Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by challenges in social communication, restricted interests, and repetitive behaviors. It is also associated with a high prevalence of eating disorders, gastrointestinal (GI) symptoms, and alterations in gut microbiota composition. One of the most pressing concerns is food selectivity. Various eating disorders, such as food neophobia, avoidant/restrictive food intake disorder (ARFID), specific dietary patterns, and poor-quality diets, are commonly observed in this population, often leading to nutrient deficiencies. Additionally, gastrointestinal problems in children with ASD are linked to imbalances in gut microbiota and immune system dysregulation. The aim of this narrative review is to identify previous associations between the gut–brain axis and gastrointestinal problems in ASD. We discuss the impact of the “microbiome–gut–brain axis”, a bidirectional connection between gut microbiota and brain function, on the development and symptoms of ASD. In gastrointestinal problems associated with ASD, a ‘vicious cycle’ may play a significant role: ASD symptoms contribute to the prevalence of ARFID, which in turn leads to microbiota degradation, ultimately worsening ASD symptoms. Current data suggest a link between gastrointestinal problems in ASD and the microbiota, but the amount of evidence is limited. Further research is needed, targeting the correlation of a patient’s microbiota status, dietary habits, and disease course.

Background: Transgenerational trauma (TT)/Intergenerational trauma (IT) is the transmission of the effects of traumatic experiences of parents to their children, who have not themselves experienced traumatic events. This transmission occurs through neurobiological and metabolic changes and the environment in which they were raised. Methods: A systematic review was conducted in accordance with the PRISMA 2020 guidelines. PubMed and Google Scholar databases were searched from 2005 to 2025. Studies focusing on adult offspring, exposure to ancestral trauma, biological markers (DNA methylation, cortisol), and psychological outcomes were included. Results: The main study results are as follows: identification of sex-specific DNA methylation patterns in the NR3C1 gene and accelerated biological aging (GrimAge) in offspring; role of parental reflective functioning (PRF) and impaired mentalization as major psychological channels of trauma transmission; and evidence confirming the impact on three generations, manifested by treatment-resistant depressive disorders, anxiety, and neuroendocrine dysregulation (low cortisol levels). Conclusions: This article highlights the intergenerational impact of trauma and highlights its epigenetic significance. The primary goal was to explore universal epigenetic mechanisms. Early understanding of ancestral history is crucial for personalized psychiatric care.