Environment as a driver of ASD

Annual Research Review: The role of the environment in the developmental psychopathology of autism spectrum condition.



Although autism spectrum condition (ASC) is strongly genetic in origin, accumulating evidence points to the critical roles of various environmental influences on its emergence and subsequent developmental course.


Before conception, advanced paternal and maternal ages may independently enhance offspring risk for ASC.

Exogenous prenatal risks are evident (e.g. valproate and toxic chemicals) or possible (e.g. selective serotonin reuptake inhibitors), and processes endogenous to the materno-foeto-placental unit (e.g. maternal diabetes, enhanced steroidogenic activities and maternal immune activation) likely heighten offspring vulnerability to ASC.

Folate intake is a prenatal protective factor, with a particular window of action around 4 weeks preconception and during the first trimester. These prenatal risks and protective mechanisms appear to involve G × E and potentially rGE.

A variety of perinatal risks are related to offspring ASC risk, possibly reflecting rGE.

Postnatal social factors (e.g. caregiver-infant interaction, severe early deprivation) during the first years of life may operate through rGE to influence the likelihood of manifesting a full ASC phenotype from a ‘prodromal’ phase (a proposal distinct to the discredited and harmful ‘refrigerator mother hypothesis’); and later postnatal risks, after the full manifestation of ASC, shape life span development through transactions mediated by rGE.

There is no evidence that vaccination is a postnatal risk for ASC.


© 2016 Association for Child and Adolescent Mental Health.

Further Readings of Interest



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