ADHD is a complex neurodevelopmental disorder with multiple contributing factors. Decades of research demonstrate a strong genetic basis for ADHD, with family, twin, and adoption studies showing linked to inherited DNA risk variants. Genome-wide analyses reveal ADHD shares genetic overlaps with autism spectrum disorder and intellectual disability, while environmental factors account for approximately 22% of variance in symptoms.
may exacerbate symptoms in some cases, but evidence does not support diet as a primary cause. While prenatal exposures to alcohol, nicotine, or pesticides show statistical associations with ADHD risk, these factors interact with genetic predispositions rather than acting independently. Studies of sugar intake and food additives find limited causal relationships, with hyperactivity patterns more likely reflecting ADHD-related impulsivity in food choices rather than dietary causation.
Micronutrient supplementation (B6, zinc, magnesium) and omega-3 fatty acids show modest symptom improvements in trials, but these interventions address secondary metabolic factors rather than root causes. The ketogenic diet’s proposed benefits for brain metabolism remain theoretical, with no robust clinical evidence demonstrating long-term efficacy for ADHD management compared to FDA-approved therapies.
Current research emphasizes , where genetic risks interact with environmental exposures during critical developmental windows. While nutritional strategies may complement treatment, they cannot replace genetic predisposition as the core biological mechanism underlying ADHD. Medications like stimulants remain first-line treatments due to extensive evidence of efficacy, despite valid concerns about side effects and overprescription trends.