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Editorial
December 2018

A Biology-First Approach in Perinatal Pharmacoepidemiology of AutismPotential and Pitfalls

Author Affiliations
  • 1The Lundbeck Foundation Initiative for Integrative Psychiatric Research (iPSYCH), Aarhus, Denmark
  • 2National Centre for Register-based Research, Department of Economics and Business, Aarhus University, Aarhus, Denmark
  • 3Department of Public Health, Aarhus University, Aarhus, Denmark
  • 4Department of Neurology, Aarhus University Hospital, Aarhus, Denmark
  • 5Centre for Academic Mental Health, Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom
  • 6Avon and Wiltshire Partnership NHS Mental Health Trust, Bristol, United Kingdom
  • 7NIHR Biomedical Research Centre, University of Bristol, Bristol, United Kingdom
JAMA Psychiatry. 2018;75(12):1213-1214. doi:10.1001/jamapsychiatry.2018.2725

In this issue of JAMA Psychiatry, Janecka et al1 conclude that maternal prenatal use of most medications that target specific neurotransmitter systems is not associated with offspring autism. This is a new perspective to consider in view of the hypothesis that there could be adverse neurodevelopmental effects of prenatal medications affecting serotonergic, GABAergic, and glutaminergic neurotransmitters. Although results vary,2,3 previous studies have warned of potential bias arising from confounding by maternal indications for prenatal drug treatments, which are stubbornly difficult to resolve.4 Janecka et al1 grouped medications into classes on the basis of each drug’s target neurotransmitter, regardless of the drug’s medical indication, and then estimated autism risk associated with maternal use of a drug in a class targeting a common neurotransmitter. They called this a biology-first approach to highlight that their autism risk assessment was linked to the drugs’ shared pharmacological effect and functional similarities while disassociated from the underlying indication.

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