|Year : 2017 | Volume
| Issue : 2 | Page : 90-96
Callous–unemotional traits in conduct disorder in relation to salivary cortisol level
Hani H Dessoki1, Heba F Abd El Reheem2, Maha E Ahmed1, Mohamed R Soltan3, Ahmed A Abdel Hakim1, Mariam E Dawoud3
1 Department of Psychiatry, Faculty of Medicine, Beni Suef University, Beni Suef, Egypt
2 Department of Psychiatry, Faculty of Medicine, Cairo University, Giza, Egypt
3 Department of Psychiatry, Faculty of Medicine, Fayoum University, Faiyum, Egypt
|Date of Web Publication||5-Jul-2017|
Mohamed R Soltan
Department of Psychiatry, Faculty of Medicine, Fayoum University, Berket El Saba City, Menoufia Governorate, Faiyum, 63514
Source of Support: None, Conflict of Interest: None
To show the correlation between items of Callous Unemotional Inventory (CUI) and Conduct Disorder and to assess correlation between salivary cortisol and Conduct Disorder.
Emerging evidence suggests that low levels of cortisol may act as a biological marker for the Callous Unemotional traits (CU Traits) subgroup of Conduct Disorder.
Materials and methods
The current study tested the presence of items of Callous Unemotional Inventory (CUI) and the salivary cortisol level among group of patients with Conduct Disorder (Forty patients from 12 to 16 years old, diagnosed according to criteria of DSM IV and recruited from Kasr El Aini Psychiatric hospital) and group of control (Forty healthy volunteers). Both groups were subjected to Callous Unemotional traits Inventory and salivary cortisol level was assessed using ELISA.
Patient group showed high levels of CU traits compared to control group. Patient group showed significant difference in salivary cortisol level (mean is 3.188 ±1.1108) compared to control group (mean is 5.01±1.846).This study found correlation between Callous traits and severity of Conduct Disorder.
The current findings build upon recent research in suggesting that low cortisol level may be a biological marker for patients with Conduct Disorder and high levels of CU traits.
Keywords: callous–unemotional traits, conduct disorder, disruptive disorder, salivary cortisol
|How to cite this article:|
Dessoki HH, Abd El Reheem HF, Ahmed ME, Soltan MR, Abdel Hakim AA, Dawoud ME. Callous–unemotional traits in conduct disorder in relation to salivary cortisol level. Egypt J Psychiatr 2017;38:90-6
|How to cite this URL:|
Dessoki HH, Abd El Reheem HF, Ahmed ME, Soltan MR, Abdel Hakim AA, Dawoud ME. Callous–unemotional traits in conduct disorder in relation to salivary cortisol level. Egypt J Psychiatr [serial online] 2017 [cited 2021 Sep 17];38:90-6. Available from: http://new.ejpsy.eg.net/text.asp?2017/38/2/90/209679
| Introduction|| |
Conduct disorder (CD) is highly prevalent during childhood and early adolescence, characterized by a repetitive and persistent pattern of behavior that violates the rights of others or in which major age-appropriate societal norms or rules are violated (Sourander et al., 2007).
Childhood-onset CD is distinguished by the presence of significant levels of callous–unemotional traits (CUI), characterized by a lack of guilt, lack of concern about the feelings of others, lack of concern about performance in important activities, and shallow or deficient affect (Hare and Neumann, 2006). The estimated prevalence of high CUI in youth with CD ranges from 10–46% in community samples to 21–59% in clinic samples (Kahn et al., 2012).
