This 2014 Stanford human study found:
“No empirical support for the OXT [oxytocin] deficit hypothesis of ASD [autism spectrum disorder], nor did plasma OXT concentrations differ by sex, OXTR [oxytocin receptor] SNPs [single nucleotide polymorphisms], or their interactions.”
Apparently, there was a:
“Prevalent but not well-interrogated OXT deficit hypothesis of ASD.”
The researchers followed up this worthwhile finding with three weak findings. The first, as stated by one of the study’s lead researchers, was:
“It didn’t matter if you were a typically developing child, a sibling or an individual with autism: Your social ability was related to a certain extent to your oxytocin levels.”
The second weak finding was that, regarding OXTR SNPs:
“The minor allele of rs2254298 predicted global social impairments on the SRS [Social Responsiveness Scale] and diagnostic severity on the ADI-R [Autism Diagnostic Interview-Revised]. In contrast, the major allele of rs53576 predicted impaired affect recognition performance on the NEPSY [A Developmental NEuroPSYchological Assessment].”
This was at odds with other relevant research, leading the researchers to state:
“The functional significance of these two intronic variants remains unknown.”
The third weak finding irked me:
“Plasma OXT concentrations were highly heritable.”
because the researchers didn’t attempt to differentiate the contribution of the environment for the observed blood oxytocin levels, as did the similar How epigenetic DNA methylation of the oxytocin receptor gene affects the perception of anger and fear study.
I wonder what the reviewer’s feedback was about these weak findings. Did he make the researchers insert specific language into the lengthy paragraph about the study’s limitations, or did he give them a pass?
http://www.pnas.org/content/111/33/12258.full “Plasma oxytocin concentrations and OXTR polymorphisms predict social impairments in children with and without autism spectrum disorder”