Autism

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Posted by motoman 03/12/2009 @ 08:16

Tags : autism, mental health, diseases, health

News headlines
NJ bill would require autism-treatment coverage - Philadelphia Inquirer
By Cynthia Henry TRENTON - After testimony from parents who had depleted their savings to provide treatment for their autistic children, New Jersey Senate and Assembly committees yesterday advanced a bill that would require insurers to cover screening...
Autism In The UK Costs More Than $41 Billion Every Year, Shows New ... - Science Daily (press release)
ScienceDaily (May 18, 2009) — Los Angeles, London, New Delhi, Singapore and Washinton DC (18 May 2009) – Research published this week in the Journal Autism, published by SAGE, estimate the annual costs of autism spectrum disorder (ASD) to be more than...
Future of autism centre in doubt - BBC News
The future of an all-Ireland centre for children with autism has been left in doubt after some of its financial backing was withdrawn. On Monday, the Irish government said they could not fund the expansion of the Middletown Centre of Excellence because...
Schools worry over autism support - BBC News
Educational institutions in Wales are "not meeting the needs" of young people with autism, a study suggests. A report by the Welsh assembly's cross-party autism group (CPAG) revealed 75% of schools surveyed felt there was a lack of adequate local help...
Insurer adds to hardship of caring for autistic child - Chicago Tribune
When their daughter, Sanai, was diagnosed with autism last summer, Keesha and Terrence Tyler vowed to do whatever it took to get her the best possible help. At the time, the toddler was non-verbal, non-expressive and did not play with her brothers....
Bill on autism coverage advances - Today's Sunbeam - NJ.com
By Trish G. Graber TRENTON - After eight years of therapy, the only sign today that Holly Masclans children have autism is their stutter. The Haddonfield mother, whose daughter was diagnosed with the disorder at 5 months old and son at 3 years old,...
Federal autism bill proposed; more sweeping than failed state bill - Arkansas News
By Rob Moritz LITTLE ROCK — Proposed federal legislation designed to improve the quality of life for people with autism would raise the premium costs on insurance plans to cover the disorder, not just insurance companies like the bill that failed in...
Autistic high school senior gets the job done - Herald Times Reporter
Pribek has autism. He is one of eight students with disabilities who are getting work experience through the school's transitional employment program, according to School to Work coordinator Don Koeser. The program is for students with any type of...
Gluten-free diets help many - San Jose Mercury News
Whether they suffer from gluten intolerance, hope to temper the symptoms of autism, or have been diagnosed with celiac disease, an autoimmune disorder that affects 1 in 133 adults and is getting overdue attention, they are going gluten-free for good,...
Extra: 'SAFER' program helps keep children with autism safe - KARE
This regular part of growing up can be a very stressful experience for parents of children with autism, children who often run, not knowing they may be headed toward danger. Like many autistic children, 6-year-old Dante Cortolezzis is attracted to...

Autism

Hans Asperger introduced the modern sense of the word autism in 1938.[37]The image above is proposed for deletion. See files for deletion to help reach a consensus on what to do.

Autism is a brain development disorder characterized by impaired social interaction and communication, and by restricted and repetitive behavior. These signs all begin before a child is three years old. The autism spectrum disorders (ASD) also include related conditions with milder signs and symptoms.

Autism has a strong genetic basis, although the genetics of autism are complex and it is unclear whether ASD is explained more by multigene interactions or by rare mutations. In rare cases, autism is strongly associated with agents that cause birth defects. Other proposed causes, such as childhood vaccines, are controversial, and the vaccine hypotheses lack any convincing scientific evidence. The prevalence of ASD is about 6 per 1,000 people, with about four times as many boys as girls. The number of people known to have autism has increased dramatically since the 1980s, partly due to changes in diagnostic practice; the question of whether actual prevalence has increased is unresolved.

Autism affects many parts of the brain; how this occurs is not understood. Parents usually notice signs in the first two years of their child's life. Although early behavioral or cognitive intervention can help children gain self-care, social, and communication skills, there is no known cure. Few children with autism live independently after reaching adulthood, but some become successful, and an autistic culture has developed, with some seeking a cure and others believing that autism is a condition rather than a disorder.

Autism is a highly variable brain development disorder that first appears during infancy or childhood, and generally follows a steady course without remission. Symptoms tend to continue through adulthood, although often in more muted form. It is distinguished not by a single symptom, but by a characteristic triad of symptoms: impairments in social interaction; impairments in communication; and restricted interests and repetitive behavior. Other aspects, such as atypical eating, are also common but are not essential for diagnosis. Autism is one of three related autism spectrum disorders (ASD; see Classification). Its individual symptoms occur in the general population and appear not to associate highly, without a sharp line separating pathologically severe from common traits.

Social deficits distinguish ASD from other developmental disorders. People with autism have social impairments and often lack the intuition about others that many people take for granted. Noted autistic Temple Grandin described her inability to understand the social communication of neurotypicals, or people with normal neural development, as leaving her feeling "like an anthropologist on Mars".

Social impairments become apparent early in childhood. Autistic infants show less attention to social stimuli, smile and look at others less often, and respond less to their own name. Autistic toddlers have more striking social deviance; for example, they have less eye contact and anticipatory postures and are more likely to communicate by manipulating another person's hand. Three- to five-year-old autistic children are less likely to exhibit social understanding, approach others spontaneously, imitate and respond to emotions, communicate nonverbally, and take turns with others. However, they do form attachments to their primary caregivers. They display moderately less attachment security than usual, although this feature disappears in children with higher mental development or less severe ASD. Older children and adults with ASD perform worse on tests of face and emotion recognition.

