Autism is not an invention of the environment or merely a behavioral anomaly – it has a deep biological foundation, as numerous studies over the past two decades have shown.
According to Thapar & Rutter (2021), the heritability of autism spectrum disorders is around 80–90% – meaning genetic factors explain the majority of variability between individuals with and without autism. It is not a single “autism gene” that plays a role, but rather a multitude of genetic variants that accumulate or occur in rare combinations:
“Autism is a complex genetic trait, with contributions from both rare variants of large effect and common variants of small effect.”
— Thapar & Rutter, 2021 (PMID 32940822)
These genetic predispositions primarily affect neural development, synaptic plasticity, and sensory integration – which directly leads to our focus.
Neuroimaging studies show that autistic brains exhibit atypical connectivity. Particularly striking is a pattern of:
This “underintegrated architecture” has been documented by Müller et al. (2011) and Maximo et al. (2014):
“Atypical functional connectivity has been consistently reported in autism, especially reduced long-range and increased local connectivity.”
— Maximo et al., 2014 (PMID 24496901)
“Underconnectivity in autism appears to reflect impaired coordination across distant regions, potentially explaining difficulties with multisensory integration and social cognition.”
— Müller et al., 2011 (PMID 21378114)
Thus, genetic predisposition leads to an atypical neural architecture – which in turn results in altered sensory processing. In this light, sensory instability does not appear as a secondary symptom but as a central consequence of altered neurobiological organization.
Our model focuses precisely on this:
Not the genes, not the behavior – but the unstable sensory interface is considered the starting point upon which autistic strategies, compulsive behaviors, and social withdrawals are built.