oxytocin levels and personality traits that are also associated with schizotypy, such as creativity and divergent thinking. However, both schizotypal personality disorder and schizotypy in the general population appear associated with the same oxytocin deficits as observed in schizophrenia, and the degree to which positive symptoms of schizophrenia and schizotypy are associated with high oxytocin—as argued by proponents—appears unclear and contradicted. Issues The broad claim that autism and schizophrenia are in opposition on the biological level is not supported by research. In samples of autistic adults, schizophrenia and other non-affective psychotic disorders occur at far higher rates than the general population, occurring in about 8-10% of the broad ASD population and as high as one-third in PDD-NOS. The same association occurs in childhood onset schizophrenia, which is considered a more homogenous form of the disorder that hews closest to the hypothetical neurodevelopmental disorder underlying schizophrenia-spectrum conditions; approximately one-quarter of children with schizophrenia fit the criteria for an autism spectrum disorder prior to the onset of psychosis, and the majority have clinical or subclinical disturbances of social, motor, or language skills similar to those seen in autistic children. Adults with schizophrenia and related psychotic disorders also have higher rates of autistic symptomatology than healthy controls. Crespi and Badcock make a number of claims about genetic disorders and their relationship to the hypothesis; for instance, that the relationship between those disorders and sex chromosome aneuploidy supports the hypothesis, with trisomy X and Klinefelter syndrome (extra X chromosomes) increasing schizophrenia risk and Turner syndrome (one X chromosome) increasing autism risk. However, polysomy X conditions are associated with increased autism as well as schizophrenia risk, and Turner syndrome is approximately three times as common in schizophrenic women as the general female population. Genetic syndromes in general lend credence to the suggestion that autism and schizophrenia are related rather than contraindicated, with conditions that sharply increase one risk tending to also increase the other. For instance, velocardiofacial syndrome, which is associated with a 20- to 30-fold increase in schizophrenia risk, also significantly increases the risk of autism. Other chromosomal disorders notable for significantly increasing the risk of both autism and schizophrenia include 15q11.2 microdeletions and 17q12 microdeletion syndrome. Moreover, the specific predictions the imprinted brain hypothesis makes about imprinting disorders are for the most part falsified. The imprinted brain hypothesis predicts that Prader-Willi syndrome, a disorder of maternal overimprinting, should have decreased autism and increased