Contrary to common belief, autistic children do not prefer to be alone. Making and maintaining friendships often proves to be difficult for those with autism. For them, the quality of friendships, not the number of friends, predicts how lonely they feel.

There are many anecdotal reports, but few systematic studies, of aggression and violence in individuals with ASD. The limited data suggest that, in children with mental retardation, autism is associated with aggression, destruction of property, and tantrums. A 2007 study interviewed parents of 67 children with ASD and reported that about two-thirds of the children had periods of severe tantrums and about one-third had a history of aggression, with tantrums significantly more common than in children with a history of language impairment. A 2008 Swedish study found that, of individuals aged 15 or older discharged from hospital with a diagnosis of ASD, those who committed violent crimes were significantly more likely to have other psychopathological conditions such as psychosis.

About a third to a half of individuals with autism do not develop enough natural speech to meet their daily communication needs. Differences in communication may be present from the first year of life, and may include delayed onset of babbling, unusual gestures, diminished responsiveness, and vocal patterns that are not synchronized with the caregiver. In the second and third years, autistic children have less frequent and less diverse babbling, consonants, words, and word combinations; their gestures are less often integrated with words. Autistic children are less likely to make requests or share experiences, and are more likely to simply repeat others' words (echolalia) or reverse pronouns. Joint attention seems to be necessary for functional speech, and deficits in joint attention seem to distinguish infants with ASD: for example, they may look at a pointing hand instead of the pointed-at object, and they consistently fail to point at objects in order to comment on or share an experience. Autistic children may have difficulty with imaginative play and with developing symbols into language.

In a pair of studies, high-functioning autistic children aged 8–15 performed equally well, and adults better than individually matched controls at basic language tasks involving vocabulary and spelling. Both autistic groups performed worse than controls at complex language tasks such as figurative language, comprehension and inference. As people are often sized up initially from their basic language skills, these studies suggest that people speaking to autistic individuals are more likely to overestimate what their audience comprehends.

Autistic individuals display many forms of repetitive or restricted behavior, which the Repetitive Behavior Scale-Revised (RBS-R) categorizes as follows.

No single repetitive behavior seems to be specific to autism, but only autism appears to have an elevated pattern of occurrence and severity of these behaviors.

Autistic individuals may have symptoms that are independent of the diagnosis, but that can affect the individual or the family. An estimated 0.5% to 10% of individuals with ASD show unusual abilities, ranging from splinter skills such as the memorization of trivia to the extraordinarily rare talents of prodigious autistic savants.

Unusual responses to sensory stimuli are more common and prominent in autistic children, although there is no good evidence that sensory symptoms differentiate autism from other developmental disorders. Differences are greater for under-responsivity (for example, walking into things) than for over-responsivity (for example, distress from loud noises) or for seeking (for example, rhythmic movements). Several studies have reported associated motor problems that include poor muscle tone, poor motor planning, and toe walking; ASD is not associated with severe motor disturbances.

Unusual eating behavior occurs in about three-quarters of children with ASD, to the extent that it was formerly a diagnostic indicator. Selectivity is the most common problem, although eating rituals and food refusal also occur; this does not appear to result in malnutrition. Although some children with autism also have gastrointestinal (GI) symptoms, there is a lack of published rigorous data to support the theory that autistic children have more or different GI symptoms than usual; studies report conflicting results, and the relationship between GI problems and ASD is unclear.

Sleep problems are known to be more common in children with developmental disabilities, and there is some evidence that children with ASD are more likely to have even more sleep problems than those with other developmental disabilities; autistic children may experience problems including difficulty in falling asleep, frequent nocturnal awakenings, and early morning awakenings. A 2007 study reported that about two-thirds of children with ASD have a history of sleep problems.

Parents of children with ASD have higher levels of stress. Siblings of children with ASD report greater admiration of and less conflict with the affected sibling; siblings of individuals with ASD have greater risk of negative well-being and poorer sibling relationships as adults.

Autism is one of the five pervasive developmental disorders (PDD), which are characterized by widespread abnormalities of social interactions and communication, and severely restricted interests and highly repetitive behavior. These symptoms do not imply sickness, fragility, or emotional disturbance.

Of the five PDD forms, Asperger syndrome is closest to autism in signs and likely causes; Rett syndrome and childhood disintegrative disorder share several signs with autism, but may have unrelated causes; PDD not otherwise specified (PDD-NOS; also called atypical autism) is diagnosed when the criteria are not met for a more specific disorder. Unlike autism, Asperger's has no substantial delay in language development. The terminology of autism can be bewildering, with autism, Asperger's and PDD-NOS often called the autism spectrum disorders (ASD) or sometimes the autistic disorders, whereas autism itself is often called autistic disorder, childhood autism, or infantile autism. In this article, autism refers to the classic autistic disorder; in clinical practice, though, autism, ASD, and PDD are often used interchangeably. ASD, in turn, is a subset of the broader autism phenotype (BAP), which describes individuals who may not have ASD but do have autistic-like traits, such as avoiding eye contact.

