Food additives and ADHD-like symptoms Numerous studies have highlighted a potential link between the intake of food additives, particularly artificial colorants, preservatives, and sweeteners, and the worsening of behavioral symptoms in individuals with ADHD and autism spectrum disorder (ASD). Among the most frequently implicated artificial colorants are tartrazine (E102), allura red (E129), and brilliant blue (E133), associated with manifestations of hyperactivity, impulsivity, irritability, and attention disorders, especially in childhood. Their action may be mediated by direct effects on the central nervous system, as well as by indirect mechanisms related to gut dysbiosis, increased permeability of the blood-brain barrier, or immunological sensitivity. Preservatives, such as benzoates (e.g., sodium benzoate, E211), commonly used to prolong the shelf life of industrial products, have been associated with increased oxidative stress and mitochondrial dysfunction. These effects can interfere with brain energy metabolism, contributing to cognitive and behavioral dysfunctions in neurodivergent individuals. Artificial sweeteners, such as aspartame (E951) and sucralose (E955), in addition to altering taste perception and satiety, can negatively influence the composition of the gut microbiota, altering the bidirectional communication along the gut–brain axis. Such alterations can worsen emotional dysregulation, stress reactivity, and behavioral disorders. In this context, the so-called “Feingold diet”, which involves eliminating artificial colorants, benzoates, and salicylates, has been successfully adopted in some children with ADHD, leading to a significant reduction in symptoms in selected subjects. Although scientific evidence is not unanimous and further randomized controlled studies are needed, the selective elimination of additives in hypersensitive individuals represents a low-risk and potentially effective therapeutic option, if integrated into a personalized nutritional approach for autism spectrum, ADHD, and AuDHD. Monosodium glutamate (MSG, E621), commonly used as a flavor enhancer in industrial foods, ready meals, and Asian cuisine, is a synthetic form of glutamate, an endogenous excitatory neurotransmitter crucial for neuronal communication. Although it is recognized as safe by most regulatory authorities, in neurodivergent individuals — in particular ADHD, autism, or AuDHD — excessive ingestion of MSG may contribute to excitotoxicity phenomena. Excess glutamate can hyperactivate NMDA and AMPA receptors, resulting in neuronal overstimulation which, in the long term, is associated with synaptic dysregulation, neuroinflammation, and potential neuronal damage. In genetically or epigenetically predisposed individuals, or those with an altered blood-brain barrier, such excitatory overload may manifest as anxiety, insomnia, hyperactivity, difficulty concentrating, irritability, and sensory hypersensitivity. The effect of MSG may also be mediated by compromised intestinal function (leaky gut), which facilitates its systemic passage, and by gut dysbiosis that amplifies vulnerability to excitotoxins. Some preclinical studies have suggested that excess glutamate may interfere with GABA homeostasis, the main inhibitory neurotransmitter, contributing to an imbalance between excitation and inhibition, characteristic of numerous neuropsychiatric disorders. A low-glutamate diet has shown promising results in small trials on neuropsychiatric disorders, showing a reduction in irritability, aggressive behavior, and sleep disorders. In AuDHD subjects with neuronal hyperexcitability or food hypersensitivity, the exclusion of monosodium glutamate and foods rich in free glutamate (stock cubes, flavor enhancers, yeast extracts, hydrolyzed vegetable proteins, soy sauce, industrial snacks) represents a reasonable nutritional intervention, in the context of a personalized and functional approach. Monosodium glutamate and excitotoxicity


