CA critical review of
‘An exploration of the serotonin system in antisocial boys with high levels of callous-unemotional traits’ by
C. Moul, C. Dobson-Stone, J. Brennan, D. Howes and M. Dadds (2013)

Introduction: Aggressiveness is a complicated study due to the fact that it does not act as an integral trait, and increased interest towards the matter of anti-social behaviour is partly explained by the apparent escalation of aggression in contemporary society (Popova, 2006). The human expression of anger is due to a combination of endocrine, neural and behavioural mechanisms and as such, a central question of human history. Children with aggressive behaviour form a heterogeneous population in relation to certain subtypes of aggressive antisocial behaviour. Callous-unemotional traits (e.g. absence of emotions and blame) are well-studied and temperamentally tied in with acute and persistent antisocial expression in children, which holds the risk for progressing psychopathy later in life (Frick & Viding, 2009) Serotonin levels are thought to contribute to childhood aggressive and antisocial behaviour, which can lead to expression later in adulthood (Raine, 2002). Thus, genetic factors are an inseparable part of the nature of antisocial behaviour, as demonstrated by twin research that has shown that heritability is likely to determine various forms of aggression and personality factors, such as impulsivity and callous-unemotional traits (Moffitt, 2005). Despite the fact that the specific genetic basis of the innate nature of antisocial behaviour has not been firmly demonstrated, a number of studies have proposed that serotonergic dysfunction acts as a trigger for deviant behaviour (Cadoret, Langbehn, Caspers, Troughton, Yucuis, Sandhu & Philibert, 2003). In their study Cadoret et al consider various factors which remain significantly important in exploring the true triggers for antisocial behaviour in children. One of these factors is the neurotransmitter serotonin or variations of the serotonin transporter gene (5HTT). In a study by Beitchman, Zai, Muir, Berall, Nowrouzi, Choi and Kennedy (2012) results suggested that there is a significant relationship between oxytocin polymorphism and CU traits in highly aggressive children, with stronger findings among boys. It has also been suggested that genetic changes in particularly sensitive developmental periods and in combination with environmental factors (e.g. parenting styles, socioeconomic status, hormones, puberty) are more likely to produce high Callous-Unemotional (CU) traits in young children (Frick & Viding, 2009). Similarly, in their study Baker, Bezdjian and Raine (2006) conclude that although heritability of antisocial traits makes a strong case, environment plays a crucial role in displaying and magnifying those genetic influences in deviant behaviour. In a study by Viding, Larsson and Jones (2008) it has been reported that high CU traits children exhibit strong genetic effects (heritability of 0.81), but are not affected by environmental factors; whereas those with low CU traits showed moderate genetic dominance (heritability of 0.30) and apparent environmental effects. In review of Moul, Dobson-Stone, Brennan, Hawes and Dadds’s (2013) evidence of the association between serotonin system and levels of callous-unemotional (CU) traits in anti-social boys the present paper acknowledges its significance of findings. Nevertheless, considering the biological factors underpinning CU traits in young anti-social children should involve other biological risk factors, for example, the role of hormones, neurotransmitters, frontal lobe function etc. Assessing the true origin of anti-social behaviour it is probably worth considering that genetic factors could be moderated by environmental variables, such as the distinct layers of the ecological micro and macro system of the child’s development (Bronfenbrenner, 1979). It is an overall satisfactory constructed study and a well operationalised experiment consistent of good methodology and systematic significant findings, which highlights a possible association between the serotonin system levels in antisocial young male population and levels of CU traits. Sample size; gender specific behavioural patterns; participants’ ethnicity limitations and the wide age range are the main weaknesses of the present study under review.