The manifestations of autism cover a wide spectrum, ranging from individuals with severe impairments—who may be silent, mentally disabled, and locked into hand flapping and rocking—to high functioning individuals who may have active but distinctly odd social approaches, narrowly focused interests, and verbose, pedantic communication. Sometimes the syndrome is divided into low-, medium- and high-functioning autism (LFA, MFA, and HFA), based on IQ thresholds, or on how much support the individual requires in daily life; these subdivisions are not standardized and are controversial. Autism can also be divided into syndromal and non-syndromal autism, where the former is associated with severe or profound mental retardation or a congenital syndrome with physical symptoms, such as tuberous sclerosis. Although individuals with Asperger's tend to perform better cognitively than those with autism, the extent of the overlap between Asperger's, HFA, and non-syndromal autism is unclear.

Some studies have reported diagnoses of autism in children due to a loss of language or social skills, as opposed to a failure to make progress, typically from 15 to 30 months of age. The validity of this distinction remains controversial; it is possible that regressive autism is a specific subtype.

Research into causes has been hampered by the inability to identify biologically meaningful subpopulations and by the traditional boundaries between the disciplines of psychiatry, psychology, neurology and pediatrics. It has been proposed to classify autism using genetics as well as behavior, with the name Type 1 autism denoting rare autism cases that test positive for a mutation in the CNTNAP2 gene.

It has long been presumed that there is a common cause at the genetic, cognitive, and neural levels for autism's characteristic triad of symptoms. However, there is increasing suspicion that autism is instead a complex disorder whose core aspects have distinct causes that often co-occur.

Autism has a strong genetic basis, although the genetics of autism are complex and it is unclear whether ASD is explained more by multigene interactions or by rare mutations with major effects. Complexity arises due to interactions among multiple genes, the environment, and epigenetic factors which do not change DNA but are heritable and influence gene expression. Early studies of twins estimated heritability explains more than 90% of the risk of autism, assuming a shared environment and no other genetic or medical syndromes. However, most of the mutations that increase autism risk have not been identified. Typically, autism cannot be traced to a Mendelian (single-gene) mutation or to a single chromosome abnormality like Angelman syndrome or fragile X syndrome, and none of the genetic syndromes associated with ASDs has been shown to selectively cause ASD. Numerous candidate genes have been located, with only small effects attributable to any particular gene. The large number of autistic individuals with unaffected family members may result from copy number variations—spontaneous deletions or duplications in genetic material during meiosis. Hence, a substantial fraction of autism cases may be traceable to genetic causes that are highly heritable but not inherited: that is, the mutation that causes the autism is not present in the parental genome.

Gene replacement studies in mice suggest that autistic symptoms are closely related to later developmental steps that depend on activity in synapses and on activity-dependent changes, and that the symptoms may be reversed or reduced by replacing or modulating gene function after birth. All known teratogens (agents that cause birth defects) related to the risk of autism appear to act during the first eight weeks from conception, and though this does not exclude the possibility that autism can be initiated or affected later, it is strong evidence that autism arises very early in development. Although evidence for other environmental causes is anecdotal and has not been confirmed by reliable studies, extensive searches are underway. Environmental factors that have been claimed to contribute to or exacerbate autism, or may be important in future research, include certain foods, infectious disease, heavy metals, solvents, diesel exhaust, PCBs, phthalates and phenols used in plastic products, pesticides, brominated flame retardants, alcohol, smoking, illicit drugs, vaccines, and prenatal stress. Although parents may first become aware of autistic symptoms in their child around the time of a routine vaccination (and parental concern about vaccines has led to a decreasing uptake of childhood immunizations and an increasing likelihood of measles outbreaks), the overwhelming majority of scientific studies show no causal association between the measles-mumps-rubella vaccine and autism, and there is no convincing scientific evidence showing that the vaccine preservative thiomersal helps cause autism.

Autism's symptoms result from maturation-related changes in various systems of the brain. Despite extensive investigation, how autism occurs is not well understood. Its mechanism can be divided into two areas: the pathophysiology of brain structures and processes associated with autism, and the neuropsychological linkages between brain structures and behaviors. The behaviors appear to have multiple pathophysiologies.

Interactions between the immune system and the nervous system begin early during the embryonic stage of life, and successful neurodevelopment depends on a balanced immune response. Several symptoms consistent with a poorly regulated immune response have been reported in autistic children. It is possible that aberrant immune activity during critical periods of neurodevelopment is part of the mechanism of some forms of ASD. As autoantibodies have not been associated with pathology, are found in diseases other than ASD, and are not always present in ASD, the relationship between immune disturbances and autism remains unclear and controversial.

Several neurotransmitter abnormalities have been detected in autism, notably increased blood levels of serotonin. Whether these lead to structural or behavioral abnormalities is unclear. Some data suggest an increase in several growth hormones; other data argue for diminished growth factors. Also, some inborn errors of metabolism are associated with autism but probably account for less than 5% of cases.

The mirror neuron system (MNS) theory of autism hypothesizes that distortion in the development of the MNS interferes with imitation and leads to autism's core features of social impairment and communication difficulties. The MNS operates when an animal performs an action or observes another animal of the same species perform the same action. The MNS may contribute to an individual's understanding of other people by enabling the modeling of their behavior via embodied simulation of their actions, intentions, and emotions. Several studies have tested this hypothesis by demonstrating structural abnormalities in MNS regions of individuals with ASD, delay in the activation in the core circuit for imitation in individuals with Asperger's, and a correlation between reduced MNS activity and severity of the syndrome in children with ASD. However, individuals with autism also have abnormal brain activation in many circuits outside the MNS and the MNS theory does not explain the normal performance of autistic children on imitation tasks that involve a goal or object.

