Diagnoses of autism have become more frequent since the 1980s, which has led to various controversies about both the cause of autism and the nature of the diagnoses themselves. Whether autism has mainly a genetic or developmental cause, and the degree of coincidence between autism and intellectual disability, are all matters of current scientific controversy as well as inquiry. There is also more sociopolitical debate as to whether autism should be considered a disability on its own. Epidemiology The current accepted prevalence of autism spectrum disorder (ASD) are around 1%, although previous research has shown far lower rates of incidence. ASD averages a 4.3:1 male-to-female ratio. The number of children on the autism spectrum has increased dramatically since the 1980s, at least partly due to changes in diagnostic practice; it is unclear whether prevalence has actually increased; and as-yet-unidentified environmental risk factors cannot be ruled out. The risk of autism is associated with several prenatal factors, including advanced parental age and diabetes in the mother during pregnancy. ASD is associated with several genetic disorders and epilepsy. Genetics The role of genetic influence on ASD has been heavily researched over the past few years. ASD is considered to have polygenic traits since there is not a single risk factor, but multiple ones. Multiple twin and family studies have been conducted in order to observe any genetic influence in diagnosing ASD. The chance of both twins having ASD was significantly higher in identical twins than fraternal twins, concluding that ASD is heritable. A reoccurring finding is that de novo (new mutation) copy number variants (CNVs) are a primary cause of ASD – they alter synaptic functions; germ line mutations can produce de novo CNVs. These mutations can only be passed on to offspring; this explains the phenomenon that occurs when the child has symptoms of ASD, but the parents have no symptoms or history of ASD. De novo variants differ from person to person, i.e. one variant can cause ASD in one person, whereas another person would need multiple variants to cause the same disorder. Loss of function variants occur in 16-18% of ASD diagnoses, which is nearly double the normal population. These loss of function variants reduce function in the protein neurexin, which connects neurons at the synapse and is important for neurological development; deletion mutations of neurexin are also very common in people with autism, as well as other neurological