Cortisol is an emotional or stress reactivity hormone that indexes activity in the hypothalamic–pituitary–adrenal (HPA) axis. A previous research revealed the relation between HPA-axis abnormalities and antisocial and aggressive behavior. Some evidence suggests that low cortisol levels may serve as a biological marker for a severe antisocial subgroup with pronounced CUI (Loney et al., 2006).
| Aim|| |
The aim of this study was to assess items of CUI and the salivary cortisol level in a group of patients with CD and a group of controls, to show the correlation between items of CUI and CD and to assess the correlation between salivary cortisol and CD.
| Patients and methods|| |
This is a cross-sectional case–control study. After taking approval from the hospital Scientific and Ethical Committee, forty patients having the diagnosis of Conduct Disorder diagnosed according to DSM IV, were recruited from the Child and Adolescent Psychiatric outpatient clinic Kasr el Aini hospitals through the period from September 2013 till March 2014. The participants were divided into two groups (groups A and B). Group A consisted of 40 patients diagnosed with CD according to Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (DSM-IV) using a diagnostic tool Kiddie-SADS-Present and Lifetime (K-SADS-PL) from the Child and Adolescent Psychiatric outpatient clinic from Kasr El Aini University Hospitals (also specific learning disorder as a comorbid condition was diagnosed according to the criteria of DSM-IV because K-SADS-PL does not include the diagnosis of this disorder). Group B consisted of 40 controls (healthy volunteers among relatives of medical and paramedical personnel staff of Kasr Al-Aini University Hospital). All scales show absence of psychopathology in the control group. The control group was matched in age and sex to exclude their possible confounding effect on the cortisol level. Both sexes were included. Their ages ranged between 12 and 16 years. Informed oral and written consent were taken from parents of all participants included in this study. Patients with mental retardation and patients on corticosteroid therapy or other hormonal treatments were excluded. Substance abuse disorder comorbidity was excluded in the patient group as it may affect cortisol level and substance abuse may result in aggression.
When selecting controls, family members of patients, although available, were excluded so as to avoid the possibility of cortisol changes as possible biological factors in disruptive behavior disorder, as serum cortisol levels in the first-degree relatives were significantly higher than that in healthy controls.
The two groups were subjected to the following: (a) the K-SADS-PL, which is a semistructured diagnostic interview designed to assess current and past episodes of psychopathology in children and adolescents according to the DSM-IV criteria; (b) the inventory of callous–unemotional traits (ICU), for assessment of four items of CUI (careless, unemotional, uncaring, and callous traits); and (c) laboratory investigations: salivary samples for cortisol level assessment were collected and preserved at −20°C in the clinical laboratories of clinical pathology Department of Fayoum University Hospitals. Free cortisol levels were assessed using enzyme-linked immunosorbent assay DRG (DRG International, Inc., USA; 841 Mountain Ave, Springfield Township, (Newjersy) NJ07081, USA) Salivary Cortisol enzyme-linked immunosorbent assay.
Data were statistically described in terms of mean±SD, median and range, or frequencies (number of cases) and percentages when appropriate. Comparison of numerical variables between the study groups was made using Student’s t-test for independent samples for comparing two groups when normally distributed and the Mann–Whitney U-test was used for independent samples when not normally distributed. Comparison of numerical variables between more than two groups was made using the Kruskal–Wallis test with post-hoc multiple two-group comparisons. For comparing categorical data, the χ2-test was performed. An exact test was used instead, when the expected frequency was less than 5. Correlation between various variables was made using Spearman’s rank correlation equation. P values less than 0.05 were considered statistically significant. All statistical calculations were carried out using the statistical package for the social science (SPSS, version 15 for Microsoft Windows; SPSS Inc., Chicago, Illinois, USA) computer program.
| Results|| |
The participants were divided into two groups, groups A and B. Group A consisted of 40 patients diagnosed with CD and group B consisted of 40 controls. [Table 1] shows some demographic data and clinical characteristics of the study participants as regards age, sex, educational level, occupation, school attendance, and family history of externalizing disorder.
|Table 1: Some demographic data and clinical characteristics of the study participants|
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On clinical assessment of cases using the K-SADS-PL, 70% (n=28) were diagnosed as having childhood-onset CD subtype, whereas 30% (n=12) were diagnosed as having adolescent-onset CD subtypes ([Figure 1]). Summary of various symptoms of CD (present and past history of threshold symptoms diagnosed according to the K-SADS-PL) in the case group is presented in [Table 2].