ASD-related patterns of low function and aberrant activation in the brain differ depending on whether the brain is doing social or nonsocial tasks. In autism there is evidence for reduced functional connectivity of the default network, a large-scale brain network involved in social and emotional processing, with intact connectivity of the task-positive network, used in sustained attention and goal-directed thinking. The two networks are not negatively correlated in people with autism, suggesting an imbalance in toggling between the two networks, possibly reflecting a disturbance of self-referential thought. A 2008 brain-imaging study found a specific pattern of signals in the cingulate cortex which differs in individuals with ASD.

The underconnectivity theory of autism hypothesizes that autism is marked by underfunctioning high-level neural connections and synchronization, along with an excess of low-level processes. Evidence for this theory has been found in functional neuroimaging studies on autistic individuals and by a brain wave study that suggested that adults with ASD have local overconnectivity in the cortex and weak functional connections between the frontal lobe and the rest of the cortex. Other evidence suggests the underconnectivity is mainly within each hemisphere of the cortex and that autism is a disorder of the association cortex.

From studies based on event-related potentials, transient changes to the brain's electrical activity in response to stimuli, there is considerable evidence for differences in autistic individuals with respect to attention, orientiation to auditory and visual stimuli, novelty detection, language and face processing, and information storage; several studies have found a preference for non-social stimuli. For example, magnetoencephalography studies have found evidence in autistic children of delayed responses in the brain's processing of auditory signals.

Two major categories of cognitive theories have been proposed about the links between autistic brains and behavior.

The first category focuses on deficits in social cognition. Hyper-systemizing hypothesizes that autistic individuals can systematize—that is, they can develop internal rules of operation to handle internal events—but are less effective at empathizing by handling events generated by other agents. It extends the extreme male brain theory, which hypothesizes that autism is an extreme case of the male brain, defined psychometrically as individuals in whom systemizing is better than empathizing. This in turn is related to the earlier theory of mind, which hypothesizes that autistic behavior arises from an inability to ascribe mental states to oneself and others. The theory of mind is supported by autistic children's atypical responses to the Sally-Anne test for reasoning about others' motivations, and is mapped well from the mirror neuron system theory of autism.

The second category focuses on nonsocial or general processing. Executive dysfunction hypothesizes that autistic behavior results in part from deficits in working memory, planning, inhibition, and other forms of executive function. Tests of core executive processes such as eye movement tasks indicate improvement from late childhood to adolescence, but performance never reaches typical adult levels. A strength of the theory is predicting stereotyped behavior and narrow interests; two weaknesses are that executive function is hard to measure and that executive function deficits have not been found in young autistic children. Weak central coherence theory hypothesizes that a limited ability to see the big picture underlies the central disturbance in autism. One strength of this theory is predicting special talents and peaks in performance in autistic people. A related theory—enhanced perceptual functioning—focuses more on the superiority of locally oriented and perceptual operations in autistic individuals. These theories map well from the underconnectivity theory of autism.

Neither category is satisfactory on its own; social cognition theories poorly address autism's rigid and repetitive behaviors, while the nonsocial theories have difficulty explaining social impairment and communication difficulties. A combined theory based on multiple deficits may prove to be more useful.

The American Academy of Pediatrics recommends that all children be screened for ASD at the 18- and 24-month well-child doctor visits, using autism-specific formal screening tests. In contrast, the UK National Screening Committee recommends against screening for ASD in the general population, because screening tools have not been fully validated and interventions lack sufficient evidence for effectiveness. Screening tools include the Modified Checklist for Autism in Toddlers (M-CHAT), the Early Screening of Autistic Traits Questionnaire, and the First Year Inventory; initial data on M-CHAT and its predecessor CHAT on children aged 18–30 months suggests that it is best used in a clinical setting and that it has low sensitivity (many false-negatives) but good specificity (few false-positives). It may be more accurate to precede these tests with a broadband screener that does not distinguish ASD from other developmental disorders. Screening tools designed for one culture's norms for behaviors like eye contact may be inappropriate for a different culture. Genetic screening for autism is generally still impractical.

Diagnosis is based on behavior, not cause or mechanism. Autism is defined in the DSM-IV-TR as exhibiting at least six symptoms total, including at least two symptoms of qualitative impairment in social interaction, at least one symptom of qualitative impairment in communication, and at least one symptom of restricted and repetitive behavior. Sample symptoms include lack of social or emotional reciprocity, stereotyped and repetitive use of language or idiosyncratic language, and persistent preoccupation with parts of objects. Onset must be prior to age three years, with delays or abnormal functioning in either social interaction, language as used in social communication, or symbolic or imaginative play. The disturbance must not be better accounted for by Rett syndrome or childhood disintegrative disorder. ICD-10 uses essentially the same definition.

Several diagnostic instruments are available. Two are commonly used in autism research: the Autism Diagnostic Interview-Revised (ADI-R) is a semistructured parent interview, and the Autism Diagnostic Observation Schedule (ADOS) uses observation and interaction with the child. The Childhood Autism Rating Scale (CARS) is used widely in clinical environments to assess severity of autism based on observation of children.

A pediatrician commonly performs a preliminary investigation by taking developmental history and physically examining the child. If warranted, diagnosis and evaluations are conducted with help from ASD specialists, observing and assessing cognitive, communication, family, and other factors using standardized tools, and taking into account any associated medical conditions. A pediatric neuropsychologist is often asked to assess behavior and cognitive skills, both to aid diagnosis and to help recommend educational interventions. A differential diagnosis for ASD at this stage might also consider mental retardation, hearing impairment, and a specific language impairment such as Landau-Kleffner syndrome.

