From ARFID to Binge Eating: A Review of the Sensory, Behavioral, and Gut–Brain Axis Mechanisms Driving Co-Occurring Eating Disorders in Children and Adolescents with Autism Spectrum Disorder

Autism spectrum disorder (ASD) is classified as a neurodevelopmental condition, marked by enduring challenges in communication, cognitive functioning, and social interaction, as well as by restricted and/or repetitive patterns of behavior, interests, or activities that typically manifest in early childhood [1]. Although various psychological assessment tools exist, and emerging research continues to explore objective neurophysiological biomarkers, the diagnosis ultimately relies on clinical evaluation [2,3].

In the DSM-5 diagnostic classification, as in ICD-11, two core symptom domains for ASD have been distinguished: deficits in social communication and social interaction, and restricted, repetitive patterns of behavior, interests, or activities (stereotypies and rituals) [1,4]. Although symptoms may manifest in early childhood, modern diagnostic classifications have abandoned a specific age criterion, as symptoms may go unnoticed until social demands exceed the child's capabilities, or they may be masked by learned coping strategies [5].

The etiology of autism spectrum disorder (ASD) remains incompletely elucidated. Current evidence strongly supports a substantial genetic contribution to its pathogenesis [6]. However, environmental influences also play an important role. ASD is viewed as a result of a multifactorial interaction between genetic predisposition and environmental influences, wherein genetic susceptibility constitutes a foundational determinant that may be modulated through epigenetic mechanisms. Additionally, sociocultural trends in Western and Central European populations, such as substance use risks or the pressure for "clean" eating, may interact with autistic cognitive rigidity to modify behavioral phenotypes [7,8,9].

The prevalence of ASD in the general population has exceeded 1%, and in the developmental age group, it is estimated to be around 1 in 54 children [10]. In a 2020 study conducted by the Centers for Disease Control and Prevention in the USA among 8-year-old children, the prevalence of ASD was estimated at an average of 27.6 per 1000, which corresponds to one in 36 children, with the prevalence among boys being 3.8 times higher than among girls [11]. The observed increase in prevalence may be attributed to improved diagnostic methods, including the exploration of objective neurofunctional assessments, as well as greater awareness among healthcare professionals, educators, and the general public [12]. High-functioning individuals with ASD often use strategies to mask their social deficits, known as "social camouflaging". Although camouflaging occurs in both sexes, it is presumed to be more frequently and effectively used by women [7,13].

Autism spectrum disorder encompasses a diverse group in terms of intellectual abilities, social functioning, and eating habits. Patients in this group often experience co-occurring neurological, psychiatric, and somatic anomalies. Additionally, specific eating habits, such as food neophobia, defined as a reluctance to try new foods that negatively impacts dietary quality and health status, significantly contribute to these risks. Coupled with challenges in self-care, self-destructive behaviors, and the side effects of pharmacotherapy, these factors predispose individuals with ASD to chronic diseases and body weight abnormalities [14].

Clinical and epidemiological data indicate a significantly elevated risk of co-occurrence between Autism Spectrum Disorder and Eating Disorders (EDs) [15]. Although eating disorders constitute a broad diagnostic category, defined as persistent disturbances of eating or eating-related behaviors that result in significant impairment of physical health or psychosocial functioning, a distinct overrepresentation of restrictive subtypes is observed within the ASD population [15,16]. It is estimated that atypical eating behaviors may affect over 70% of children with ASD, compared to less than 5% in the neurotypical population [16]. Concurrently, difficulties in emotion regulation and sensory dysfunctions may predispose individuals to Binge-Eating Disorder (BED). This mechanism may be associated with the use of food as a strategy for affect regulation ("emotional eating") or the pursuit of sensory stimulation, distinguishing the etiology of these disorders in ASD from classical models driven by body image concerns [15].

In recent years, there has been growing interest in the gut–brain axis as a multidirectional communication channel integrating the nervous, endocrine, and immune systems [17]. Currently, this concept is expanded to the "microbiome–gut–mucosa–immune–brain axis", highlighting the pivotal role of Neuro-Immuno-Gastroenterology in the pathogenesis of neurodevelopmental disorders [18]. In ASD, a selective diet frequently leads to dysbiosis, which may compromise the integrity of the intestinal barrier ("leaky gut") and facilitate the translocation of bacterial metabolites, such as lipopolysaccharides, into the bloodstream [18]. The resulting systemic inflammatory state influences neurotransmission and emotional regulation, creating a "vicious cycle" mechanism that secondarily exacerbates behavioral symptoms [18].

The extant literature, including recently published original studies, has provided crucial data on specific aspects of nutritional problems in ASD [19,20]. Despite the value of this information, the literature still lacks a synthesis that integrates these distinct domains, including sensory, behavioral, and metabolic factors, with the role of the gut microbiota and the gut–brain axis. Crucially, no review has yet elucidated how these complex mechanisms contribute to the full spectrum of co-occurring, formally diagnosed eating disorders—ranging from restrictive disorders such as ARFID and Anorexia Nervosa to emotional and binge-eating patterns leading to obesity.

