Abstract
Attention-deficit/hyperactivity disorder (ADHD) has been linked to dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis, indexed by salivary cortisol. The phenotypic and aetiological association of cortisol productivity with ADHD was investigated. A selected twin design using 68 male twin-pairs aged 12–15, concordant or discordant for high ADHD symptom scores, or control twin-pairs with low ADHD symptoms, based on developmentally stable parental ADHD ratings. A genetic growth curve model was applied to cortisol samples obtained across three points during a cognitive-electroencephalography assessment, to examine the aetiological overlap of ADHD affection status (high versus low ADHD symptom scores) with latent intercept and slope factors. A significant phenotypic correlation emerged between ADHD and the slope factor, with cortisol levels dropping faster for the group with high ADHD symptom scores. The analyses further suggested this overlap was mostly driven by correlated genetic effects. We identified change in cortisol activity over time as significantly associated with ADHD affection status, primarily explained by shared genetic effects, suggesting that blunted cortisol productivity can be a marker of genetic risk in ADHD.
Highlights
Attention deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterised by age-inappropriate levels of inattention and hyperactivity-impulsivity
Other group mean differences include that the group with high Attention-deficit/hyperactivity disorder (ADHD) symptom scores was significantly younger than controls and were more likely to have participated during months with more light (March–September)
The high ADHD symptom group had lower cortisol concentration levels throughout the cognitive-EEG session, this was only significant at the last sampling point and did not retain significance (t = -1.34, p = 0.18) after regressing out potential confounders
Summary
Attention deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterised by age-inappropriate levels of inattention and hyperactivity-impulsivity. Studies on children with diagnosed ADHD versus control groups examining overall diurnal cortisol levels and rhythm have reported significantly lower basal cortisol concentrations in morning sampling (Blomqvist et al 2007; Isaksson et al 2012; Ma et al 2011), and significantly lower incidence of typical diurnal variation (defined as having a maximum and minimum cortisol level, respectively, at morning and evening sampling (Kaneko et al 1993). A recent meta-analysis of case–control studies of baseline cortisol found a significant, though modest effect (d = -0.31, p = 0.0001) of ADHD, with lower levels in ADHD versus controls (Scassellati et al 2012). Some studies suggest that the covariation between ADHD and HPA-axis dysregulation is further complicated by ADHD subtype and/or comorbidity (Freitag et al 2009; Hastings et al 2009), but in the largest study to date with over 300 children (Isaksson et al 2012), the negative association of morning cortisol measures with ADHD symptoms in children aged over 10 years did not differ according to ADHD subtype or co-occurring symptoms
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