OBJECTIVES: The objective is to evaluate possible mechanisms explaining the link between polyunsaturated fatty acid (PUFA) deficiencies and ADHD, based on findings from animal research. METHOD: The authors consulted peer-reviewed publications from the last 10 years (Medline and resulting reference lists). RESULTS: PUFA deficiency in rodents results in behavioral changes (increased motor activity and decreased learning abilities) and dysregulations of monoamine neurotransmission. Behavioral improvement following a PUFA recovery diet is observed, but recovery of brain monoamine dysregulation is not fully demonstrated. Anti-inflammatory processes could damage neural membranes, but the direct link with ADHD model is not documented. Synaptic growth and neurogenesis impairment could account for working memory dysregulations, but research is at its early start. CONCLUSION: Induced PUFA deficiencies in animals show several noteworthy similarities with brain dysregulations seen in ADHD human children. However, the mechanisms of partial recovery after PUFA supplementation are not fully understood, and rigorous clinical trials have yet to show PUFA supplementation is an effective complementary treatment for ADHD.
OBJECTIVES: The objective is to evaluate possible mechanisms explaining the link between polyunsaturated fatty acid (PUFA) deficiencies and ADHD, based on findings from animal research. METHOD: The authors consulted peer-reviewed publications from the last 10 years (Medline and resulting reference lists). RESULTS:PUFA deficiency in rodents results in behavioral changes (increased motor activity and decreased learning abilities) and dysregulations of monoamine neurotransmission. Behavioral improvement following a PUFA recovery diet is observed, but recovery of brain monoamine dysregulation is not fully demonstrated. Anti-inflammatory processes could damage neural membranes, but the direct link with ADHD model is not documented. Synaptic growth and neurogenesis impairment could account for working memory dysregulations, but research is at its early start. CONCLUSION: Induced PUFA deficiencies in animals show several noteworthy similarities with brain dysregulations seen in ADHDhumanchildren. However, the mechanisms of partial recovery after PUFA supplementation are not fully understood, and rigorous clinical trials have yet to show PUFA supplementation is an effective complementary treatment for ADHD.