|Figure 1: Childhood-onset and adolescent-onset conduct disorder subtypes among cases.|
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|Table 2: Summary of various symptoms of conduct disorder (present and past history of threshold symptoms diagnosed according to the Kiddie-SADS-Present and Lifetime in the case group|
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Items of ICU were compared between the case and control groups [Figure 2] shows that the four items of ICU (careless traits, unemotional traits, callous traits, and unemotional traits) were statistically significantly higher in the case group than in the control group (P≤0.000). However, on comparing items of CUI between cases of childhood-onset CD and adolescent-onset CD, [Figure 3] shows that there was no significant difference in items of ICU between cases of childhood-onset type of CD and cases of adolescent-onset type of CD.
|Figure 2: Comparison of items of callous–unemotional traits inventory between the case and the control group.|
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|Figure 3: Comparison of items of callous–unemotional traits inventory between cases of childhood-onset conduct disorder and adolescent-onset conduct disorder.|
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On comparing salivary cortisol level between the case and control groups, [Figure 4] shows that salivary cortisol level among participants of the case group was lower than that in the control group. The difference was statistically significant (P≤0.000). As regards sex differences in salivary cortisol level in the case group, [Figure 4] shows that there was no statistically significant difference between male (mean salivary cortisol level was 3.214±1.1362) and female patients (mean salivary cortisol was 3.125±1.095) (P=0.896).
|Figure 4: Comparison of salivary cortisol between both the case and the control group and sex difference in salivary cortisol level in the case group.|
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As regards sex differences in items of ICU in the case group, [Figure 5] shows that there was no significant difference between male and female patients with respect to items of ICU.
|Figure 5: Sex difference in items of callous–unemotional traits in the case group.|
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On studying the correlation between items of ICU and age of onset of CD and salivary cortisol level, [Table 3] shows that there was no significant correlation between items of CUI and age of onset of CD. Moreover, there was no significant correlation between items of CUI and salivary cortisol level.
|Table 3: Correlation between the items of callous–unemotional traits inventory and the age of onset of conduct disorder and salivary cortisol level)|
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| Discussion|| |
In this study, participants between 12 and 16 years of age were selected. This is guided by studies in the literature that studied aggression in adolescents with conduct problems (Waldman et al., 2011), and studies using the self-report of ICU (Forsman et al., 2008). The factor structure of ICU has been tested in a large community sample of German adolescents between 12 and 18 years of age (Essau et al., 2006) and a moderately sized sample of juvenile offenders between 12 and 20 years of age in the USA (Kimonis and Frick, 2011).
In total, 70% of patients were male and 30% were female ([Table 1]). This is consistent with the findings of Keith and Kathleen (2005), who found that boys show approximately three to four times higher rates of CD compared with girls. The sex difference can be attributed to the more consistent parental expectations and reinforcement of girls and more unresponsive and rejective parenting of boys; in addition, greater predispositions toward responding in more aggressive ways to boys’ behavior compared with girls’ behavior may be a contributing factor.
In this study, 70% (n=28) of cases were diagnosed as having childhood-onset CD subtype, whereas 30% (n=12) of cases were diagnosed as having adolescent-onset subtype. Such subtyping was supported by the research by Moffitt et al. (2008), who defined meaningful groups of CD according to age as follows: childhood-onset CD, characterized by the presence of at least one symptom before the age of 10 years, and adolescent-onset CD, characterized by appearance of symptoms after the age of 10 years.
The finding of this study supported that there was an increase in the percentage of symptoms from past to present history, which may indicate the progressive course of CD. It is in line with the findings of Moffitt et al. (2002), who found that children often begin showing mild conduct problems as early as preschool or early elementary school and their behavioral problems tend to increase in rate and severity throughout childhood and into adolescence, and that they continue to show antisocial and criminal behavior into adulthood. Conduct problems can also be aggravated by interpersonal problems within family and school and poor outcome in school achievement, which may be a cause and a result for symptom progression.
