ADHD (Attention-Deficit/Hyperactivity Disorder)

ADHD is a neurodevelopmental condition characterized by persistent patterns of inattention, hyperactivity-impulsivity, or both, that interfere with functioning across multiple settings. Though historically framed as a childhood disorder, longitudinal research demonstrates that 50-65% of diagnosed children continue to meet criteria in adulthood, and adult-onset presentations are increasingly recognized as valid. Current prevalence estimates place adult ADHD at approximately 2.5-4.4% globally.

Neurobiologically, ADHD involves reduced dopaminergic and noradrenergic signaling in prefrontal-striatal circuits, with substantial genetic heritability (estimates of 70-80%). Imaging studies show reduced gray matter volume in specific regions and altered default mode network dynamics. Recent evidence reframes ADHD partially as a circadian rhythm disorder: 73-78% of adults with ADHD show delayed sleep-wake timing with melatonin onset approximately 90 minutes later than controls (Luu & Fabiano, 2025), and clock gene expression (BMAL1, PER2) is attenuated.

First-line pharmacotherapy (stimulants) produces large effect sizes (SMD approximately 0.7-1.0) and remains the most evidence-supported intervention. Nutritional interventions function as adjuncts, most strongly in the presence of measured deficiency: ferritin optimization (target above 50 ng/mL), vitamin D repletion (4000 IU/day if deficient), and zinc supplementation (SMD −0.62 for ADHD symptoms in meta-analysis) show meaningful effects. Omega-3 EPA-dominant formulas require 4+ months for modest effect. L-tyrosine develops tolerance within weeks and is not recommended. Stimulant-induced insomnia is counterintuitively often reduced by stimulants in adults with ADHD by decreasing pre-sleep rumination (Adamis et al., 2026).