Opioids and autism spectrum disorder: liaisons dangereuses?

A recent laboratory study in the Journal examined the effects of repeated exposures of neonatal mice to fentanyl on autism-like behaviour via opioid receptor-mediated DNA hypermethylation of the Grin2B gene, which encodes the GluN2B subunit of the NMDA receptor. These experiments provide mechanisms and biological plausibility but do not directly demonstrate that opioid exposure in early life induces autism spectrum disorder in humans. Experimental modelling of human neuropsychiatric disorders is extremely challenging since most subjective psychiatric symptoms used to establish diagnosis in humans cannot be convincingly ascertained in laboratory rodents. While some human epidemiological data show associations between repeated exposures to opioids during early life, it remains undeter-mined whether opioid exposure is an independent risk factor for developing autism spectrum disorder in the young.

Automated summary

A recent laboratory study examined the effects of repeated exposures of neonatal mice to fentanyl on autism-like behavior, indicating a potential mechanism through opioid receptor-mediated DNA hypermethylation. However, it is still uncertain whether opioid exposure in early life is an independent risk factor for developing autism spectrum disorder in humans due to the challenges of experimental modeling and the subjective nature of diagnosis in human neuropsychiatric disorders. Epidemiological data suggest associations, but further research is needed for a conclusive understanding.