Callous-unemotional (CU) traits, which include characteristics such as lack of empathy, lack of guilt and shallow affect, are a well-documented temperamental risk factor for severe and persistent conduct problems in youth (Fontaine et al.
2011; Frick et al.
2003b). In addition, CU traits have been identified as a precursor to adult psychopathy (Lynam et al.
2007) and are considered the clinical hallmark of this syndrome (Cleckley
1976; Hare
2003). Evidence for a subset of youth with severe conduct problems distinguished by their high levels of CU traits led to the inclusion of CU traits as a specifier (labeled ‘limited prosocial emotions’) to conduct disorder in the
Diagnostic and Statistical Manual of Mental Disorders – 5th edition (DSM; American Psychiatric Association
2013).
While there is evidence suggesting that CU traits are associated with externalizing problems, such as conduct problems (Frick et al.
2014) and that externalizing problems are associated with internalizing problems, such as depression and anxiety (Russo and Beidel
1994), the nature of the association between CU traits and internalizing problems is less clear. Based on theory and clinical work, CU traits are expected to be negatively associated with anxiety (Cleckley
1976). A number of empirical studies support this negative association (Frick et al.
1999; Pardini and Fite
2010). In particular, it has been shown that low levels of fearfulness in youth, a trait closely related to anxiety (Kochanska
1993), may be an important risk factor for the later development of CU traits (Glenn et al.
2007; Waller et al.
2016). However, other studies have reported no significant association between CU traits and anxiety (Loney et al.
2003; Neumann and Pardini
2014). In addition, there are even findings suggesting a positive association between CU traits and anxiety (Essau et al.
2006; Fontaine et al.
2011). However, these findings could be notably explained by the fact that the unique and contrasting contributions of CU traits and conduct problems to anxiety were not explored: conduct problems, when controlling for CU traits, tend to be positively correlated with anxiety, whereas CU traits, when controlling for conduct problems, tend to be negatively correlated with anxiety (Frick and Dickens
2006).
Etiology of CU Traits, Conduct Problems, Hyperactivity and Emotional Problems
Research based on twin samples has yielded important information concerning the etiology of CU traits, conduct problems, hyperactivity and emotional problems. Findings showed moderate to strong heritability of CU traits in youth, especially in boys (Fontaine et al.
2010), with estimates indicating that 40–78% of the variation in CU traits across the population was due to genetic contributions (Viding et al.
2013; Viding and McCrory
2012). These studies have also suggested that non-shared environmental contributions were important to explain variation in CU traits. On the other hand, shared environmental contributions to CU traits were reported in only a small number of studies (Fontaine et al.
2010; Viding et al.
2007), although they may be especially important for a small subset of girls with stable and high levels of CU traits (Fontaine et al.
2010).
Moderate to strong genetic and non-shared environmental contributions have been found to explain the variation in conduct problems (Forsman et al.
2010; Viding et al.
2007) and emotional problems (Blonigen et al.
2005; Mann et al.
2015) in youth samples. Shared environmental contributions were often modest or not significant. As for hyperactivity in youth samples, high heritability estimates and relatively modest to moderate non-shared environmental estimates were reported (Biederman
2005; Kuntsi and Stevensen
2001).
A number of studies have examined the etiological association between CU traits and conduct problems. Genetic and non-shared environmental correlations were reported, but the strength of these correlations varied across studies (Bezdjian et al.
2011; Blonigen et al.
2005; Larsson et al.
2007; Viding et al.
2007). Importantly, moderate (Blonigen et al.
2005) to relatively strong (Viding et al.
2007) genetic correlations were found.
The etiological association between CU traits and other phenotypes, including hyperactivity and emotional problems, has been less explored. To our knowledge, no published twin study has specifically examined the etiological association between CU traits and hyperactivity in youth. However, one twin study tested whether symptoms of ADHD were associated with different dimensions of psychopathic traits (including CU traits) in adolescence (Forsman et al.
2007). A modest phenotypic correlation was observed between CU traits and symptoms of ADHD, but the authors did not examine whether this association was explained by genetic, shared or non-shared environmental factors. The genetic association between CU traits (more specifically fearless dominance, which encompasses interpersonal-affective traits such as fearlessness and social potency) and emotional problems (i.e., major depression, social phobia and simple phobia) was examined in a study of 17-year-old twins (Blonigen et al.
