W. R. Hunter
Gut microbiome differences are frequently interpreted as reflecting underlying biological differences between individuals. When outcomes are mediated by behaviour, however, this mapping may be fundamentally non-unique. This limits causal inference in gut-brain research, where microbiome differences in autism and depression are routinely attributed to intrinsic neurobiology despite highly variable, overlapping findings. I built a minimal agent-based model grounded in the known sensory variation across the autism spectrum. Dietary behaviour emerges from latent sensory traits, including sensory drive, predictability preference, and context sensitivity, through reinforcement learning and environmental interaction. This behaviour shapes gut microbiome composition. Behavioural variation organizes endogenously into a continuum of specialist, opportunist, and explorer strategies that maps onto the autism sensory spectrum. The system is fundamentally degenerate. Similar microbiome states arise from distinct behavioural pathways. Similar dietary patterns emerge from divergent latent traits. This many-to-one mapping reflects the structural interaction of behaviour, learning, and environmental variability, not stochasticity alone. Microbiome similarity therefore does not uniquely identify underlying cause. As such, the model provides a theoretical framework for interpreting heterogeneity in gut microbiome research, particularly in autism, and generalizes to any condition where behaviour mediates between neural processes and ecological outcomes.