Cibo, stress & neurodivergenze

Stress, early traumatic experiences, chronic life conditions with high adaptive demand, and genetic vulnerability can leave a “biological trace” that manifests as endocrine, immune, and neurochemical alterations. In particular, the repeated activation of the HPA axis can lead to a true “allostatic load,” that is, an overload of adaptation that alters the functioning of stress regulation and emotional response systems. A fundamental component concerns the neurobiology of interoception. The brain structures responsible for the perception of bodily sensations—particularly the anterior insula and the anterior cingulate cortex—play a key role in integrating visceral signals, emotions, and behavior. Alterations in these areas have been observed both in eating disorders and in neurodivergence, contributing to difficulties in recognizing hunger and satiety, altered body awareness, hyperattention to internal signals or, conversely, hypo–interoceptive sensitivity. This explains why some neurodivergent people may not clearly perceive hunger signals, forget to eat, or, on the contrary, seek food as a means of self-regulation. The endocrine system represents another central node. Cortisol, thyroid hormones, insulin, leptin, ghrelin, and sex hormones interact with the brain’s reward circuits, influencing appetite, motivation, and eating behavior. States of chronic stress and inflammation profoundly alter these balances, contributing to oscillations between hyperphagia, restriction, and eating dysregulation. In neurodivergent women, moreover, hormonal fluctuations can amplify emotional instability, cravings, and attentional symptoms, impacting both eating behavior and emotional regulation. In ASD and ADHD, structural and functional differences are also observed in the brain networks of reward, motivation, and inhibitory control. In the case of ADHD, dopaminergic and noradrenergic dysfunction is associated with difficulties in modulating impulsivity, delayed gratification, and reward prediction error (a key concept in neuroscience and reinforcement learning, describing the difference between expected and actually received reward), elements directly involved in food management and the tendency toward compulsive or disorganized eating behaviors. In autism, on the other hand, cognitive rigidity, hyper– or hypo–sensory sensitivity, and selective preferences interact with biological and gastrointestinal factors, structuring eating patterns that are often repetitive, avoidant, or highly selective. A further level of complexity is represented by the epigenetic dimension. Environmental experiences, nutrition, early stress, and affective relationships can modulate the gene expression of stress systems, the immune system, and neurotransmitter pathways. This suggests that eating disorders and neurodivergence are not simply “psychological” or “biological,” but the result of a continuous interaction between genetic predisposition and environment, according to a fully PNEI logic. Overall, therefore, the PNEI model allows us to overcome the reductionist mind/body view and to understand how the relationship with food, emotional functioning, and neurodivergent characteristics derive from the dynamic integration of neurobiological, endocrine, immune, and psychological processes in constant dialogue with each other.