Could oxytocin administration during labor contribute to autism and related behavioral disorders?--A look at the literature.
This literature review summarizes recent potential evidence, most of which is at the molecular/mechanistic level, in support of Hollander's hypothesis that excess oxytocin (OT), possibly through OT administration at birth, could contribute to the development of autistic spectrum disorders and related syndromes by proposed down regulation of the OT receptor (OTR). In this review, recent molecular evidence for OTR internalization by excess OT is related to OT's reported effects on animal social behavior, favoring social bondage, notably in sheep, voles, rats and especially mice. Adding indications for OT's capability of crossing the maternal placenta and OT's possibility of crossing an underdeveloped or stressed infantile blood brain barrier at birth, a causal connection between OT excess and behavioral disorders such as autism can be supported from a molecular perspective. Possible strategies such as a thorough statistical analysis of numerous birth records as well as molecular studies such as radiotracing using labeled OT are proposed to test this hypothesis.
Wahl
Roy U Rojas
RU
Initiative for Molecular Studies in Autism (IMSA), 516 North Street, Teaneck, NJ 07666, USA. rrojaswahl@msn.com
D001321:Autistic Disorder / Q000139:chemically induced* / Q000378:metabolism*; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D002653:Child Behavior Disorders / Q000139:chemically induced* / Q000378:metabolism*; D019317:Evidence-Based Medicine; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D007751:Labor, Induced / Q000009:adverse effects; D008431:Maternal-Fetal Exchange; D008954:Models, Biological; D010121:Oxytocin / Q000008:administration & dosage / Q000009:adverse effects* / Q000378:metabolism*; D011247:Pregnancy; D018045:Receptors, Oxytocin / Q000378:metabolism
D018045:Receptors, Oxytocin; D010121:Oxytocin