Adolescent inattention/overactivity/impulsivity as an outcome of early institutional deprivation : the role of genetic factors

This longitudinal study examined the association between early institutional deprivation and inattention/overactivity/impulsivity (IOI) in a sample of institutionreared children adopted from severely depriving conditions in Romania before the age of 43 months. The total sample comprised 144 institution-reared and 21 noninstitution-reared Romanian adoptees, and a comparison group of 52 nondeprived, U.K. born children, adopted between the ages of 0 and 6 months. Their development was assessed at ages 6, 11 and 15 years, with particular attention given to their outcome in mid-adolescence. The current study tested the hypothesis that the risk for IOI following early deprivation is moderated by individual genetic make-up, using a subsample of 129 children. Candidate genes were selected using two strategies (Moffitt et al., 2005): i) a phenotype-based strategy that employed genes implicated in the aetiology of ADHD (dopamine transporter and receptor genes); ii) a process-based strategy that used polymorphisms with functional significance in terms of individual’s responsivity to early deprivation (glucocorticoid receptor gene). The introductory section of the current thesis is organised into three sections: i) an overview of ERA study and the association between adversity and IOI; ii) a review of literature on the broader phenotype of ADHD; iii) a discussion of the role that genetic factors may play in the putative causal pathways to IOI and ADHD. The following section outlines the study sample, methods and instruments. The subsequent empirical section is divided into three chapters: the first presents the results on the persistence and presentation of IOI; the second and third chapters present the analysis of the role of genetic factors in the risk for IOI following early deprivation. There were three main study findings: First, institutional deprivation lasting around 6 months or more was associated with an increased risk for IOI impairment from childhood into midadolescence. Second, the phenotypic presentation of IOI shared several features in common with nondeprivation-related ADHD. Despite showing persistence and pervasiveness across settings, the effects of early deprivation were not deterministic, suggesting other risk factors may be moderating the association. The third main finding suggested that the adverse effects of institutional deprivation on IOI were moderated by specific polymorphisms within the dopamine transporter gene. The effects were seen over time and across measures of IOI. The results are then brought together in the final discussion chapter. When the GxE interaction findings are integrated with the observation of persistence of IOI impairment and the commonalities in phenotypic presentation with nondeprivation-related ADHD, the results provide support for the hypothesised gene-environment interaction model, whereby ADHD susceptibility genes moderate the risk for of IOI from prolonged institutional deprivation.