Summary: The authors of the study hypothesised that boys with antisocial behaviour problems and high levels of CU traits would have lower levels of serum serotonin than boys with antisocial behaviour problems and low levels of CU traits. In order to test their hypothesis they have employed 157 boys (3-16 years for the genetic sample and 4-12 years for the serum sample). The sample sizes used for the main measures were split in three separate groups: serotonin system single nucleotide polymorphisms (SNP’s) – Caucasian only (N=157); serotonin serum levels with no ethnicity restrictions (N=66) and both genetic and serum serotonin level data – Caucasian only (N=35). Parents were asked to complete the Antisocial Processes Screening Device (APSD) and the Strengths and Difficulties Questionnaire (SDQ) – testing traits and behaviours associated with psychopathy. Family dynamics were assessed through Family Assessment Device (FAD) – 12-item brief version questionnaire, exploring the family structure and organisation. Subsequently, parental psychopathology was measured with the Depression Anxiety Stress Scales (DASS) - 21-item self-report sub-scales. Home address was recorded for each family and consulted with the Australian Bureau of Statistics (ABS) Socio-Economic Index of Area – a ten-point scale which estimates the children’s surrounding environment. Callous-Unemotional (CU) traits were measured combining items from the APSD and the prosocial scale of the SDQ. Subsequently, participants have been divided into two groups – high CU trait boy group and low CU trait boy. Participants were rated by clinical psychologists on levels of antisocial behaviour problems, ADHD, autism spectrum disorders, anxiety and depression, unaware of levels of CU traits. Child distress was measured by a clinical rating scale, namely the Quality of the Family Environment (QFE). CU groups were first compared by means of ANOVA, Chi square was subsequently conducted in order to compare frequencies of genotypes and logistic regression was the final statistical analysis method to determine whether serum serotonin levels were a predictor of CU traits. Findings have noted that functional single nucleotide polymorphisms (SNP’s) from the serotonin 1b receptor gene (HTR1B) and 2a receptor gene (HTR2A) were associated with callous-unemotional traits. Therefore, it was proposed that serum serotonin level served as a significant predictor of CU traits where boys with high CU traits had lower levels of serum serotonin than boys with low CU traits. The authors have concluded that their findings provide support for the genetic aetiology of callous-unemotional traits through an alteration in the serotonin function and suggested that future research should replicate and further assess their results.

Evaluation: The present study under review argues that the levels of CU traits, characterised by cognitive and emotional deficits and also directly associated with the causes of aggression and antisocial behaviour, are dependent on serum serotonin levels. In this paper an important prediction has suggested that the relationship between serotonin and aggression is inverse. The study by Moul, Dobson-Stone, Brennan, Hawes and Dadds is an important piece of work considering the neurobiological components underlying aggressive behaviours. Understanding the complex nature of the relationship between serotonin and aggressiveness requires the consideration of numerous factors, including the kind of aggression, the genetic history and the quintessential phenotype for it, the individual traits and the situational factors surrounding the behaviour (Takahashi, Quadros, de Almeida & Miczek, 2011). Combining the specific individual and environmental characteristics could help in further exploring the association between serotonin and aggression, facilitating future interventions. Furthermore, an interesting finding from a recent research by Moul, Dobson-Stone, Brennan, Hawes and Dadds (2015) suggests the possibility of two hypothetical pathways leading to high CU traits considering the HTR1B gene. The authors proposed that one of them would be more demonstrative of a genetic factor (analogous to primary level of psychopathy) and the second route characterised by high level of methylation related to environmental factors (linked to secondary psychopathy progression). Moreover, in search of the genetic explanations for CU traits in young boys Jones, Laurens, Herba, Barker and Viding (2009) have found that when children with high CU traits have been exposed to fearful facial expressions their amygdala activity proved lower in comparison to those exhibiting ADHD problems. More recent research has reported that reduction in amygdala action was found in high CU traits children when presented with pre-attentive stimuli resulting in a negative correlation between high CU traits and low levels of amygdala activity, which possibly compromises childrens’ estimation of affective social cues (Viding, Sebastian, Dadds, Lockwood, Cecil, De Brito, McCrory, 2012). Therefore, a more balanced explanation for the broad variations of human behaviour could be the interaction between genetic and environmental factors (Baker, Bezdjian & Raine, 2006). The work of Moul et al. had