at least 18 years of age (American Psychiatric Association, 2013). The diagnostic criteria for CD and ASPD are based on the same anti-social behaviors.
When comparing theses disorders, it is notable that CD and ASPD are largely similar, the disorders differ by age of diagnosis, by definition ASPD cannot be diagnosed before the age of 18 but the underlying mechanisms of the disorders—based on their symptoms—seem be shared and ASPD seems to be an escalation of CD. In addition, oppositional behaviors and ODD often precede and predict later CD onset (American Psychiatric Association, 2013). A group of individuals—likely beginning with ODD—who exhibit early anti-social behaviors that persist are at higher risk for various negative adult outcomes (Moore et al., 2017). Meaning that anti-social behaviors may be at root of ODD, CD and ASPD, this idea will be revisited later.
Genetics
While some argue that ODD and CD are different due to the distinction between oppositional patterns of behavior and patters of violations of the rights of others characteristic of their respective disorders. The genetic underpinnings of these disorders suggest they are more similar than they are different; and they often share the same genetic risk factors.
Surly there is some common genetic factor across all three disorders being discussed in this paper. Children who have siblings with CD or parents who had CD—or exhibit other psychopathology, such as substance use disorders and mood disorders—are at higher risk themselves to develop a conduct problem disorder (American Psychiatric Association, 2013). Whether the development of psychopathology in children with relatives is a result of inherited conduct disorder vulnerabilities or they learn symptomatic behaviors through modeling is unclear. In reality, the development of conduct disorders likely involves the interaction of genes and the environment. In addition, evidence suggests that ASPD is also somewhat heritable, it is more common among biological relatives than in the general population (American Psychiatric Association, 2013). Similar findings are true for other externalizing disorders.
Neurobiological makers such as lower heart rate, reduced basal cortisol activity and abnormalities in the prefrontal cortex (PFC) have been previously associated with both ODD and CD (American Psychiatric Association, 2013). Such neurobiological makers can be observed relatively early in life and are predictive of all the disorders at the center of this paper—ODD, CD and ASPD—suggesting some kind of common etiological factor. The exact etiological factor is yet unknown.
Certain behaviors and aspects of personality are thought to be heritable. Oppositional behavior has been found to be various degrees of heritable, it has been found to be somewhat to substantially heritable in a study looking at young children (Lahey & Waldman, 1999). Another trait that is thought to be heritable and at the core of various conduct problem disorders is impulsively. Trait impulsivity seems to be a shared risk factor for externalizing disorders. Trait impulsivity refers to impulsivity as a result of mesolimbic dopamine dysfunction, the dysfunction is exhibited behaviorally as a proclivity for immediate rewards over delayed rewards that may be larger (Beauchaine & McNulty, 2013). The mesolimbic dopamine dysfunction discussed above is thought to be an etiological factor in multiple or even all externalizing disorders and is likely a vulnerability across DBDs (Beauchaine & McNulty, 2013; Sauder, Beauchaine, Gatzke-Kopp, Shannon, & Aylward, 2012). Behavioral genetics studies also suggest that conduct problem disorders share genetic etiological factors.
Behavioral genetic studies suggest that comorbidity among conduct problem disorders and externalizing syndromes result in large part due to heritable mechanism (Beauchaine, Hinshaw, & Pang, 2010). The literature related to comorbidity in externalizing disorders is expansive and cannot be summarized in this paper. Comorbidity rates are very high for conduct problem disorder and other externalizing disorders (Beauchaine, Hinshaw, & Pang, 2010). From the perspective of this paper, it is thought that the high rates of comorbidity can be explained in part by artifactual comorbidity.
Heritability estimates for various behavioral aspects have been studied, thus far it appears that h2 for oppositional behaviors is highest, h2 for aggression, property violations and status violation are considerably lower than that of oppositional behaviors (Lahey & Waldman, 1999). Although some relevant behaviors are more heritable than others, they all have a notable genetic component (Martin, Levy & Pieka, 2006). Thus, given that oppositional behaviors are highly heritable and are often observed not only in ODD but CD and ASPD as well suggest that some genetic risk factors are the same across the disorders . Furthermore, this would suggest genetic etiological mechanisms across these conduct problem disorders are the same—though heterogeneous symptomatic behaviors are observed and therefore lead to different, separate diagnoses.
Environment
Not only do ODD, CD and ASPD share genetic etiological risk factors and mechanisms, they also often share environmental risk factors. Environmental risk factors for ODD include: harsh and neglectful home environments (American Psychiatric Association, 2013). Similarly, neglectful home environments, along with tough discipline and abuse is linked to the development of CD (American Psychiatric Association, 2013). Substance abuse by parents is also linked to conduct problem disorders, substance use disorders (SUDs) of parents is also associated with an increased the risk of SUDs in their offspring. Substance use disorders and conduct problem disorders are often comorbid (Burke, Loeber, & Birmaher, 2002). Particularly, fathers who had children with DBDs such as ODD or CD in studies have exhibited higher rates of substance use than fathers in the control group (McKinney & Renk, 2007). Clearly, similar home environments are shared among conduct problem disorders.
