ADHD and Differences in Brain Function as Measured by EEG

Cause or Effect?

Ahn, Kwangmi
Jean, Jenny
Norman, Luke J.
Shaw, Philip

¹National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA
²National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA
³Institute of Psychiatry, Psychology and Neuroscience, King’s College London, UK

Philip Shaw, Kings Maudsley Partnership for Children and Young People, Pears Maudsley Centre, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, Denmark Hill, London SE5 8AZ, UK. Email: [email protected]

* These authors contributed equally as co-first authors.

** These authors contributed equally as co-senior authors.

Journal of Attention Disorders 29(12):p 1107-1117, October 2025. | DOI: 10.1177/10870547251349253

Objectives:

Although extensive research has documented associations between Attention-Deficit/Hyperactivity Disorder (ADHD) and differences in resting-state electroencephalography (EEG) oscillatory activity, the causal nature of these relationships remains uncertain. This study aimed to determine whether there is a causal relationship between resting-state EEG activity and ADHD using genetic methods.

Methods:

We performed a bidirectional two-sample Mendelian Randomization analysis using summary-level genome-wide association study data. EEG data were obtained from the ENIGMA-EEG consortium, including resting-state EEG spectral power measurements from 7,983 subjects. ADHD genome-wide association study summary statistics were derived from 225,534 individuals, alongside data for six additional psychiatric disorders from the Psychiatric Genomics Consortium. Mendelian Randomization analysis was used to test for causal relationships in both directions between EEG activity and ADHD.

Results:

We identified a significant unidirectional causal relationship, with genetic variants influencing resting alpha-band EEG activity conferring risk for ADHD (odds ratio = 0.89, 95% confidence interval [0.82, 0.96], p = 1.52 × 10-³). No evidence was found for reverse causation from ADHD liability to alpha EEG power band activity (odds ratio = 1.07, 95% confidence interval [0.88, 1.30], p = .52).

Conclusions:

Our findings provide genetic evidence that reduced resting-state alpha power is not merely correlated with ADHD but may causally predispose individuals to developing the disorder. This supports previous observational studies linking lower alpha activity to ADHD and establishes a causal pathway from altered EEG activity to ADHD risk, with important implications for understanding ADHD pathophysiology and potential biomarker development.