The aetiological association between the dynamics of cortisol productivity and ADHD

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.

Temperament Dimensions and Awakening Cortisol Levels in Attention-Deficit/Hyperactivity Disorder

“…We did not find significant associations between cortisol levels and the surgency-extraversion, negative affect, and effortful control regulation dimensions. To further examine this relationship and confirm that arousal does not share similar underlying mechanisms with temperament in ADHD, studies using repeated measures of cortisol productivity under different active tasks [e.g., such as those used in ( 30 )] and in larger samples are warranted.…”

“…Studies have found low awakening cortisol levels concerning ADHD diagnosis and symptoms. However, this evidence is currently inconsistent ( 26 ), with some studies showing reduced cortisol levels in ADHD ( 27 – 29 ) and others showing no associations with ADHD traits ( 30 ) or case-control differences ( 31 ) requiring further replication. Additionally, only children with ADHD and ODD, but not those without comorbid disruptive behavior disorders, showed lower awakening cortisol levels than controls in an earlier study ( 32 ).…”

No evidence of associations between ADHD and event-related brain potentials from a continuous performance task in a population-based sample of adolescent twins

“…Participants were from the Neurophysiological Study of Activity and Attention in Twins (NEAAT), which has also been described elsewhere [15,52–54]. The NEAAT sample consisted of a subset of adolescent twin pairs from the Twins’ Early Development Study (TEDS), which is a longitudinal population-based study of all twins born in England and Wales in 1994 to 1996 [55].…”

“…MZ and DZ cross-twin correlations on ADHD status were fixed based on heritability estimates from a meta-analysis [4], with the following parameters: h 2 = .76, c 2 = .00, e 2 = .24, consistent with rMZ = .76 ( h 2 + c 2 ) and rDZ = .38 (.5 h 2 + c 2 ). We have established, validated and successfully applied this model to investigate the link between EEG [15,52,53] and cortisol outcomes [54] with ADHD, as well as the link between brain-based measures and other low-prevalence conditions, such as schizophrenia [76–79], bipolar disorder [80,81], and psychopathy [82].…”

Diverse Autonomic Nervous System Stress Response Patterns in Childhood Sensory Modulation

“…Children with ADHD and SOR displayed similar cortisol patterns to typically developing children, while children with ADHD without SOR displayed lower, possibly blunted, cortisol responses . While blunted cortisol is frequently observed in children with ADHD (Ma et al, 2011;Pinto et al, 2016), it is also observed in individuals with early adversity (Bunea et al, 2017;Kuras et al, 2017), illustrating the complex relationship between sensory modulation and stress arousal patterns. Emerging models of HPA reactivity also support various trajectories of ''typical'' daily cortisol patterns (Van Ryzin et al, 2009).…”