Although all the DBDs share hostile or harsh home environments as risk factors, the relationship between at home environments and socio-economic status (SES) must be considered. Anti-social personality disorder appears to be related to low SES and urban setting (American Psychiatric Association, 2013). Also, there is an inverse relationship between anti-social behaviors and family income and parental education (Lahey & Waldman, 1999). This means that children with genetic anti-social vulnerabilities in poorer and urban neighborhoods are at an increased risk for developing ASPD. More generally, disruptive behavior—characteristic of conduct problem disorders—in both boys and girls is associated with poorer, low SES neighborhoods (Burke, Loeber, & Birmaher, 2002). The mechanisms thought which low SES neighborhoods influence anti-social behaviors in individuals remains unclear—though some say SES and neighborhoods may influence behaviors characteristic of conduct problem disorders through their influence on parenting behaviors (Burke, Loeber, & Birmaher, 2002; McKinney & Renk, 2007). Other environmental factors that seem to be associated with DBDs are pregnancy and birth complications and parental psychopathology (Burke, Loeber, & Birmaher, 2002). Though these factors are associated with DBDs, they are also associated with a general risk for developing psychopathology and not specific to DBDs. Given the evidence, it can be concluded that environmental etiological factors are similar, if not the same across conduct problem disorders and the externalizing spectrum disorders.
Temperament
Temperament is also thought to be somewhat heritable, the emerging literature regarding temperament related to conduct problem disorders is particularly interesting since detecting temperament type can be done relatively early on and is a great step towards early intervention. Temperament is thought to represent innate qualities in an individual (Burke, Loeber, & Birmaher, 2002). These innate qualities can be predictive of later outcomes and certain types of temperament are thought to be risk factors for psychopathology such as conduct problem disorders.
Early temperament, including inflexibility and negative emotionality have been shown to be predictive of externalizing syndromes including conduct problem disorders (Burke, Loeber, & Birmaher, 2002). High emotional reactivity and low tolerance for frustrations have been associated with ODD; CD has been associated with under-controlled temperament during infancy (American Psychiatric Association, 2013). Temperaments including restlessness, negativisms, and short attention span have been identified as precursors to behavioral problems characteristic of conduct problem disorders (McKinney & Renk, 2007). All discussed temperament types thus far are shared risk factors among ODD and CD—and therefore ASPD.
Protective factors are also shared among conduct problem disorders. On the topic of temperament, inhibited and approach withdrawal temperaments have been related to less externalizing behavioral problems later in development (Burke, Loeber, & Birmaher, 2002). In addition, children who were rated high on scales measuring harm avoidance were also less likely to engage in anti-social behaviors in early adolescence (Lahey & Waldman, 1999). According to temperament research, conduct disorders marginally differ from each other, but of course temperament is only one aspect of these disorders.
Lastly in regard to temperament, some have proposed new ways to view ODD. It is argued that oppositional behaviors—instead of being view as a disorder (ODD)—can be viewed as a dimension of temperament because oppositional behaviors are non specific, emerge early in life and are significantly heritable (Lahey& Waldman, 1999). If ODD is viewed as a dimension of temperament, it could be seen as a driver for the early development of anti-social behaviors characteristic of CD and ASPD. In this view, ODD would not be a disorder but a significant predictor of future anti-social behaviors, like evidence previously stated suggests.
Temperamental risk factors are similar and even the same for ODD and CD, which also supports the need to further researcher in order to determine whether keeping these disorders separate is useful.
Conclusion
Genetic, environmental and temperamental factors related to conduct problem disorders all seem to suggest that these disorders are largely similar and share many of the same risk factors and processes. According to these aspects of etiology, these disorders may be better represented by a spectrum model with heterogeneous presentations. In this paper, only a few aspects of etiology were covered, other aspects of the disorders must be reviewed before such a model can be proposed.
Other facets of these disorders seem to suggest that the underlying mechanisms of these disorders may be similar if not the same as well. Comorbidity rates among conduct problem disorders—and externalizing disorders—are notably high. Whether the high comorbidity rates are due to artifactual, spurious or true comorbidity is not yet known for certain, but given the overlap of symptoms between ODD and CD, artifactual comorbidity likely accounts for a significant portion of the high rates observed.
In the future, more research into the etiology of specific conduct disorders is needed and the use of terms such as DBDs should be limited in order identify unique etiological characteristics that would strongly support the perseverance of the current state of differential diagnoses of child conduct problem disorders. Otherwise, the etiological case for a conduct problem spectrum model is strong. Though not covered in this paper, the evidenced for an even broader spectrum model for externalizing disorders is interesting and maybe a direction for future research.