Editorial: Integrating neurobiological, genetic, and environmental risk factors in cognitive and behavioral conditions


The January issue brings together several important topics related to the etiology and treatment of cognitive and behavioral disorders. The issue begins with two excellent narrative reviews of the literature. First, Thapar and colleagues1 reviewed the longstanding literature related to genetic and environmental factors associated with ADHD. The most consistent risk factors for ADHD are having a relative with the disorder, large rare copy number variations, extreme early adversity, low birth weight/prematurity, and pre/postnatal exposure to lead. The authors concluded that, although heritable, genetic risks related to ADHD have either small effect sizes or are rare, that noninherited factors are also important, and that genetic and environmental sources are noncausal in effect.

In contrast to the mature ADHD literature, Betancourt and colleagues reviewed the emerging literature examining psychosocial adjustment and mental health in former child soldiers. The authors found that the persistence and prevalence of mental health problems varied widely. However, the authors also noted that coordinated efforts are also necessary to increase the scientific rigor in this important area of study.

In addition to these two reviews, the January issue includes several primary articles. First, Loman and colleagues examined international adoptees, in particular the relationship between early institutionalization and later executive attention in middle childhood. Notably, the authors employed both behavioral and neurobiological measures, finding that children who experienced institutionalization were more likely to demonstrate problems with sustained attention, which may be associated with inhibitory control and error monitoring. The authors suggested that these behavioral and neurobiological patterns may be the result of a lack of early consistent and responsive caregiving. Perren and colleagues examined the impact of peer victimization on later maladjustment, focusing on the mediating and moderating effects of hostile and self-blaming attributions. The authors found that peer victimization was associated with increased internalizing and externalizing problems. Importantly, the negative impact of victimization may be mediated or moderated by child attributions. The authors concluded that changing child attributions may be an important potential lever to reduce the negative consequences of peer victimization. Ramchandani and colleagues examined the relationship between early father–infant interactions and later externalizing behavior problems. The authors found that disengaged and remote interactions between fathers and their 3-month infants predicted externalizing behavior problems in the same children at one year. This study adds to a relatively small but important literature examining the effects of fathers. In his commentary to this article, Shaw highlighted the potential interactions between maternal and paternal caregiving as well as the potential role of paternal depressive symptoms.

The January issue also presents two quantitative genetic studies. Taylor and colleagues conducted a quantitative genetic study of the relationship between socioemotional dispositions and externalizing behavior. In particular, the authors found that ADHD and ODD formed a latent externalizing factor, and that socioemotional dispositions such as prosocial behavior, negative emotionality, and daring were linked with externalizing behavior via genetic and environmental factors. The authors concluded that these results highlight the importance of considering temperament/personality when considering the development of externalizing behavior disorders. Tucker-Drob and Harden employed a quantitative genetic design to examine gene x preschool interactions and the development of externalizing problems. The authors suggested that attending preschool may differentiate externalizing behavioral problems as a result of genetic factors.

Finally, the January issue presents a series of studies examining the relationship between brain structure and psychological/psychiatric outcomes and conditions. Fairchild and colleagues examined the relationship between brain structure and conduct disorder, notably, in adolescent girls. The authors found abnormalities in brain areas related to emotion processing, reward, and empathy. Ghassabian and colleagues examined the relationship between infant brain structure and later preschool executive function and attention/hyperactivity problems. The authors were not able to demonstrate that structural variations in infancy predicted symptoms of ADHD, but were able to show that brain structure predicted subtle impairments in later inhibition and emotional control. Debrito and colleagues found that children who experienced maltreatment presented with reduced grey matter in brain areas related to reinforcement-based decision making, autobiographical memory, and emotion regulation. The authors concluded that these regions may represent a neurobiological risk factor for later risk-taking behavior and risk for psychopathology.

Taken together, these studies are emblematic of the exciting yet daunting state of affairs in psychology and psychiatry. On one hand, we are in an unprecedented position to examine the underlying neurobiological, genetic, and environmental risk factors for highly important clinical outcomes such as ADHD and behavioral adjustment. Several of the studies in the January issue operate across multiple levels of analysis. This opens up the possibility of discovering etiological markers that may aid in our understanding of these important conditions. On the other hand, it is also abundantly clear that causal reductionist thinking is unable to explain the vast amount of variance in the population, which complicates efforts to translate etiological findings into clinical practice. An interesting review by Manolio (2009) explores this state of affairs in genetics, suggesting that, although explaining all of the variance may be elusive, identifying a large number of risk factors of small effect may allow the identification of clinically meaningful subgroups that may be particularly amenable to targeted prevention/intervention strategies.