Oxytocin & Autism Spectrum Disorder Research Abstracts

We have included a small collection of research abstracts about the relationship between oxytocin levels, social behaviors, and autism spectrum disorders. For further research, we suggest visiting the US National Library of Medicine / National Institutes of Health website: http://www.pubmed.gov.


Biol Psychiatry. 2010 Apr 1;67(7):692-4. Epub 2009 Nov 7.
Intranasal oxytocin improves emotion recognition for youth with autism spectrum disorders.
Guastella AJ, Einfeld SL, Gray KM, Rinehart NJ, Tonge BJ, Lambert TJ, Hickie IB.
Brain & Mind Research Institute, University of Sydney, Sydney, NSW 2050, Australia.

BACKGROUND: A diagnostic hallmark of autism spectrum disorders is a qualitative impairment in social communication and interaction. Deficits in the ability to recognize the emotions of others are believed to contribute to this. There is currently no effective treatment for these problems. METHODS: In a double-blind, randomized, placebo-controlled, crossover design, we administered oxytocin nasal spray (18 or 24 IU) or a placebo to 16 male youth aged 12 to 19 who were diagnosed with Autistic or Asperger’s Disorder. Participants then completed the Reading the Mind in the Eyes Task, a widely used and reliable test of emotion recognition. RESULTS: In comparison with placebo, oxytocin administration improved performance on the Reading the Mind in the Eyes Task. This effect was also shown when analysis was restricted to the younger participants aged 12 to 15 who received the lower dose. CONCLUSIONS: This study provides the first evidence that oxytocin nasal spray improves emotion recognition in young people diagnosed with autism spectrum disorders. Findings suggest the potential of earlier intervention and further evaluation of oxytocin nasal spray as a treatment to improve social communication and interaction in young people with autism spectrum disorders. PMID: 19897177


 
Biol Psychiatry. 2007 Feb 15;61(4):498-503. Epub 2006 Aug 14.
Oxytocin increases retention of social cognition in autism.
Hollander E, Bartz J, Chaplin W, Phillips A, Sumner J, Soorya L, Anagnostou E, Wasserman S.
Mount Sinai School of Medicine, New York, New York, USA.

BACKGROUND: Oxytocin dysfunction might contribute to the development of social deficits in autism, a core symptom domain and potential target for intervention. This study explored the effect of intravenous oxytocin administration on the retention of social information in autism. METHODS: Oxytocin and placebo challenges were administered to 15 adult subjects diagnosed with autism or Asperger’s disorder, and comprehension of affective speech (happy, indifferent, angry, and sad) in neutral content sentences was tested. RESULTS: All subjects showed improvements in affective speech comprehension from pre- to post-infusion; however, whereas those who received placebo first tended to revert to baseline after a delay, those who received oxytocin first retained the ability to accurately assign emotional significance to speech intonation on the speech comprehension task. CONCLUSIONS: These results are consistent with studies linking oxytocin to social recognition in rodents as well as studies linking oxytocin to prosocial behavior in humans and suggest that oxytocin might facilitate social information processing in those with autism. These findings also provide preliminary support for the use of oxytocin in the treatment of autism.  PMID: 16904652


Proc Natl Acad Sci U S A. 2010 Mar 2;107(9):4389-94. Epub 2010 Feb 16.
Promoting social behavior with oxytocin in high-functioning autism spectrum disorders.
Andari E, Duhamel JR, Zalla T, Herbrecht E, Leboyer M, Sirigu A.
Centre de Neuroscience Cognitive, Unité Mixte de Recherche 5229, Centre National de la Recherche Scientifique, France.