Clinical genetics evaluations are often done once ASD is diagnosed, particularly when other symptoms already suggest a genetic cause. Although genetic technology allows clinical geneticists to link an estimated 40% of cases to genetic causes, consensus guidelines in the U.S. and UK are limited to high-resolution chromosome and fragile X testing. A genotype-first model of diagnosis has been proposed, which would routinely assess the genome's copy number variations. As new genetic tests are developed several ethical, legal, and social issues will emerge. Commercial availability of tests may precede adequate understanding of how to use test results, given the complexity of autism's genetics. Metabolic and neuroimaging tests are sometimes helpful, but are not routine.

ASD can sometimes be diagnosed by age 14 months, although diagnosis becomes increasingly stable over the first three years of life: for example, a one-year-old who meets diagnostic criteria for ASD is less likely than a three-year-old to continue to do so a few years later. In the UK the National Autism Plan for Children recommends at most 30 weeks from first concern to completed diagnosis and assessment, though few cases are handled that quickly in practice. A 2006 U.S. study found the average age of first evaluation by a qualified professional was 48 months and of formal ASD diagnosis was 61 months, reflecting an average 13-month delay, all far above recommendations. Although the symptoms of autism and ASD begin early in childhood, they are sometimes missed; adults may seek diagnoses to help them or their friends and family understand themselves, to help their employers make adjustments, or in some locations to claim disability living allowances or other benefits.

Underdiagnosis and overdiagnosis are problems in marginal cases, and much of the recent increase in the number of reported ASD cases is likely due to changes in diagnostic practices. The increasing popularity of drug treatment options and the expansion of benefits has given providers incentives to diagnose ASD, resulting in some overdiagnosis of children with uncertain symptoms. Conversely, the cost of screening and diagnosis and the challenge of obtaining payment can inhibit or delay diagnosis. It is particularly hard to diagnose autism among the visually impaired, partly because some of its diagnostic criteria depend on vision, and partly because autistic symptoms overlap with those of common blindness syndromes.

The main goals of treatment are to lessen associated deficits and family distress, and to increase quality of life and functional independence. No single treatment is best and treatment is typically tailored to the child's needs. Studies of interventions have methodological problems that prevent definitive conclusions about efficacy. Although many psychosocial interventions have some positive evidence, suggesting that some form of treatment is preferable to no treatment, the methodological quality of systematic reviews of these studies has generally been poor, their clinical results are mostly tentative, and there is little evidence for the relative effectiveness of treatment options. Intensive, sustained special education programs and behavior therapy early in life can help children acquire self-care, social, and job skills, and often improve functioning and decrease symptom severity and maladaptive behaviors; claims that intervention by around age three years is crucial are not substantiated. Available approaches include applied behavior analysis (ABA), developmental models, structured teaching, speech and language therapy, social skills therapy, and occupational therapy. Educational interventions have some effectiveness in children: intensive ABA treatment has demonstrated effectiveness in enhancing global functioning in preschool children and is well-established for improving intellectual performance of young children. Neuropsychological reports are often poorly communicated to educators, resulting in a gap between what a report recommends and what education is provided. It is not known whether treatment programs for children lead to significant improvements after the children grow up, and the limited research on the effectiveness of adult residential programs shows mixed results.

Many medications are used to treat ASD symptoms that interfere with integrating a child into home or school when behavioral treatment fails. More than half of U.S. children diagnosed with ASD are prescribed psychoactive drugs or anticonvulsants, with the most common drug classes being antidepressants, stimulants, and antipsychotics. Aside from antipsychotics, there is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD. A person with ASD may respond atypically to medications, the medications can have adverse effects, and no known medication relieves autism's core symptoms of social and communication impairments.

Although many alternative therapies and interventions are available, few are supported by scientific studies. Treatment approaches have little empirical support in quality-of-life contexts, and many programs focus on success measures that lack predictive validity and real-world relevance. Scientific evidence appears to matter less to service providers than program marketing, training availability, and parent requests. Though most alternative treatments, such as melatonin, have only mild adverse effects some may place the child at risk. A 2008 study found that compared to their peers, autistic boys have significantly thinner bones if on casein-free diets; in 2005, botched chelation therapy killed a five-year-old child with autism.

Treatment is expensive; indirect costs are more so. A U.S. study estimated an average cost of $3.2 million in 2003 U.S. dollars for someone born in 2000, with about 10% medical care, 30% extra education and other care, and 60% lost economic productivity. Publicly supported programs are often inadequate or inappropriate for a given child, and unreimbursed out-of-pocket medical or therapy expenses are associated with likelihood of family financial problems; one 2008 U.S. study found a 14% average loss of annual income in families of children with ASD, and a related study found that ASD is associated with higher probability that child care problems will greatly affect parental employment. After childhood, key treatment issues include residential care, job training and placement, sexuality, social skills, and estate planning.

