Dietary glycemic index modulates the behavioral and biochemical abnormalities associated with autism spectrum disorder

• Published in: Molecular psychiatry 2016-03, Vol.21 (3), p.426-436
• Main Authors: Currais, A, Farrokhi, C, Dargusch, R, Goujon-Svrzic, M, Maher, P
• Format: Article
• Language: English
• Subjects: 13; 14; 38; 64; 64/60; 692/699/476/1373; 82; 82/58; Animals; Autism; Autism Spectrum Disorder - complications; Autism Spectrum Disorder - genetics; Autism Spectrum Disorder - metabolism; Behavioral Sciences; Behavioral Symptoms - etiology; Biological Psychology; C-Reactive Protein - metabolism; Calcium-Binding Proteins - metabolism; Care and treatment; Carrier Proteins - genetics; Carrier Proteins - metabolism; Diet; Disease Models, Animal; Environmental factors; Etiology; Glial Fibrillary Acidic Protein - genetics; Glial Fibrillary Acidic Protein - metabolism; Gliosis - etiology; Glycemic Index; Grooming - physiology; Homer Scaffolding Proteins; Humans; Immune system; Inbreeding; Inflammation; Inositol 1,4,5-Trisphosphate Receptors - genetics; Interpersonal Relations; Maze Learning - classification; Maze Learning - drug effects; Maze Learning - physiology; Medicine; Medicine & Public Health; Mice; Mice, Transgenic; Microfilament Proteins - metabolism; Microtubule-Associated Proteins - metabolism; Mutation - genetics; Nerve Tissue Proteins - metabolism; Neurodevelopmental disorders; Neurogenesis; Neuropeptides - metabolism; Neurosciences; original-article; Oxidoreductases - metabolism; Pervasive developmental disorders; Pharmacotherapy; Phenotypes; Psychiatry; ras GTPase-Activating Proteins - metabolism; Risk factors
• ISSN: 1359-4184; 1476-5578
• DOI: 10.1038/mp.2015.64

Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder of unknown etiology, but very likely resulting from both genetic and environmental factors. There is good evidence for immune system dysregulation in individuals with ASD. However, the contribution of insults such as dietary factors that can also activate the immune system have not been explored in the context of ASD. In this paper, we show that the dietary glycemic index has a significant impact on the ASD phenotype. By using BTBR mice, an inbred strain that displays behavioral traits that reflect the diagnostic symptoms of human ASD, we found that the diet modulates plasma metabolites, neuroinflammation and brain markers of neurogenesis in a manner that is highly reflective of ASD in humans. Overall, the manuscript supports the idea that ASD results from gene–environment interactions and that in the presence of a genetic predisposition to ASD, diet can make a large difference in the expression of the condition.