a number of strengths and weaknesses. One of its strengths is the use of validated measures for determining levels of CU traits (the Antisocial Processes Screening Device-APSD and the prosocial scale of the Strengths and Difficulties Questionnaire-SDQ) and serotonin levels (blood sample, saliva sample and a combination of blood-saliva sample). To avoid predicted bias in the study sample the authors have kept boys using prescription drugs included. Also, clinical psychologists, unaware of levels of CU traits were used to rate the participants, again avoiding possible bias. The study included a well selected participant sample in accordance to the criteria of DSM-IV diagnosis of antisocial behaviour problems (ODD or CD). The findings of the study were also consistent with some of the prior research about the subject and after significance of the results was found, a regression analysis was conducted with an exclusion of boys who were taking prescription medications, in order to avoid results bias. Last, but not least another strength of their study based on prior research findings is that Moul et al. have used entirely antisocial cohort in their search for a possible relationship between serotonin levels and CU traits. The paper under review has also pointed at its possible weaknesses and limitations. One of these was sample size due to the fact that fewer participants were willing to give a blood sample and as such the study results require a replication with a larger population. Findings of the study are not suitable for generalisation, as it was an entirely male sample where there could be testosterone level of effects on the degree of aggressiveness in boys. Participants’ ethnicity limitation is another of the study’s weaknesses; despite the need of a homogenous population for the genetic analyses, findings cannot be reliably relevant to all ethnic backgrounds. Age range used for this research was quite large and behavioural patterns could vary considerably across this age range, whereas a longitudinal design could be more relevant in testing serotonin levels in association with CU traits in order to prescribe pharmacological interventions. This paper failed to properly describe some of its method procedures, especially in the Participants section it appears unclear how many participants in total have been used and how they have been split in groups i.e. 56 of the boys were not accounted for. Nevertheless, the work of Moul et al.is a prominent piece of scientific investigation in the field of neuropsychology exploring the genetic factors, that could be responsible for high CU traits found in some children. The current study under review could benefit from a future inclusion and analyses of a variety environmental factors, which will enrich the data in search of the true triggers of anti-social behaviour and in particular discovering the factors shaping CU traits in the young population.

Conclusion: In conclusion it might be said that the neurobiology of CU traits in boys varies in accordance with the types of aggression and the type of factors analysed. In humans, as in animals, the evidence suggests that serotonergic dysfunction appears to be linked to reduced threshold for aggressiveness (Dadds & Rhodes, 2008). The complex interrelations between hormonal and neurobiological factors, as in the case of testosterone and 5-HT, which appear in critical developmental stages may prove to be one explanation for the aggressive expression in boys. Moreover, any conclusions about the factors responsible for the negative correlation between brain serotonin levels and CU traits call for the consideration that biological risks may not be completely genetically founded, and similarly social risk factors may not necessarily be environmentally based. Thus, the association between risk factors and various types of antisocial behaviour should be highlighted as one of a complex nature. An overall satisfactory study, the work of Moul et al. has provided the opportunity for further investigation of the subject given the basis for predicting that at least one of the factors for observed high CU traits in some children could have genetic grounds. Considering the strengths and the weaknesses of the study by Moul et al.it might be suggested that by employing a larger, homogeneous sample of smaller age range, but of a wider ethnicity population, the same study could have a greater predictive validity. Therefore, future research should consider the nature and the development of CU traits by better understanding of the characteristics of these traits and the functionality of the neurochemical systems across gender, including all developmental stages. Incorporating ethnical diversity could help generalisations to be made over a larger sample. Findings from future adolescence samples may change the associations between the functions of the serotonin system and CU traits. Nevertheless, in search of objectively identifying the grounds of callous-unemotional traits in children it could be suggested that further research should consider amalgamating biological and environmental variables as an alternative approach to the scientific study of anti-social behaviour.
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