There is no known cure. Children recover occasionally, so that they lose their diagnosis of ASD; this occurs sometimes after intensive treatment and sometimes not. It is not known how often recovery happens; reported rates in unselected samples of children with ASD have ranged from 3% to 25%. Most children with autism lack social support, meaningful relationships, future employment opportunities or self-determination. Although core difficulties tend to persist, symptoms often become less severe with age. Few high-quality studies address long-term prognosis. Some adults show modest improvement in communication skills, but a few decline; no study has focused on autism after midlife. Acquiring language before age six, having an IQ above 50, and having a marketable skill all predict better outcomes; independent living is unlikely with severe autism. A 2004 British study of 68 adults who were diagnosed before 1980 as autistic children with IQ above 50 found that 12% achieved a high level of independence as adults, 10% had some friends and were generally in work but required some support, 19% had some independence but were generally living at home and needed considerable support and supervision in daily living, 46% needed specialist residential provision from facilities specializing in ASD with a high level of support and very limited autonomy, and 12% needed high-level hospital care. A 2005 Swedish study of 78 adults that did not exclude low IQ found worse prognosis; for example, only 4% achieved independence. A 2008 Canadian study of 48 young adults diagnosed with ASD as preschoolers found outcomes ranging through poor (46%), fair (32%), good (17%), and very good (4%); 56% of these young adults had been employed at some point during their lives, mostly in volunteer, sheltered or part time work. Changes in diagnostic practice and increased availability of effective early intervention make it unclear whether these findings can be generalized to recently diagnosed children.

Most recent reviews tend to estimate a prevalence of 1–2 per 1,000 for autism and close to 6 per 1,000 for ASD; because of inadequate data, these numbers may underestimate ASD's true prevalence. PDD-NOS's prevalence has been estimated at 3.7 per 1,000, Asperger's at roughly 0.6 per 1,000, and childhood disintegrative disorder at 0.02 per 1,000. The number of reported cases of autism increased dramatically in the 1990s and early 2000s. This increase is largely attributable to changes in diagnostic practices, referral patterns, availability of services, age at diagnosis, and public awareness, though unidentified contributing environmental risk factors cannot be ruled out. The available evidence does not rule out the possibility that autism's true prevalence has increased; a real increase would suggest directing more attention and funding toward changing environmental factors instead of continuing to focus on genetics.

Boys are at higher risk for ASD than girls. The sex ratio averages 4.3:1 and is greatly modified by cognitive impairment: it may be close to 2:1 with mental retardation and more than 5.5:1 without. The risk of autism is also associated with several prenatal and perinatal risk factors. A 2007 review of risk factors found associated parental characteristics that included advanced maternal age, advanced paternal age, and maternal place of birth outside Europe or North America, and also found associated obstetric conditions that included low birth weight and gestation duration, and hypoxia during childbirth. Most professionals believe that race, ethnicity, and socioeconomic background do not affect the occurrence of autism.

A few examples of autistic symptoms and treatments were described long before autism was named. The Table Talk of Martin Luther contains the story of a 12-year-old boy who may have been severely autistic. According to Luther's notetaker Mathesius, Luther thought the boy was a soulless mass of flesh possessed by the devil, and suggested that he be suffocated. The Wild Boy of Aveyron, a feral child caught in 1798, showed several signs of autism; the medical student Jean Itard treated him with a behavioral program designed to help him form social attachments and to induce speech via imitation.

The New Latin word autismus (English translation autism) was coined by the Swiss psychiatrist Eugen Bleuler in 1910 as he was defining symptoms of schizophrenia. He derived it from the Greek word autos (αὐτός, meaning self), and used it to mean morbid self-admiration, referring to "autistic withdrawal of the patient to his fantasies, against which any influence from outside becomes an intolerable disturbance".

The word autism first took its modern sense in 1938 when Hans Asperger of the Vienna University Hospital adopted Bleuler's terminology autistic psychopaths in a lecture in German about child psychology. Asperger was investigating a form of ASD now known as Asperger syndrome, though for various reasons it was not widely recognized as a separate diagnosis until 1981. Leo Kanner of the Johns Hopkins Hospital first used autism in its modern sense in English when he introduced the label early infantile autism in a 1943 report of 11 children with striking behavioral similarities. Almost all the characteristics described in Kanner's first paper on the subject, notably "autistic aloneness" and "insistence on sameness", are still regarded as typical of the autistic spectrum of disorders. It is not known whether Kanner derived the term independently of Asperger.

Kanner's reuse of autism led to decades of confused terminology like infantile schizophrenia, and child psychiatry's focus on maternal deprivation during the mid-1900s led to misconceptions of autism as an infant's response to "refrigerator mothers". Starting in the late 1960s autism was established as a separate syndrome by demonstrating that it is lifelong, distinguishing it from mental retardation and schizophrenia and from other developmental disorders, and demonstrating the benefits of involving parents in active programs of therapy. As late as the mid-1970s there was little evidence of a genetic role in autism; now it is thought to be one of the most heritable of all psychiatric conditions. Although the rise of parent organizations and the destigmatization of childhood ASD have deeply affected how we view ASD, parents continue to feel social stigma in situations where their autistic children's behaviors are perceived negatively by others, and many primary care physicians and medical specialists still express some beliefs consistent with outdated autism research. The Internet has helped autistic individuals bypass nonverbal cues and emotional sharing that they find so hard to deal with, and has given them a way to form online communities and work remotely. Sociological and cultural aspects of autism have developed: some in the community seek a cure, while others believe that autism is simply another way of being.

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Causes of autism

Autism and autism spectrum disorders are complex neurodevelopmental disorders. Many causes of autism have been proposed, but its theory of causation is still incomplete. Heritability contributes about 90% of the risk of a child developing autism, but the genetics of autism are complex and typically it is unclear which genes are responsible. In rare cases, autism is strongly associated with agents that cause birth defects. Many other causes have been proposed, such as exposure of children to vaccines; these proposals are controversial and the vaccine hypotheses have no convincing scientific evidence.

