Autism Spectrum Disorder (ASD) is a disorder defined by the heterogeneity of its presentations, making diagnosis and treatment for those who need it difficult. Here I examine a set of causal mechanisms which lead to the development of ASD. I support the idea that within and between those mechanisms, what may look like a singular causal tale may instead account for a large variety of individual presentations. I examine how an understanding of the low-level neurobiological mechanisms underlying ASD allows us to begin unraveling the nature of the heterogeneity found in individual and sub-group presentations of ASD.

Understanding the diverse etiologies of ASD can facilitate diagnosis and treatment. It is therefore critical that our understanding of ASD is as nuanced as possible. Here I explore three precipitants of ASD: SHANK3 haploinsufficiency, pre-natal organophosphate exposure, and pre-natal neonicotinoid exposure. I explore why the precipitant is important, how disruption in the mechanisms relevant to the precipitant can lead to ASD, and how mitigating or agitating ancillary factors affect the likelihood of precipitation, severity of effect, and phenotype of presentation of ASD within subgroups and individuals.