This study found that the case group showed significantly higher values in the four items of ICU compared with the control group. It is consistent with the findings of Frick and Dickens (2006), who reviewed 24 published studies using child or adolescent samples in which either psychopathic traits in general, or CUI specifically, were associated with more severe conduct problems.
CUI were important for designating a more severe (Christian et al., 1997) and stable (Frick et al., 2005) pattern of antisocial behavior within children who showed serious conduct problems. Moreover, Kahn et al. (2012) suggested that the proposed callous–unemotional (CU) specifier would designate between 10 and 32% of children with CD in the community sample. Further, the base rates of the CU specifier and the individual CU symptoms were fairly low in children without CD.
This is consistent with the findings of Frick (2012), who indicated that between 20 and 50% of children with serious conduct problems exhibit non-normative levels of CUI. This subgroup of youths with severe conduct problems and elevated CUI seem to exhibit a more severe and stable pattern of antisocial behavior compared with other youths.
In a national representative sample (n=5326) of children between 5 and 16 years of age, Rowe et al. (2009) reported that 46% of children with CD had high rates of CUI, and those with CUI showed a more stable pattern of CD.
It is consistent with the findings of Larson and Lochman (2003), Taylor et al. (2003), Viding et al. (2007), Bezdjian et al. (2011), and Waldman et al. (2011), who found an association between CUI and conduct problems, and also found that unique genetic influences both constructs and supports partially distinct etiological underpinnings.
Accumulating evidence indicates that youth with elevated CUI are at risk for exhibiting severe and persistent antisocial behavior, even after controlling for co-occurring disruptive behavior disorder symptoms (Pardini and Fite, 2010).
In this study, difference in salivary cortisol level between cases and controls was statistically significant (P≤0.000) (in the case group salivary cortisol level ranged from 1.9 to 6.2, with a mean of 3.188±1.1108, whereas in the control group salivary cortisol level ranged from 2 to 8.5, with a mean of 5.01±1.846).
This finding is consistent with that of Alink et al. (2008), who examined data from 82 studies conducted between 1978 and 2006. The results supported an inverse relationship between cortisol and antisocial behavior – that is, the development of antisocial behavior is associated with low cortisol levels.
The finding of this study is not consistent with that of Sondeijker et al. (2007), who indicated that, in a large representative general population sample of preadolescent boys and girls, the association between disruptive behaviors and indices of the basal HPA-axis functioning were weak, and not always in the direction expected. To explain discrepancies with previous studies, the severity of problems in high-risk groups versus general population samples could be of importance. In clinical samples, problems are more severe and likely to have persisted for several years before referral to mental health services takes place. Hence, the HPA-axis may have become less sensitive to stress. As a result, in these individuals, much more stress may be needed to activate the HPA-axis, which would result in decreased basal levels of cortisol (underarousal) in individuals with severe disruptive behaviors. Such a phenomenon might play a less important role in the general population (Van de Wiel et al., 2004).
This study found that there was no significant correlation between items of CUI and age of onset of CD. It is not consistent with the findings of Pardini et al. (2006), who found that CUI seem to further delineate childhood-onset CD cases that are more likely to persist in their antisocial behavior into adulthood. There also appears to be unique causal factors underlying the conduct problems found in children with CUI, such as low temperamental fear. This may be attributed to the small sample size of this study and usage of the self-report of the ICU, and not only the teacher-reported or the parent-reported ICU.
The presence of CUI seems to be more highly associated with the childhood-onset conduct problems (Silverthorn et al., 2001). However, these traits seem to designate a more severe, chronic, and aggressive subgroup within this trajectory, and a subgroup with distinct temperamental characteristics (Frick, 2006).
