A brain-chemistry deficit in children with autism may help to explain their social difficulties, according to new findings from the Stanford University School of Medicine.
The research team found a correlation between low levels of vasopressin, a hormone involved in social behavior, and the inability of autistic children to understand that other people’s thoughts and motivations can differ from their own.
The research was published July 22 in PLOS ONE.
“Autistic children who had the lowest vasopressin levels in their blood also had the greatest social impairment,” said the study’s senior author, Karen Parker, PhD, associate professor of psychiatry and behavioral sciences.
The findings raise the possibility that treatment with vasopressin might reduce social problems for autistic children who have low vasopressin levels, a hypothesis that Parker and her team are now testing in a clinical trial. However, the new research also showed that children without autism can have low vasopressin levels without displaying social impairment, Parker noted; in other words, autism is not explained by a vasopressin deficit alone.
Investigating vasopressin
Autism is a developmental disorder that affects 1 out of every 68 children in the United States. It is characterized by social and communication deficits and repetitive behaviors. The new study examined a social trait that psychologists call “theory of mind”: the ability to understand that others have different perspectives. Poor “theory of mind” makes it harder for people with autism to empathize and form relationships with others.
Vasopressin is a small-protein hormone that is structurally similar to oxytocin. Like oxytocin, it has roles in social behavior. Vasopressin also helps regulate blood pressure.
In the new study, the researchers first verified that vasopressin levels in the blood accurately reflected vasopressin levels in the brain by measuring the hormone’s levels simultaneously in the blood and cerebrospinal fluid of 28 people who were having the fluid collected for medical reasons.
They then recruited 159 children ages 3-12 for behavioral testing. Of these children, 57 had autism, 47 did not have autism but had a sibling who did, and 55 were typically developing children with no autistic siblings. All of the children completed standard psychiatric assessments of their neurocognitive abilities, social responsiveness, theory of mind, and ability to recognize others’ emotions, which is known as affect recognition. All children gave blood samples that were measured for vasopressin.
In all three groups, children had a wide range of vasopressin levels, with some children in each group having low, medium and high levels. Children without autism had similar scores on theory of mind tests regardless of their blood vasopressin level, but in children with autism, low blood vasopressin was a marker of low theory of mind ability.
Testing the hormone’s effects
Parker and her collaborator, Antonio Hardan, MD, professor of psychiatry and behavioral sciences, are now investigating whether vasopressin treatment improves social ability in children with autism. They are interested in whether the hormone is beneficial only for autistic children who start with low vasopressin levels or whether it might benefit all children with autism. More information about the team’s vasopressin clinical trial is available at http://med.stanford.edu/clinicaltrials/trials/NCT01962870or by calling Robin Libove at (650) 736-1235.
Other Stanford-affiliated authors of the paper are Dean Carson, PhD, postdoctoral scholar; Joseph Garner, PhD, associate professor of comparative medicine; laboratory managers Shellie Hyde and Raena Sumiyoshi; Robin Libove, social science research assistant; Sean Berquist, former social science research assistant now at the University of California-San Diego; Kirsten Hornbeak, medical resident; Lisa Jackson, graduate student; Christopher Howerton, PhD, former postdoctoral scholar; Sadie Hannah, RN, nurse practitioner in pediatric oncology; Sonia Partap, MD, clinical assistant professor of neurology and neurological sciences and a pediatric neuro-oncologist at Lucile Packard Children’s Hospital Stanford; Jennifer Phillips, PhD, clinical associate professor of psychiatry and behavioral sciences and co-director of the Autism and Developmental Disabilities Clinic at Lucile Packard Children’s Hospital Stanford; and Hardan, who is division chief of child and adolescent psychiatry, and director of the Autism and Developmental Disabilities Clinic.
Parker and Hardan are members of Stanford’s Child Health Research Institute, the Stanford Autism Center, Bio-X and Stanford Neurosciences Institute. Garner is a member of the Child Health Research Institute and Bio-X.
The research was funded by a Simons Foundation Autism Research Initiative Pilot Award, the Katherine D. McCormick Fund, the Mosbacher Family Fund for Autism Research, Stanford’s Bio-X NeuroVentures Program, the Weston Havens Foundation, Stanford’s Child Health Research Institute, an Autism Speaks Meixner Fellowship in Translational Research, a Stanford School of Medicine Dean’s Postdoctoral Fellowship, and the National Institutes of Health (grants 1R21MH10038701, UL1RR025774 and RR000167).
More information about the Department of Psychiatry and Behavioral Sciences, which also supported the research, is available at http://med.stanford.edu/psychiatry.html.
