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Early psychosocial adversity and cortisol levels in children with attention-deficit/hyperactivity disorder
Johan Isaksson1, Kent W Nilsson, Frank Lindblad
1Department of Neuroscience, Child and Adolescent Psychiatry Unit, Uppsala University, 751 85, Uppsala, Sweden. johan.isaksson@neuro.uu.se
Insights
Children with ADHD showed higher rates of early adversity but not lower morning cortisol levels, challenging the hypothesis that psychosocial adversity programs the HPA-axis to cause low cortisol in ADHD.
Area of Science:
- Neuroendocrinology
- Developmental Psychology
- Child Psychiatry
Background:
- Children with ADHD often exhibit altered hypothalamus-pituitary-adrenal (HPA) axis regulation, characterized by lower diurnal cortisol levels.
- Psychosocial adversity in fetal development and childhood is linked to both ADHD and HPA-axis dysfunction.
- Early life adversity may program the HPA-axis, potentially explaining low cortisol levels observed in ADHD.
Purpose of the Study:
- To retrospectively investigate fetal and early childhood psychosocial adversity exposures in children with ADHD.
- To examine the relationship between these exposures and cortisol levels in children with ADHD.
- To test the hypothesis that early adversity influences the HPA-axis, leading to lower cortisol in ADHD.
Main Methods:
- Saliva samples were collected from children aged 6-17 with confirmed ADHD (n=197) and controls (n=221) for cortisol analysis.
- Parental rating scales assessed ADHD subtypes and degree of psychosocial adversity exposure.
- Radioimmunoassay was used for cortisol level determination.
Main Results:
- Children with ADHD reported significantly more fetal and childhood adversity than controls.
- Low morning cortisol levels remained associated with ADHD symptoms even after adjusting for adversity and other factors.
- No direct relationship was found between fetal/childhood adversity and cortisol levels, except a positive association between childhood adversity and morning cortisol increase in ADHD.
Conclusions:
- The study did not support the hypothesis that early adversity leads to lower cortisol levels in children with ADHD.
- While ADHD is associated with increased early adversity, this adversity does not appear to be the primary driver of altered HPA-axis cortisol regulation in this cohort.
- Further research is needed to elucidate the complex interplay between ADHD, HPA-axis function, and environmental factors.
Abstract:
Previous studies suggest a different regulation of the hypothalamus-pituitary-adrenal axis (HPA-axis) with lower diurnal cortisol levels, especially in the morning, in children with attention-deficit/hyperactivity disorder (ADHD) compared with controls. Since exposure to foetal and childhood psychosocial adversity has been associated with both ADHD and HPA-axis functioning, such exposures may explain these low cortisol levels in ADHD via early programming of the HPA-axis. Thus, our main aim was to retrospectively study foetal and early childhood exposures to psychosocial adversity in children with ADHD and to relate these exposures to cortisol levels. Saliva samples were collected during a regular weekday in children, 6-17 years old, with clinically confirmed ADHD (n = 197) and non-affected comparisons (n = 221) for radioimmunoassay analysis of cortisol. Parental rating scales were used for categorising subtypes of ADHD and degree of exposure to adversity. Children with ADHD had more reports of at least one rated foetal adversity (p = 0.041) and childhood adversity (p < 0.001) than comparisons. The association between low morning cortisol levels and ADHD-symptoms remained when analyses were adjusted for adversities, age, sex, sampling time and symptoms of oppositional defiant disorder. No relation was found between exposures to foetal/childhood adversity and cortisol levels except for a positive relation between childhood adversity and cortisol morning increase in children with ADHD. The hypothesis that early adversity may influence the HPA-axis, leading to lower cortisol levels in children with ADHD, was not supported by our findings.
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