It has long been presumed that there is a common cause at the genetic, cognitive, and neural levels for<unk> 's characteristic triad of symptoms. However, there is increasing suspicion that<unk>  is instead a complex disorder whose core aspects have distinct causes that often co-occur. Deletion (1), duplication (2), and inversion (3) are all chromosome abnormalities that have been implicated in<unk> .<unk>  has a strong genetic basis, although the genetics of<unk>  are complex and it is unclear whether ASD is explained more by rare mutations with major effects, or by rare multigene interactions of common genetic variants. Complexity arises due to interactions among multiple genes, the environment, and epigenetic factors which do not change DNA sequencing but are heritable and influence gene expression. Many genes have been associated with<unk>  through sequencing the genomes of affected individuals and their parents. Studies of twins suggest that heritability is 0.7 for<unk>  and as high as 0.9 for ASD, and siblings of those with<unk>  are about 25 times more likely to be<unk> ic than the general population. However, most of the mutations that increase<unk>  risk have not been identified. Typically,<unk>  cannot be traced to a Mendelian (single-gene) mutation or to a single chromosome abnormality, and none of the genetic syndromes associated with ASDs have been shown to selectively cause ASD. Numerous candidate genes have been located, with only small effects attributable to any particular gene. Most loci individually explain less than 1% of cases of<unk> . The large number of<unk> ic individuals with unaffected family members may result from spontaneous structural variation—such as deletions, duplications or inversions in genetic material during meiosis. Hence, a substantial fraction of<unk>  cases may be traceable to genetic causes that are highly heritable but not inherited: that is, the mutation that causes the<unk>  is not present in the parental genome.<unk>  may be underdiagnosed in women and girls due to an assumption that it is primarily a male condition, but genetic phenomena such as imprinting and X linkage have the ability to raise the frequency and severity of conditions in males, and theories have been put forward for a genetic reason why males are diagnosed more often, such as the imprinted brain hypothesis and the extreme male brain theory. Maternal nutrition and inflammation during preconception and pregnancy influences fetal neurodevelopment. Intrauterine growth restriction is associated with ASD, in both term and preterm infants. Maternal inflammatory and autoimmune diseases may damage fetal tissues, aggravating a genetic problem or damaging the nervous system. Exposure to air pollution during pregnancy, especially heavy metals and particulates, may increase the risk of<unk> . Environmental factors that have been claimed without evidence to contribute to or exacerbate<unk>  include certain foods, infectious diseases, solvents, PCBs, phthalates and phenols used in plastic products, pesticides, brominated flame retardants, alcohol, smoking, illicit drugs, vaccines, and prenatal stress. Some, such as the MMR vaccine, have been completely disproven. Parents may first become aware of<unk> ic symptoms in their child around the time of a routine vaccination. This has led to unsupported theories blaming vaccine "overload", a vaccine preservative, or the MMR vaccine for causing<unk> . The latter theory was supported by a litigation-funded study that has since been shown to have been "an elaborate fraud". Although these theories lack convincing scientific evidence and are biologically implausible, parental concern about a potential vaccine link with<unk>  has led to lower rates of childhood immunizations, outbreaks of previously controlled childhood diseases in some countries, and the preventable deaths of several children.
Autism
Schizophrenia
Tourettism
Reactive attachment disorder
Puberphonia
Intellectual disability
Selective mutism
Lesch–Nyhan syndrome