Clinical nutrition for neurodevelopmental disorders

Overview The childhood disorders known collectively as neurodevelopmental disorders are associated with various dysfunctions in cognition, learning, communication and behaviour, and include: attention deficit hyperactivity disorder (ADHD), autism spectrum disorder (ASD), dyspraxia and dyslexia. Evidence suggests that neurodevelopmental disorders are the result of genetic and environmental factors which, when present together in early life, result in neurological and mental/cognitive dysfunction. Breakdowns in several neurotransmitter pathways, disturbances in neurotransmission and dysfunction of the hypothalamus-pituitary-adrenal (HPA) axis activity are all associated with the development and progression of neurodevelopmental disorders.[1, 2] Deficiencies in key micronutrients including zinc and magnesium, important for neurotransmission, coupled with deficiencies or imbalances in the long-chain omega-3 fatty acids have also been implicated in their predisposition and development. [3, 4] The use of omega-3 supplementation is widely recognised as an effective treatment, especially for ADHD – with the ratio of EPA to DHA within dietary supplements directly linked to the efficacy of the treatment regime. [5] The use of pure EPA has been shown to be a highly effective therapy for ADHD, [6] in particular for those individuals resistant to commonly used pharmaceuticals, [7] with greater improvements observed in combination with micronutrients – specifically zinc, magnesium and vitamin B6. [8-10] Oxidative stress and dysregulation of cellular redox activity has also been observed in neurodevelopmental disorders, particularly autism, with ubiquinol proving a useful tool in providing antioxidant and redox support, as well as reducing symptom severity.[37] Omega-3 and neurodevelopmental disorders Clinical and biochemical evidence suggests that deficiencies of the long-chain polyunsaturated fatty acids (PUFA) are related to neurodevelopmental disorders, as lower omega-3 blood levels and a higher omega-6 to omega-3 ratio (specifically AA to EPA) are consistently observed in both children and adolescents with the condition when compared with healthy controls. [9-11] The delta-6-desaturase (FADS2) enzyme presents a major rate-limiting step in the biosynthesis of polyunsaturated fatty acids (PUFA) and variants in the genes coding FADS2 have been found to correlate with neurodevelopmental disorders, in particular in ADHD. This strongly suggests a pathogenic role of endogenous variations in PUFA metabolism in ADHD and new research suggests that the ratio between omega-3 long-chain PUFA levels and desaturase enzyme activity may provide valuable insights into the biological factors that contribute to ADHD. [12]