A systematic review of circadian function, chronotype and chronotherapy in attention deficit hyperactivity disorder.
Study Goal
The researchers aimed to analyze evidence for circadian rhythm changes in ADHD and assess therapeutic approaches involving the circadian clock, including melatonin treatment.
Results Summary
The study found consistent evidence linking ADHD to eveningness/later chronotype, phase delay in circadian markers, and delayed sleep onset. Melatonin treatment showed efficacy in addressing ADHD-related sleep problems, but other chronotherapeutic approaches were understudied.
Population
ADHD patients (children and adults), totaling 4462 participants across 62 studies.
Effective Dosage
Not specified
Duration
Not specified
Interactions
None mentioned
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
- | increase | more eveningness/later chronotype | ADHD patients | - | associated with | #1 |
- | increase | phase delay of circadian phase markers | ADHD patients | - | associated with | #2 |
melatonin treatment | decrease | ADHD-related sleep problems | ADHD patients | - | may be efficacious in addressing | #3 |
- | neutral | polymorphisms in circadian clock genes and ADHD symptoms | - | - | linkages between | #4 |
Reports of sleep disturbances in attention deficit hyperactivity disorder (ADHD) are common in both children and adults; however, the aetiology of such disturbances is poorly understood. One potentially important mechanism which may be implicated in disrupted sleep in ADHD is the circadian clock, a known key regulator of the sleep/wake cycle. In this systematic review, we analyse the evidence for circadian rhythm changes associated with ADHD, as well as assessing evidence for therapeutic approaches involving the circadian clock in ADHD. We identify 62 relevant studies involving a total of 4462 ADHD patients. We find consistent evidence indicating that ADHD is associated with more eveningness/later chronotype and with phase delay of circadian phase markers such as dim light melatonin onset and delayed sleep onset. We find that there is evidence that melatonin treatment may be efficacious in addressing ADHD-related sleep problems, although there are few studies to date addressing other chronotherapeutic approaches in ADHD. There are only a small number of genetic association studies which report linkages between polymorphisms in circadian clock genes and ADHD symptoms. In conclusion, we find that there is consistent evidence for circadian rhythm disruption in ADHD and that such disruption may present a therapeutic target that future ADHD research might concentrate explicitly on.