2005). This study revealed that fearless dominance exhibited a moderate negative genetic correlation with emotional problems, indicating that the same genetic factors that contributed to fearless dominance traits also contributed to
reduced levels of emotional problems.
In sum, previous research showed that CU traits in youth are under the influence of moderate to strong heritability and that a modest to strong proportion of the factors explaining the genetic variance of conduct problems also explains the genetic variance of CU traits. The degree of etiological association between CU traits and other phenotypes, more specifically hyperactivity and emotional problems, has been less explored. To address these limitations, the current study, employing a twin model-fitting approach, aimed to 1) replicate findings on the etiology of CU traits and their etiological association with conduct problems in a sample of adolescent twins screened for neurodevelopmental problems, and 2) extend research by examining further the etiological associations between CU traits and symptoms of hyperactivity and emotional problems separately. Findings from the current study have the potential to clarify the underlying etiological bases of CU traits and their associations with other psychopathological symptoms.
Discussion
In this study, we examined the etiological associations between CU traits and symptoms of conduct problems, hyperactivity and emotional problems through the use of a twin design. This allowed us 1) to replicate findings on the relatively high heritability of CU traits and the genetic correlation between CU traits and conduct problems in a sample of adolescent twins screened for neurodevelopmental problems, and 2) to investigate further the etiological associations between CU traits and symptoms of hyperactivity and emotional problems separately. Findings from this study extend research in three main respects.
First, we found substantial genetic contributions to CU traits and a strong genetic correlation between CU traits and conduct problems. These findings are consistent with previous research examining the etiological association between CU traits and conduct problems in youth (Bezdjian et al.
2011; Viding et al.
2007). However, unlike previous studies (Bezdjian et al.
2011; Viding et al.
2007), we did not find a significant non-shared environmental correlation between CU traits and conduct problems. The substantial genetic correlation suggests that future molecular genetic research should focus on the identification of common genes that contribute to CU traits and conduct problems (Viding et al.
2007). Still, the non-overlapping genetic variance suggests some independence in the underlying biological mechanisms leading to the development of CU traits and conduct problems (Taylor et al.
2003; Viding et al.
2007). For instance, biological mechanisms related to temperamental characteristics (e.g., fearlessness; Glenn et al.
2007; Waller et al.
2016), emotion regulation and empathy could be represented in the residual genetic variance found for CU traits (Taylor et al.
2003).
Second, to our knowledge, this is the first published study to examine the etiological association between CU traits and hyperactivity in youth. Although past research showed that the two phenotypes often co-occur (Fontaine et al.
2008; Fontaine et al.
2011; Frick et al.
2003a; Nagin and Tremblay
2001), our findings suggest that they share genetic etiological factors, but only to some extent. Indeed, unlike CU traits and conduct problems, the genetic correlation between CU traits and hyperactivity was not strong. The substantial non-overlapping genetic variance suggests important independence in the underlying biological mechanisms leading to the development of CU traits and hyperactivity, which appears to be in line with past research suggesting that hyperactivity is not a significant risk factor associated with the development of CU/psychopathic traits (Barry et al.
2000; Forsman et al.
2007). Biological mechanisms related to temperamental characteristics (e.g., fearlessness), emotional regulation and empathy could be represented in the residual variance found for CU traits, but to a greater extent than when examining the etiological overlap between CU traits and conduct problems. Future research is needed to further our understanding about the etiological associations between these phenotypes.
Third, we found a relatively modest, but significant negative genetic correlation between CU traits and emotional problems, which is in line with the findings reported by Blonigen et al. (
2005). In this previous study, a negative genetic correlation was reported between fearless dominance, which covered a wide range of interpersonal-affective traits associated with psychopathy, and emotional problems, which included symptoms of phobia and depression. Because we focused on CU traits, instead of a wider range of interpersonal-affective traits, the current study extends previous findings by increasing the level of specificity in the examination of the etiological association between psychopathic traits and emotional problems. The negative genetic correlation between CU traits and emotional problems suggests that the genetic factors influencing the
increase of one phenotype contribute to the
decrease of the other. This could suggest that CU traits may act as a protective factor for emotional problems (or that emotional problems may act as a protective factor for CU traits). It could be that the biological mechanisms associated with fearlessness in CU traits (Glenn et al.