This review aims to provide a critical synthesis of these three domains, proposing the thesis that sensory hypersensitivity and behavioral rigidity in ASD lead to restrictive eating patterns, which in turn induce gut dysbiosis. This dysbiosis, through neuroinflammation and dysregulation of the gut–brain axis, secondarily affects emotional regulation and cognitive functions, predisposing individuals to the development of the full spectrum of eating disorders, ranging from ARFID to binge-eating disorders.

Given the heterogeneous and interdisciplinary nature of the research question, which encompasses neurodevelopmental psychiatry, sensory processing, gastroenterology, and microbiology, a narrative review methodology was adopted. This approach allows for the broad synthesis of diverse evidence streams required to construct an integrated pathogenetic model, a task often constrained by the rigid inclusion criteria of systematic reviews. The review aims to critically evaluate current theoretical frameworks, identify mechanistic overlaps, and highlight gaps in the existing literature to inform future clinical and research directions. To ensure rigor and minimize bias, a structured search strategy and defined eligibility criteria were implemented as detailed below.

Feeding difficulties in ASD arise from a complex interplay between sensory processing abnormalities and cognitive-behavioral rigidity. Research indicates that sensory hypersensitivity, particularly within the oral domain (oral defensiveness), is a primary driver of food refusal [22,23]. This hyper-reactivity to texture, consistency, temperature, and color often co-occurs with a profound need for predictability and sameness—a core behavioral feature of ASD [24,25]. Consequently, the introduction of novel foods (neophobia) triggers anxiety and resistance, leading to a highly restrictive diet often limited to specific "safe" foods rich in carbohydrates and processed fats, while lacking essential nutrients found in fruits and vegetables [22]. These sensory-behavioral patterns also extend to oral hygiene and health. Atypical oral habits (e.g., bruxism, pouching) and self-injurious behaviors in the head and neck region, observed in up to 75% of cases with severe ASD, further complicate feeding by causing dental pathology and discomfort [14]. Thus, sensory aversion and behavioral inflexibility act synergistically to establish a restrictive eating phenotype, which serves as the behavioral starting point for the physiological dysregulation discussed below. To provide a comprehensive overview of these complex interactions, the key determinants of atypical eating patterns in ASD are summarized in Table 1.

Selective dietary habits in ASD induce significant alterations in the gut microbiome composition, leading to a state of dysbiosis characterized by a reduction in beneficial fermentative bacteria (e.g., Bifidobacterium) and an overgrowth of potentially pathogenic species (e.g., Clostridium species) [18,26]. This dysbiosis state may compromise the intestinal epithelial barrier ("leaky gut"), facilitating the translocation of bacterial metabolites such as lipopolysaccharides (LPS) into the systemic circulation. This process is hypothesized to trigger a chronic, low-grade inflammatory response, characterized by elevated levels of pro-inflammatory cytokines (e.g., TNF-α, IL-6), which can cross the blood–brain barrier and modulate neurodevelopmental and behavioral trajectories via neuroimmune and neuroendocrine pathways [18,27].

While the "microbiome–gut–mucosal–immune–brain" axis offers a compelling mechanistic model, it is essential to interpret current findings with caution. A substantial portion of the existing literature relies on cross-sectional studies with relatively small sample sizes and high heterogeneity in methodology (e.g., differences in DNA sequencing techniques, lack of dietary control). Furthermore, most human studies demonstrate correlations rather than causation. It remains a subject of debate whether gut dysbiosis is a primary driver of ASD symptoms or a secondary consequence of the restricted "autistic diet" [20,28]. Nevertheless, bidirectional signaling is evident, where diet-induced dysbiosis exacerbates behavioral symptoms, creating a feedback loop that further entrenches restrictive eating patterns.

Specific microbial alterations driving this feedback loop include an increased abundance of Enterobacteriaceae, Salmonella, Escherichia/Shigella and Clostridium XIVa [29]. These shifts are frequently correlated with the severity of gastrointestinal symptoms, such as abdominal pain, constipation, and diarrhea, commonly reported in this population [26].

Beyond immune activation, the microbiome exerts influence via neurochemical pathways. A critical mechanism involves the stimulation of serotonin synthesis through tryptophan hydroxylation in intestinal cells. Given that polymorphisms in the serotonin transporter gene are established risk factors for ASD, dysbiosis-induced irregularities in serotonin production may directly exacerbate behavioral rigidity and mood dysregulation. The functional impact of these microbial shifts is supported by intervention studies, for instance, treatment with antibiotics such as vancomycin has been shown to temporarily alleviate behavioral difficulties. Furthermore, a recent study on fecal microbiota transplantation (FMT) in 18 children with ASD demonstrated increased bacterial diversity and concurrent improvements in both gastrointestinal and behavioral symptoms, persisting for up to eight weeks post-intervention [14].

