The science of love in ASD and ADHD

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Science Translational Medicine  11 Oct 2017:
Vol. 9, Issue 411, eaap8168
DOI: 10.1126/scitranslmed.aap8168


Genetic variations in the oxytocin receptor gene affect patients with ASD and ADHD differently.

Often called “the love hormone,” oxytocin is a neuropeptide that plays a role in the modulation of social behaviors and sexual reproduction. It is involved in contraction during labor, establishing maternal-infant bonding, enhancing interpersonal trust, increasing gaze to the eye region of human faces, and modulating social recognition.

Twins and family studies have shown that social behaviors are highly heritable. Thus, it is possible that variations in the oxytocin receptor gene (OXTR) might be involved in behavioral impairments in individuals with disorders associated with social deficits.

In a new study, Baribeau and colleagues built on previously published analyses to understand how single nucleotide polymorphisms (SNPs) in OXTR affect social cognition in individuals with either autism spectrum disorders (ASD) or attention deficit hyperactivity disorders (ADHD), two common groups of neurodevelopmental conditions associated with impairment of social abilities. The authors compared previously reported SNPs with social abilities in a cohort of over 600 patients with ASD or ADHD.

Baribeau and colleagues could confirm a positive association between three OXTR SNPs and the severity of social deficits in patients with ASD, supporting the role of oxytocin in social behavior modulation and the combinatorial effect of multiple alleles on the clinical presentation of ASD patients. In contrast and in disagreement with previously published results in smaller cohorts, the authors found no association or reduced severity of social cognition deficits associated with OXTR SNPs in patients with ADHD.

As confirmation, combining the entire data set, the authors found that OXTR risk variants in ASD show a significantly different effect in ADHD. In other words, the same OXTR genotype can exert a different influence on social deficits in ADS and ADHD patients. Given the well-described role of oxytocin in stress and fear, the authors controlled for the effect of the OXTR SNPs on anxiety disorders in the two diagnostic groups in their cohort, finding no association.

Although other confounding factors may explain the differences between the two groups of patients, these results raise the interesting possibility that social deficits in ASD and ADHD are the result of impairment of distinct neural circuits and thus are differentially influenced by OXTR genetic variations.

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