It is not in line with other studies that reported that CUI were more common in youths with childhood-onset to their antisocial behavior compared with those with an adolescent-onset type (Dandreaux and Frick, 2009).
In this study, there was no correlation between items of ICU and salivary cortisol. It is not consistent with the findings of Stadler et al. (2011), who found that CU+ patients with disruptive behavior problems showed a blunted cortisol reactivity to stress. The strengths of latter study were the large sample size, use of multiple informants to assess disruptive behaviors, and assessment of three cortisol measures on relevant time points during the day.
This is not in line with previous results reporting blunted HPA-axis function in a nonreferred adolescent sample with high CUI, which was not observed in those without high CUI (Loney et al., 2006). This is can be attributed to the small sample size of this study and assessment of only one sample of salivary cortisol without stress provocation. Barry et al. (2003) explained that stress sensitivity may be a key factor in the link between HPA-axis functioning and disruptive behaviors.
In this study, there was no significant difference in cortisol level between male and female patients in the case group. This is contradictory to the findings of Bryan et al. (2006), who reported the absence of a statistically significant CU-low cortisol relation for female participants (in contrast to male CUI with conduct problems) and that female CUI with conduct problems may not be associated with cortisol abnormalities. It is important to note that it would not entirely rule out an emotional under-reactivity component to female psychopathy, which may be attributed to various biological, cognitive, emotional, and behavioral responses that subsume a fear response, and it is possible that male psychopathy is simply more robustly tied to low emotional reactivity (i.e. across a number of indices such as passive avoidance impairment, heart rate, hormone, and skin conductance findings).
It is not consistent with the findings of Keith and Kathleen (2005), who found that girls had higher cortisol levels compared with boys. Netherton et al. (2004) suggested that gonadal steroids might play an important role in this finding. Gonadal steroids, and estrogens in particular, are known to interact with the HPA-axis. Increased HPA-axis activity in girls might be related to the direct effect of estrogens on corticotropin-releasing hormone Vanyukov et al. (1993).
According to Sondeijker et al. (2007), sex interaction effects were found, indicating that associations between cortisol levels and disruptive behaviors were different in boys versus girls.
Higher rates of CD problems were associated with higher morning cortisol levels in girls and lower cortisol levels in boys. The finding that lower cortisol levels in boys were associated with higher levels of CD problems is in accordance with previous studies (McBurnett et al., 2000).
For instance, estrogens, which are known to influence HPA-axis activity, might play a role (Vanyukov et al., 1993).
The small sample size of the participants and the small number of female participants could support this inconsistence.
Future research could compare and contrast resting hormone levels to hormone levels assessed following perceived threat or emotional provocation. This provocation might exacerbate group differences and/or suggest important contextual variables related to underlying emotional impairments (Bryan et al., 2006).
In this study there was no significant difference in items of ICU between male and female patients in the case group. It is not consistent with the findings of Essau et al. (2006), who found that boys had significantly higher scores on ICU, both for total and subscale scores. Moreover, the finding of this study is not consistent with past research indicating that men tend to score higher than women on all dimensions of psychopathy, including the CU dimension (Vitacco et al., 2006). The small sample size of the participants and the small number of female participants could support this inconsistence.
| Conclusion|| |
It is important to study items of CUI in patients with CD and its relation with cortisol level. The patients with CD show high levels of CUI compared with normal children and adolescents. The level of cortisol is lower in patients with CD than in the control group. There was no correlation between cortisol level and items of CUI. There was no correlation between the age of onset of CD and items of CUI.
Limitations of the study
The data collection was confined to specific age group among cases of CD (aged 12–16) in whom the ICU could be applied. The number of participants interviewed was small, as the patients who met the inclusion criteria (cases of CD aged 12–16) were few as their parents consider that their treatment would not be promising and so do not seek medical advice. Another obvious limitation of the study was the use of only self-reported inventory, and so data may not be enough to generalize the current results into larger scale. The cross-sectional study together with number of participants may not be enough to generalize the current results to the population-based cases. 
