this years ago.............more info now......
Oxytocin is what is used to induce labor in a product called pitocin
ScienceDaily (Oct. 22, 2009) Researchers at Duke University Medical Center
have uncovered a new genetic signature that correlates strongly with autism and
which doesn't involve changes to the DNA sequence itself. Rather, the changes
are in the way the genes are turned on and off. The finding may suggest new
approaches to diagnosis and treatment of autism.
Possible Link Between Autism And Oxytocin Gene Via Non-DNA
The researchers found higher-than-usual numbers of gene-regulating molecules
called methyl groups in a region of the genome that regulates oxytocin receptor
expression in people with autism.
"In both blood samples and brain tissue, the methylation status of specific
nucleotides in the oxytocin receptor gene is significantly higher in someone
with autism, about 70 percent, compared to the control population, where it is
about 40 percent," said co-lead author Simon G. Gregory, Ph.D., assistant
professor in the Duke Department of Medicine. The work appears in BMC
Medicine journal online.
Oxytocin is a hormone secreted into the bloodstream from the brain, and also
released within the brain, where it has a bearing on social interaction.
Previous studies have shown that giving oxytocin can improve an autistic
person's social engagement behavior and it is being explored as a potential
treatment of the disorder. Higher methylation of the oxytocin receptor gene may
make a person less sensitive to the hormone.
The findings by Dr. Gregory and his colleagues will potentially provide
information about which individuals will respond better to treatment with
"We are excited about our findings because they represent one of the few
occasions in which a mechanism other than genetic susceptibility or genome
instability is implicated in the development of autism, Gregory said.
"These results provide a possible explanation of why social isolation forms part
of the autism spectrum -- because an autistic individual's ability to respond to
oxytocin may be limited," Gregory said. " Oxytocin has been tied to levels of
trust and ability to read social cues."
Although the methylation status of the OXTR gene is not a definitive diagnosis
of autism by itself, a test for methylation might be used along with other
clinical tests for diagnosing autism. Gregory said that methylation-modifying
drugs also may be a new avenue for treatments.
Though not a change to the DNA sequence itself, methylation status can be
inherited, by what is known as epigenetics -- inherited changes in gene
"The epigenetic link to autism is extremely exciting as it provides another
opportunity for us to explore the heritability of this disorder and argues the
importance of exploring epigenetic markers in complex disease," said co-lead
author Jessica J. Connelly, Ph.D., assistant professor in the Department of
Medicine at the University of Virginia.
The identification of differences in methylation status of OXTR in people with
and without autism was discovered through a genome-wide study of genomic
The researchers examined 119 individuals with autism to identify genomic
rearrangements. One of these individuals had a DNA deletion of a region
containing the OXTR gene. The group then examined the genomic make-up of the
individual's family members and established that the boy with the deletion had a
brother with autism who didn't have the deletion. (Their mother had symptoms of
an obsessive-compulsive disorder, but not autism; autism and OCD share the
symptom of intensely repetitive thoughts and behaviors).
The researchers examined the brother's genome and found instances of elevated
methylation. With this discovery, they looked again at independent collections
of blood samples and brain tissue from a repository of specimens, and found
consistent differences in OXTR methylation.
This research was supported by the JP Hussman Foundation and National Institutes
of Health grants.
Other authors include co-lead-author Jessica J. Connelly, now with the
University of Virginia and formerly of the Duke Center for Human Genetics; Aaron
Towers, J. Johnson, D Biscocho, and Christina Markunas of the Duke Center for
Human Genetics; G.R. Delong of the Duke Department of Medicine; S.K. Murphy of
the Duke Departments of Obstetrics and Gynecology, and Pathology; Carla Lintas
and Antonio. Persico of the Laboratory of Molecular Psychiatry and Neurogenetics,
University Campus Bio-Medico, and the Department of Experimental Neurosciences,
IRCCS "Fondazione Santa Lucia," both in Rome; R.K. Abramson and H.H. Wright of
the Department of Neuropsychiatry, SOM-USC in Columbia, S.C.; P. Ellis and C.F.
Langford of Wellcome Trust Sanger Institute in Hinxton, U.K.; and Michael L.
Cuccaro and Margaret A. Pericak-Vance of the John P. Hussman Institute for Human
Genomics of the University of Miami Miller School of Medicine in Miami, Fla.
Adapted from materials provided by Duke
University Medical Center, via
EurekAlert!, a service of AAAS.
- Simon G Gregory, Jessica J Connelly, Aaron J Towers, Jessica Johnson,
Dhani Biscocho, Christina A Markunas, Carla Lintas, Ruth K Abramson, Harry H
Wright, Peter Ellis, Cordelia F Langford, Gordon Worley, G Robert Delong,
Susan K Murphy, Michael L Cuccaro, Antonello Persico and Margaret A Pericak-Vance.
Genomic and epigenetic evidence for oxytocin receptor deficiency in
autism. BMC Medicine, 2009; (in press) [link]
Sheri Nakken, R.N., MA, Hahnemannian Homeopath
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