2007; Waller et al.
2016) provide a resiliency to developing a broad range of emotional problems, such as anxiety and depression symptoms (Blonigen et al.
2005). Still, the relatively modest negative genetic correlation between the two phenotypes suggests important independence in their respective underlying biological mechanisms.
There are a number of strengths to this study, including the use of a measure of CU traits over a broader measure of psychopathic traits, which increases the specificity of our findings. Moreover, to our knowledge, this was the first published study to explore the etiological association between CU traits and hyperactivity in youth. However, this study has a number of limitations. First, we were unable to conduct the analyses separately for boys and girls due to our sample size. Taking sex differences into account may be important because boys tend to have higher scores than girls on CU traits, conduct problems, and hyperactivity, but lower scores on emotional problems (Essau et al.
2006; Fontaine et al.
2008; Lewinsohn, Gotlib, Lewinsohn, Seeley, & Allen
1998). In addition, sex differences in the etiology of the behaviours and traits at study have been previously reported. For instance, lower heritability and higher shared environmental contributions for CU traits (Fontaine et al.
2010; Viding et al.
2007) as well as lower shared and non-shared environmental correlations between CU traits and conduct problems have been found in girls (Viding et al.
2007). Second, the sample size may have influenced the results. More specifically, the non-significant findings for environmental influences could potentially be related to the relative small sample size and limited statistical power.
Third, the internal consistency of the measure of conduct problems was moderate (α = .67). This may have produced relatively lower heritability estimates for our measure of conduct problems and a more conservative estimate of the magnitude of the association between CU traits and conduct problems. Indeed, in samples of adolescents, higher estimates of genetic influences to conduct problems based on the parent-report version of the SDQ have been reported (e.g., a
2 = .73; Pingault et al.
2015). However, estimates of genetic influences to conduct problems based on the self-report version of the SDQ tend to be lower than for parent-reports (e.g., a
2 = .35 for self-reports and a
2 = .54 for parent-reports; Scourfield et al.
2004). Fourth, we used the emotional problems scale of the SDQ, which is a brief screening instrument (Goodman
2001). Replications of our findings using more comprehensive measures of different types of emotional problems (e.g., anxiety and depression separately) are needed.
Fifth, because all the measures were based on the youths’ reports, there is a possibility that our findings were partly influenced by shared method variance. Finally, as in all twin studies, it must be noted that the non-shared environment influences can be affected by unsystematic, chance events that, when compounded over time, make twins different in unpredictable ways (Plomin and Daniels
1987). This makes non-shared environmental influences difficult to interpret. However, our study mainly focuses on the significant genetic correlations, and as such, this prospect does not appear to overly affect our findings or our conclusions. Finally, the CATSS-15/DOGSS is mainly composed of children who screened positive for neurodevelopmental problems/mental health problems or at-risk children (i.e., screen-negative children who are considered to be genetically at-risk siblings). This provided a unique opportunity to replicate and extend previous findings based on population-based twin samples to a sample composed of clinical and at-risk children identified from a population-based sample of twins. Replications involving youth from various backgrounds are needed to increase the generalizability of the findings. Although replications of our findings using larger twin samples would be crucial, our study is a step further toward a better understanding of the etiological overlap between CU traits and other symptoms of psychopathology.
This study raises a number of implications. It is important to note that genetic vulnerability does not mean immutability. Genetically-influenced behaviours can be buffered by preventive and treatment strategies, which could be considered as positive gene-environment interactions (Fontaine et al.
2018). We found a genetic correlation between CU traits and conduct problems, but contrary to previous studies (Bezdjian et al.
2011; Viding et al.
2007), we did not find a significant non-shared environmental correlation. Given the past and the current findings, future research is needed to identify measured environmental factors (e.g., parenting behaviours) that may be common or specific to CU traits and related symptoms of psychopathology, which in turn could be targeted in the context of intervention programs. Investigations focusing on child-specific environmental factors within twin designs may be particularly promising.
In sum, we found a strong positive genetic correlation between CU traits and conduct problems, a relatively moderate genetic correlation between CU traits and hyperactivity, and a modest negative genetic correlation between CU traits and emotional problems. Studies based on prospective longitudinal data would be needed to advance further our understanding of the potential etiological mechanisms underlying the development of CU traits and related psychopathological symptoms.