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Alink LR, van Ijzendoorn MH, Bakermans-Kranenburg MJ, Mesman J, Juffer F, Koot HM (2008). Cortisol and externalizing behavior in children and adolescents: mixed meta-analytic evidence for the inverse relation of basal cortisol and cortisol reactivity with externalizing behavior. Dev Psychobiol 50:427–450.
Barry CT, Frick PJ, Killian AL (2003). The relation of narcissism and self-esteem to conduct problems in children: a preliminary investigation. J Clin Child Adolesc Psychol 32:139–152.
Bezdjian S, Raine A, Baker LA, Lynam DR (2011). Psychopathic personality in children: genetic and environmental contributions. Psychol Med 41:589–600.
Bryan RL, Melanie AB, Elizabeth NL, Counts CA, Eckel LA (2006). The relation between salivary cortisol, callous unemotional traits, and conduct problems in an adolescent non-referred sample. J Child Psychol Psychiatry 47:30–36.
Christian RE, Frick PJ, Hill NL, Tyler L, Frazer DR (1997). Psychopathy and conduct problems in children: II. Implications for subtyping children with conduct problems. J Am Acad Child Adolesc Psychiatry 36:233–241.
Dandreaux DM, Frick PJ (2009). Developmental pathways to conduct problems: A further test of the childhood and adolescent-onset distinction. J Abnorm Child Psychol 37:375–385.
Essau CA, Sasagawa S, Frick PJ (2006). Callous unemotional traits in a community sample of adolescents. Assessment 13:454–469.
Forsman M, Lichtenstein P, Andershed H, Larsson H (2008). Genetic effects explain the stability of psychopathic personality from mid- to late adolescence. J Abnorm Psychol 117:606–617.
Frick PJ (2006). Developmental pathways to conduct disorder. Child Adolesc Psychiatr Clin N Am 15:311–331.
Frick PJ (2012). Developmental pathways to conduct disorder: implications for future directions in research, assessment, and treatment. J Clin Child Adolesc Psychol 41:378–389.
Frick PJ, Dickens C (2006). Current perspectives on conduct disorder. Curr Psychiatry Rep 8:59–72.
Frick PJ, Stickle TR, Dandreaux DM, Farrell JM, Kimonis ER (2005). Callous unemotional traits in predicting the severity and stability of conduct problems and delinquency. J Abnorm Child Psychol 33:471–487.
Hare RD, Neumann CS (2006). The PCL-R assessment of psychopathy: development, structural properties, and new directions. In: Patrick CJ, editor. Handbook of psychopathy
. New York, NY: Guilford. 58–90.
Kahn RE, Frick PJ, Youngstrom E, Findling RL, Youngstrom JK (2012). The effects of including a callous unemotional specifier for the diagnosis of conduct disorder. J Child Psychol Psychiatry 53:271–282.
Keith CH, Kathleen M (2005). Child and adolescent psychiatry: the essential
. XXXX: Lippincott Williams & Wilkins.
Kimonis ER, Frick PJ (2011). Etiology of oppositional defiant disorder and conduct disorder: biological, familial and environmental factors identified in the development of disruptive behavior disorders. In: Murrihy RC, Kidman AD, Ollendick TH, editors. Handbook of clinical assessment and treatment of conduct problems in youth
. New York, NY: Springer. 407–433.
Larson J, Lochman JE (2003). Helping school children cope with anger
. New York, NY: Guilford Press.
Loney BR, Butler MA, Lima EN, Counts CA, Eckel LA (2006). The relation between salivary cortisol, callous unemotional traits, and conduct problems, in an adolescent nonreferred sample. J Child Psychol Psychiatry 47:30–36.
McBurnett K, Lahey BB, Rathouz PJ, Loeber R (2000). Low salivary cortisol and persistent aggression in boys referred for disruptive behavior. Arch Gen Psychiatry 57:38–43.