To address the limitations of current cross-sectional research, ongoing prospective initiatives such as the GEMMA (Genomic, Environmental, Microbiome, and Metabolomic Assessment) project aim to elucidate the longitudinal interactions between host genetics, environmental factors (e.g., birth mode, early feeding), and immune-metabolic trajectories [28]. By identifying specific metagenomic phenotypes, such studies seek to validate biomarkers for early diagnosis and shift the treatment paradigm toward targeted microbiota manipulation [28]. Collectively, the dysregulation of the oral and gut microbiota constitutes a key node in the "microbiome–gut–brain" axis, contributing to the clinical expression of ASD symptoms, as summarized in Figure 1 [14,27,28].

The interplay of sensory sensitivity, behavioral rigidity, and gut–brain axis dysfunction predisposes individuals with ASD to a wide spectrum of specific Feeding and Eating Disorders (FEDs)—Table 2.

The bimodal distribution of eating problems in ASD leads to distinct somatic risks (Figure 2). Restrictive behaviors often result in a monotonous diet, which has been observed from infancy [24,71,72]. The long-term consequences include severe micronutrient deficiencies, particularly of vitamins A, D, C, E, and the B-complex (B6, B12, folic acid), as well as essential minerals like iron, zinc, calcium, and magnesium [73,74,75]. These deficits have systemic implications: insufficient vitamin D and calcium compromise bone density, increasing fracture risk, while deficiencies in immune-modulating nutrients (zinc, vitamins A/C) heighten susceptibility to infections [73]. In extreme cases, critical conditions such as scurvy or vitamin A deficiency-related visual impairments have been reported due to severe food selectivity [74,76]. Furthermore, malnutrition can lead to oral health issues, including gingivitis and delayed wound healing [30,77,78].

Conversely, the preference for energy-dense, low-fiber foods, combined with sedentary habits and pharmacotherapy, contributes to a high prevalence of overweight and obesity, estimated at over 30% in some ASD cohorts [71,79,80]. This metabolic phenotype increases the long-term risk of cardiovascular disease and diabetes [81,82]. Additionally, chronic gastrointestinal dysfunction, manifesting as constipation or diarrhea, affects up to 70% of patients. While often linked to diet and dysbiosis, these GI symptoms can exacerbate behavioral irritability and sleep disturbances, creating a vicious cycle of somatic discomfort and behavioral dysregulation [73,75,83]. Importantly, deficiencies in omega-3 fatty acids and iron may further impair cognitive functions, such as attention and memory—domains that are fundamentally disrupted in neurodevelopmental disorders—directly impacting the child's developmental trajectory [73,84].

The complex co-occurrence of Eating Disorders and Autism Spectrum Disorder is driven by a pathogenic feedback loop involving sensory hypersensitivity, behavioral rigidity, and dysfunction of the gut–brain axis.

This review demonstrates that feeding difficulties in ASD should be understood not merely as behavioral comorbidities but as the result of intricate neurobiological interactions. From a clinical perspective, this necessitates a shift in diagnostic protocols to carefully differentiate between classic eating disorders driven by body image distortion and phenotypes specific to ASD. In cases of severe restriction, such as ARFID or Anorexia Nervosa, routine screening for sensory processing disorders and gastrointestinal dysfunction is imperative, as these are often the primary drivers of food refusal [22,23,75]. Moreover, standard therapeutic interventions, such as rapid refeeding, may be ineffective or traumatic for patients with sensory defensiveness. Therefore, effective management requires a multidisciplinary strategy integrating sensory integration therapy, nutritional rehabilitation respectful of "safe foods", and behavioral interventions targeting cognitive rigidity [73,78].

The recognition of gut dysbiosis as a mediator of behavioral symptoms also highlights new therapeutic targets. While microbiological interventions like probiotics or fecal microbiota transplantation offer promise, their routine clinical application awaits validation through longitudinal studies, such as the GEMMA project [18,28]. Ultimately, moving beyond purely behavioral management toward a holistic biopsychosocial model is essential to improve long-term health outcomes and quality of life for this population.

Finally, given the complex neurobiological underpinnings of these disorders, future clinical protocols might benefit from integrating nutritional rehabilitation with neurophysiological monitoring [5]. Tools such as quantitative electroencephalography (QEEG) and event-related potentials (ERPs) could serve as objective biomarkers to assess functional brain changes resulting from dietary interventions, while neurotherapeutic modalities like Neurofeedback may support the emotional regulation necessary to break the cycle of binge eating [85,86,87]. However, further research is needed to validate these integrative approaches in the ASD population.