Autism is a condition involving abnormalities of brain development and behavior which manifests itself before a child is three years old and has a steady course with no remission. It is characterized by impairments in social interaction and communication, as well as restricted and repetitive behavior. It is part of a larger family called the autism spectrum disorders (ASD) or pervasive developmental disorders (PDD), which include closely related syndromes such as Asperger syndrome and PDD-NOS. This article uses autism to denote the classic autistic disorder and ASD to denote the wider family.

Autism's theory of causation is still incomplete. It has long been presumed that there is a common cause at the genetic, cognitive, and neural levels for autism's characteristic triad of symptoms. However, there is increasing suspicion among researchers that autism does not have a single cause, but is instead a complex disorder with a set of core aspects that have distinct causes. Although these distinct causes have been hypothesized to often co-occur, it has also been suggested that the correlation between the causes has been exaggerated. The number of people known to have autism has increased dramatically since the 1980s, at least partly due to changes in diagnostic practice; it is unknown whether prevalence has increased as well. An increase in prevalence would suggest directing more attention and funding toward changing environmental factors instead of continuing to focus on genetics.

The consensus among mainstream autism researchers is that genetic factors predominate, but some are concerned, as one anonymous researcher put it, that "geneticists are running the show, and ignoring the environmental aspects." Environmental factors that have been claimed to contribute to autism or exacerbate its symptoms, or may be important to consider in future research, include certain foods, infectious disease, heavy metals, solvents, diesel exhaust, PCBs, phthalates and phenols used in plastic products, pesticides, brominated flame retardants, alcohol, smoking, illicit drugs, and vaccines. Among these factors, vaccines have attracted much attention, as parents may first become aware of autistic symptoms in their child around the time of a routine vaccination, and parental concern about vaccines has led to a decreasing uptake of childhood immunizations and an increasing likelihood of measles outbreaks. However, as described in Mercury and MMR vaccine below, there is overwhelming scientific evidence showing no causal association between the measles-mumps-rubella vaccine and autism, and there is no scientific evidence that the vaccine preservative thiomersal helps cause autism.

In 2007 the National Institutes of Health announced an Autism Centers of Excellence (ACE) research program to find the causes of autism and identify new treatments for the disorder. Initial recipients are focusing on genetic factors, brain imaging, brain chemicals and functions including mirror neurons, effect of early parent-child behavior on autism, and learning in autistic children.

Genetic factors are the most significant cause for autism spectrum disorders. Early studies of twins estimated heritability to be over 90%, in other words, that genetics explains over 90% of whether a child will develop autism. This may be an overestimate; new twin data and models with structural genetic variation are needed. Many of the non-autistic co-twins had learning or social disabilities. For adult siblings the risk for having one or more features of the broader autism phenotype might be as high as 30%.

The genetics of autism is complex. Linkage analysis has been inconclusive; many association analyses have had inadequate power. More than one gene may be implicated, different genes may be involved in different individuals, and the genes may interact with each other or with environmental factors. Several candidate genes have been located, but the mutations that increase autism risk have not been identified for most candidate genes. A substantial fraction of autism may be highly heritable but not inherited: that is, the mutation that causes the autism is not present in the parental genome. One hypothesis is that autism is in some sense diametrically opposite to schizophrenia, and that autism involves increased effects via genomic imprinting of paternally expressed genes that regulate overgrowth in the brain, whereas schizophrenia involves maternally expressed genes and undergrowth.

Though autism's genetic factors explain most of autism risk, they do not explain all of it. A common hypothesis is that autism is caused by the interaction of a genetic predisposition and an early environmental insult. Several theories based on environmental factors have been proposed to address the remaining risk. Some of these theories focus on prenatal environmental factors, such as agents that cause birth defects; others focus on the environment after birth, such as children's diets.

A 2007 review of risk factors found associated parental characteristics that included advanced maternal age, advanced paternal age, and maternal place of birth outside Europe or North America. It is not known whether these associations reflect genetic, epigenetic, or environmental factors.

The risk of autism is associated with several prenatal risk factors. Autism has been linked to birth defect agents acting during the first eight weeks from conception, though these cases are rare. Other potential prenatal environmental factors do not have convincing scientific evidence.

Prenatal viral infection has been called the principal non-genetic cause of autism. Prenatal exposure to rubella or cytomegalovirus activates the mother's immune response and greatly increases the risk for autism. Congenital rubella syndrome is the most convincing environmental cause. Infection-associated immunological events in early pregnancy may affect neural development more than infections in late pregnancy, not only for autism, but also for other psychiatric disorders of presumed neurodevelopmental origin, notably schizophrenia.

The maternal antibody theory hypothesizes that immunoglobulin G (IgG) in a mother's blood can cross the placenta, enter into the fetus's brain, react against fetal brain proteins, and cause autism. The theory is related to the autoimmune disease hypothesis, except it focuses on maternal antibodies rather than the child's. A 2008 study found that these antibodies bind to fetal brain cells, most commonly in mothers of children with regressive autism. A 2008 study found that rhesus monkeys exposed during gestation to IgG from mothers of children with ASD demonstrated stereotypies, one of the three main symptoms of autism.