Moffitt TE, Caspi A, Harrington H, Milne BJ (2002). Males on the life-course persistent and adolescence-limited pathways: follow-up at age 26 years. Dev Psychopathol 14:179–207.
Moffitt TE, Arseneault L, Jaffee SR, Kim-Cohen J, Koenen KC, Odgers CL et al.
(2008). DSM-V conduct disorder: research needs for an evidence base. J Child Psychol Psychiatry 49:3–33.
Netherton C, Goodyer I, Tamplin A, Herbert J (2004). Salivary cortisol and dehydroepiandrosterone in relation to puberty and gender. Psychoneuroendocrinology 29:125–140.
Pardini DA, Fite PJ (2010). Symptoms of conduct disorder, oppositional defiant disorder, attention deficit/hyperactivity disorder, and callous unemotional traits as unique predictors of psychosocial maladjustment in boys: advancing an evidence base for DSM-V. J Am Acad Child Adolesc Psychiatry 49:1134–1144.
Pardini DA, Obradović J, Loeber R (2006). Interpersonal callousness, hyperactivity/impulsivity, inattention, and conduct problems as precursors to delinquency persistence in boys: a comparison of three grade-based cohorts. J Clin Child Adolesc Psychol 35:46–59.
Rowe R, Maughan B, Moran P, Ford T, Briskman J, Goodman R, (2009). The role of callous unemotinal traits in the diagnosis of conduct disorder. J Child Psychol Psychiatry 51:688–695.
Silverthorn P, Frick PJ, Reynolds R (2001). Timing of onset and correlates of severe conduct problems in adjudicated girls and boys. J Psychopathol Behav Assess 23:171–181.
Sondeijker FE, Ferdinand RF, Oldehinkel AJ, Veenstra R, Tiemeier H, Ormel J, Verhulst FC (2007). Disruptive behaviors and HPA-axis activity in young adolescent boys and girls from the general population. J Psychiatr Res 41:570–578.
Sourander A, Jensen P, Davies M, Niemelä S, Elonheimo H, Ristkari T et al.
(2007). Who is at greatest risk of adverse long-term outcomes? the Finnish from a boy to a man study. J Am Acad Child Adolesc Psychiatry 46:1148–1161.
Stadler C, Kroeger A, Weyers P, Grasmann D, Horschinek M, Freitag C, Clement HW, (2011). Cortisol reactivity in boys with attention deficit hyperactivity disorder and disruptive behavior problems: the impact of callous unemotional traits. Psychiatry Res 187:204–209.
Taylor J, Loney BR, Bobadilla L, Lacono WG, McGue M, (2003). Genetic and environmental influences on psychopathy trait dimensions in a community sample of male twins. J Abnorm Child Psychol 31:633–645.
Van de Wiel NMH, van Goozen SH, Matthys W, Snoek H, van Engeland H, (2004). Cortisol and treatment effect in children with disruptive behavior disorders: a preliminary study. J Am Acad Child Adolesc Psychiatry 43:1011–1018.
Vanyukov MM, Moss HB, Plial JA, Blackson T, Mezzich AC, Tarter RE (1993). Antisocial symptoms in preadolescent boys and in their parents: associations with cortisol. Psychiatry Res 46:9–17.
Viding E, Frick PJ, Plomin R (2007). Aetiology of the relationship between callous unemotional traits and conduct problems in childhood. Br J Psychiatry Suppl 190:s33–s38.
Vitacco MJ, Neumann CS, Caldwell MF, Leistico AM, van Rybroek GJ (2006). Testing factor models of the psychopathy checklist: youth version and their association with instrumental aggression. J Pers Assess 87:74–83.
Waldman ID, Tackett JL, van Hulle CA, Applegate B, Pardini D, Frick PJ, Lahey BB (2011). Child and adolescent conduct disorder substantially shares genetic influences with three socioemotional dispositions. J Abnorm Psychol 120:57–70.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
[Table 1], [Table 2], [Table 3]