The perspective article reviews evidence that attention-deficit/hyperactivity disorder (ADHD) frequently co-occurs with circadian rhythm disruptions, particularly an evening chronotype and phase-delayed biological markers. It reports that insomnia and sleep disturbances affect up to 80% of adults with ADHD and up to 82% of children, while delayed sleep-wake timing occurs in up to 78% of patients. Dim-light melatonin onset (DLMO) is delayed by approximately 45 minutes in children and 90 minutes in adults compared to neurotypical controls, and these findings persist after controlling for comorbid anxiety and depression.
Beyond sleep timing, the article describes multiple biological indicators of circadian dysfunction in ADHD. Melatonin rhythms show not only delayed onset but also altered patterns, with some studies noting abnormally high daytime melatonin levels in children that improve with stimulant medication. Cortisol rhythms are described as blunted and delayed, and peripheral clock genes such as BMAL1 and PER2 exhibit attenuated rhythms, with symptom severity tracking with reduced PER2 rhythmicity. The authors also note reduced pineal gland volume, which correlates with eveningness preferences. Intervention studies demonstrate that melatonin supplementation can advance DLMO by 88 minutes in adults with ADHD while reducing ADHD symptoms by 14%, and bright light therapy—especially when combined with melatonin—can produce phase advances of up to two hours, improving both sleep and core ADHD symptoms.
This image complements the article's discussion of biological markers such as delayed melatonin onset and altered cortisol rhythms in ADHD.
Despite these associations, the perspective highlights important limitations. The direction of causality remains unclear; ADHD-related behaviors could alter light exposure and subsequently affect circadian rhythms, creating a bidirectional relationship. The authors caution that circadian dysfunction is not universal among ADHD patients and that evidence on whether circadian interventions lead to remission of core ADHD symptoms is still lacking. They propose a pragmatic, behavioral-first clinical pathway involving routine screening for sleep/circadian disturbances, phenotypic characterization through chronotype assessment and DLMO measurement when feasible, and implementation of fixed wake times, morning bright light exposure, evening light restriction with screen hygiene, and selective low-dose melatonin for confirmed or probable DLMO delays, while calling for future stratified trials to quantify effects on core outcomes and define responder phenotypes.