Social adaptation requires specific cognitive and emotional competences. Individuals with high-functioning autism or with Asperger syndrome cannot understand or engage in social situations despite preserved intellectual abilities. Recently, it has been suggested that oxytocin, a hormone known to promote mother-infant bonds, may be implicated in the social deficit of autism. We investigated the behavioral effects of oxytocin in 13 subjects with autism. In a simulated ball game where participants interacted with fictitious partners, we found that after oxytocin inhalation, patients exhibited stronger interactions with the most socially cooperative partner and reported enhanced feelings of trust and preference. Also, during free viewing of pictures of faces, oxytocin selectively increased patients’ gazing time on the socially informative region of the face, namely the eyes. Thus, under oxytocin, patients respond more strongly to others and exhibit more appropriate social behavior and affect, suggesting a therapeutic potential of oxytocin through its action on a core dimension of autism. PMID: 20160081


Front Neuroendocrinol. 2011 Oct;32(4):426-50. Epub 2011 Jul 23.
Prosocial effects of oxytocin and clinical evidence for its therapeutic potential.
Striepens N, Kendrick KM, Maier W, Hurlemann R.
Department of Psychiatry, University of Bonn, 53105 Bonn, Germany.

There has been unprecedented interest in the prosocial effects of the neuropeptide oxytocin in humans over the last decade. A range of studies has demonstrated correlations between basal oxytocin levels and the strength of social and bonding behaviors both in healthy individuals and in those suffering from psychiatric disorders. Mounting evidence suggests associations between polymorphisms in the oxytocin receptor gene and prosocial behaviors and there may also be important epigenetic effects. Many studies have now reported a plethora of prosocial effects of intranasal application of oxytocin, including the domains of trust, generosity, socially reinforced learning, and emotional empathy. The main focus of this review will be to summarize human preclinical work and particularly the rapidly growing number of clinical studies which have identified important links between oxytocin and a wide range of psychiatric disorders, and have now started to directly assess its therapeutic potential.  PMID: 21802441


BMC Med. 2009 Oct 22;7:62.
Genomic and epigenetic evidence for oxytocin receptor deficiency in autism.
Gregory SG, Connelly JJ, Towers AJ, Johnson J, Biscocho D, Markunas CA, Lintas C, Abramson RK, Wright HH, Ellis P, Langford CF, Worley G, Delong GR, Murphy SK, Cuccaro ML, Persico A, Pericak-Vance MA. Duke Center for Human Genetics, DUMC, Durham, NC, USA.

BACKGROUND: Autism comprises a spectrum of behavioral and cognitive disturbances of childhood development and is known to be highly heritable. Although numerous approaches have been used to identify genes implicated in the development of autism, less than 10% of autism cases have been attributed to single gene disorders. METHODS: We describe the use of high-resolution genome-wide tilepath microarrays and comparative genomic hybridization to identify copy number variants within 119 probands from multiplex autism families. We next carried out DNA methylation analysis by bisulfite sequencing in a proband and his family, expanding this analysis to methylation analysis of peripheral blood and temporal cortex DNA of autism cases and matched controls from independent datasets. We also assessed oxytocin receptor (OXTR) gene expression within the temporal cortex tissue by quantitative real-time polymerase chain reaction (PCR). RESULTS: Our analysis revealed a genomic deletion containing the oxytocin receptor gene, OXTR (MIM accession no.: 167055), previously implicated in autism, was present in an autism proband and his mother who exhibits symptoms of obsessive-compulsive disorder. The proband’s affected sibling did not harbor this deletion but instead may exhibit epigenetic misregulation of this gene through aberrant gene silencing by DNA methylation. Further DNA methylation analysis of the CpG island known to regulate OXTR expression identified several CpG dinucleotides that show independent statistically significant increases in the DNA methylation status in the peripheral blood cells and temporal cortex in independent datasets of individuals with autism as compared to control samples. Associated with the increase in methylation of these CpG dinucleotides is our finding that OXTR mRNA showed decreased expression in the temporal cortex tissue of autism cases matched for age and sex compared to controls. CONCLUSION: Together, these data provide further evidence for the role of OXTR and the oxytocin signaling pathway in the etiology of autism and, for the first time, implicate the epigenetic regulation of OXTR in the development of the disorder.  PMID: 19845972