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Growing evidence continues to expand the biological landscape of neurodevelopmental and psychiatric disorders beyond traditional neural mechanisms. A recent pediatric microbiome study from Comenius University (Slovakia) adds an important layer to this evolving perspective. The study demonstrates that children with autism spectrum disorder (ASD), attention deficit/hyperactivity disorder (ADHD), and anorexia nervosa (AN) exhibit overlapping gut microbial signatures, despite their distinct clinical phenotypes.
These findings support a multidimensional model in which the gut microbiome influences neuroimmune maturation, metabolic regulation, and behavior, reinforcing the gut–brain axis as a critical component of child and adolescent mental health.
This cross-sectional analysis included 117 children, distributed across ASD (n=30), ADHD (n=14), AN (n=21), and age- and sex-matched neurotypical controls. Stool samples were analyzed using 16S rRNA sequencing, enabling high-resolution taxonomic profiling. While exploratory, the study is among the first to compare microbiome signatures across these three disorders within a unified methodological framework, allowing meaningful cross-condition inferences.
Children with ASD, ADHD, and AN displayed a consistently elevated Bacteroidetes /Firmicutes (B/F) ratio relative to controls. This phylum-level imbalance is frequently associated with:
• Altered energy harvest and glucose metabolism.
• Enhanced mucosal and systemic inflammation.
• Perturbed satiety and appetite regulation.
The convergence of B/F ratio shifts across these conditions suggests a shared metabolic and immunological perturbation.
Both ASD and ADHD groups demonstrated lower α-diversity, indicating decreased microbial richness and ecological stability. Reduced diversity is known to correlate with:
• Increased intestinal permeability,
• Chronic low-grade immune activation,
• Diminished microbial production of neuroactive metabolites (e.g., SCFAs, GABA precursors).
These alterations may contribute to the gastrointestinal symptoms, immune dysregulation, and behavioral variability frequently observed in these disorders.
Two bacterial groups showed notable elevation:
• Escherichia/Shigella (ASD and ADHD): taxa capable of promoting mucosal inflammation and disrupting epithelial integrity when overrepresented.
• Desulfovibrio (ADHD and AN): sulfate-reducing organisms that produce hydrogen sulfide, a compound that can impair epithelial function and increase oxidative stress when abundant.
These signatures indicate a shift toward a pro-inflammatory gut environment, potentially influencing both immune and neural pathways.
Reduced abundance of key commensals was observed, particularly in ADHD and AN:
• Faecalibacteriuma dominant butyrate producer essential for anti-inflammatory signaling, gut barrier maintenance, and epithelial repair,
• Bifidobacterium important for early immune programming, gut barrier development, and synthesis of neuroactive compounds.
Loss of these beneficial microbes may impair microbial-host metabolic interactions and disrupt the gut-brain signaling networks that regulate mood, cognition, and appetite.
Diet plays a disproportionately influential role in shaping the pediatric microbiome.
• ASD: sensory sensitivities often narrow dietary variety.
• ADHD: irregular food intake and impulsive eating patterns are common.
• AN: caloric restriction and severe food avoidance are diagnostic features.
Limited dietary diversity is strongly correlated with reduced microbial diversity. In turn, dysbiosis may exacerbate behavioral rigidity, mood dysregulation, and appetite disturbances, perpetuating a bidirectional gut–brain feedback loop.
Microbiome disturbances were accompanied by alterations in appetite-regulating and metabolic hormones:
• Lower peptide YY (PYY) in ADHD and AN,
• Disrupted leptin and ghrelin signaling in AN.
These hormonal changes parallel microbial shifts known to affect satiety, reward pathways, and metabolic homeostasis, underscoring the physiological relevance of gut dysbiosis in these disorders.
Because the gut microbiome can be reshaped through dietary interventions, prebiotics, probiotics, and lifestyle-based strategies, it represents a promising adjunctive target alongside behavioral, nutritional, and pharmacological treatments.
Recurring microbial signatures such as elevated B/F ratios and reduced Faecalibacterium, may serve as biomarkers for early identification, risk stratification, or treatment monitoring.
These findings support a paradigm that views ASD, ADHD, and AN as multisystem disorders, influenced by interactions between neural circuitry, immune function, metabolism, and microbial ecology.
• Modest sample sizes limit statistical power and generalizability,
• Cross-sectional design restricts causal interpretation,
• Limited stratification of dietary variables reduces clarity on diet–microbiome interactions,
• Absence of metabolomic profiling leaves functional microbial outputs unexplored.
Even with these constraints, the consistent cross-condition microbial patterns provide a robust foundation for larger longitudinal and mechanistic research.
The identification of shared gut microbiome disturbances across ASD, ADHD, and anorexia nervosa highlights the gut ecosystem as a potential unifying biological pathway in pediatric neurodevelopmental and psychiatric conditions. Altered phylum-level ratios, reduction in beneficial SCFA-producing taxa, and enrichment of inflammation-associated microorganisms suggest a common microbial milieu that may influence immune maturation, metabolic function, and behavioral regulation.
As research continues to uncover the complexity of the microbiota-brain interface, these insights offer promising avenues for novel diagnostic tools and microbiome-centered interventions, broadening the clinical horizon from a brain-only model to a more integrated, systems-based understanding of childhood neurodevelopmental health.
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