Teratogens are environmental agents that cause birth defects. Some agents that are known to cause other birth defects have also been found to be related to autism risk. These include exposure of the embryo to thalidomide, valproic acid, or misoprostol. These cases are rare. Questions have also been raised whether ethanol (grain alcohol) increases autism risk, as part of fetal alcohol syndrome or alcohol-related birth defects, but current evidence is insufficient to determine whether autism risk is actually elevated with ethanol. All known teratogens appear to act during the first eight weeks from conception, and though this does not exclude the possibility that autism can be initiated or affected later, it is strong evidence that autism arises very early in development.

A 2007 study by the California Department of Public Health found that women in the first eight weeks of pregnancy who live near farm fields sprayed with the organochlorine pesticides dicofol and endosulfan are several times more likely to give birth to children with autism. The association appeared to increase with dose and decrease with distance from field site to residence. The study's findings suggest that on the order of 7% of autism cases in the California Central Valley might have been connected to exposure to the insecticides drifting off fields into residential areas. These results are highly preliminary due to the small number of women and children involved and lack of evidence from other studies. It is not known whether these pesticides are human teratogens, though endosulfan has significant teratogenic effects in laboratory rats.

A 2005 study showed indirect evidence that prenatal exposure to organophosphate pesticides such as diazinon and chlorpyrifos may contribute to autism in genetically vulnerable children. Several other studies demonstrate the neurodevelopmental toxicity of these agents at relatively low exposure levels.

Thyroid problems that lead to thyroxine deficiency in the mother in weeks 8–12 of pregnancy has been postulated to produce changes in the fetal brain leading to autism. Thyroxine deficiencies can be caused by inadequate iodine in the diet, and by environmental agents that interfere with iodine uptake or act against thyroid hormones. Possible environmental agents include flavonoids in food, tobacco smoke, and most herbicides. This hypothesis has not been tested.

It has been hypothesized that folic acid taken during pregnancy could play a role in causing autism by modulating gene expression through epigenetic mechanism. This hypothesis is untested.

Prenatal stress, consisting of exposure to life events or environmental factors that distress an expectant mother, has been hypothesized to contribute to autism, possibly as part of a gene-environment interaction. Autism has been reported to be associated with prenatal stress both with retrospective studies that examined stressors such as job loss and family discord, and with natural experiments involving prenatal exposure to storms; animal studies have reported that prenatal stress can disrupt brain development and produce behaviors resembling symptoms of autism.

The fetal testosterone theory hypothesizes that higher levels of testosterone in the amniotic fluid of mothers pushes brain development towards improved ability to see patterns and analyze complex systems while diminishing communication and empathy, emphasizing "male" traits over "female", or in EQ SQ Theory terminology, emphasizing "systemizing" over "empathizing". One project has published several reports suggesting that high levels of fetal testosterone could produce behaviors relevant to those seen in autism. The theory and findings are controversial and many studies contradict the idea that baby boys and girls respond differently to people and objects.

A 2006 study found that sustained exposure of mouse embryos to ultrasound waves caused a small but statistically significant number of neurons to fail to acquire their proper position during neuronal migration. It is highly unlikely that this result speaks directly to risks of fetal ultrasound as practiced in competent and responsible medical centers. There is no scientific evidence of an association between prenatal ultrasound exposure and autism, but there are very little data on human fetal exposure during diagnostic ultrasound, and the lack of recent epidemiological research and human data in the field has been called "appalling".

Autism is associated with some perinatal and obstetric conditions. A 2007 review of risk factors found associated obstetric conditions that included low birth weight and gestation duration, and hypoxia during childbirth. This association does not demonstrate a causal relationship; an underlying cause could explain both autism and these associated conditions. A 2007 study of premature infants found that those who survived cerebellar hemorrhagic injury (bleeding in the brain that injures the cerebellum) were significantly more likely to show symptoms of autism than controls without the injury.

A wide variety of postnatal contributors to autism have been proposed, including gastrointestinal or immune system abnormalities, allergies, and exposure of children to drugs, vaccines, infection, certain foods, or heavy metals. The evidence for these risk factors is anecdotal and has not been confirmed by reliable studies. The subject remains controversial and extensive further searches for environmental factors are underway.

This theory hypothesizes that autoantibodies that target the brain may cause or exacerbate autism. It is related to the maternal antibodies theory, except that it postulates that the effect is caused by the individual's own antibodies, possibly due to an environmental trigger after birth. It is also related to several other hypothesized causes; for example, viral infection has been hypothesized to cause autism via an autoimmune mechanism.

Interactions between the immune system and the nervous system begin early during embryogenesis, and successful neurodevelopment depends on a balanced immune response. Several symptoms consistent with a poorly regulated immune response have been reported in autistic children. It is possible that aberrant immune activity during critical periods of neurodevelopment is part of the mechanism of some forms of ASD. As autoantibodies have not been associated with pathology, are found in diseases other than ASD, and are not always present in ASD, the relationship between immune disturbances and autism remains unclear and controversial.

Parents have reported gastrointestinal (GI) disturbances in autistic children, and several studies have investigated possible associations between autism and the gut. The controversial Wakefield et al. vaccine paper discussed in MMR vaccine below also suggested that some bowel disorders may allow antigens to pass from food into the bloodstream and then to contribute to brain dysfunction. Although Wakefield later proposed the term autistic enterocolitis, his studies' methodology has been criticized, their results have not been replicated by other groups, and Wakefield has been accused of manipulating patient data and misreporting results.

In another example, a 1998 study of three children with ASD treated with secretin infusion reported improved GI function and dramatic improvement in behavior, which suggested an association between GI and brain function in autistic children. After this study, many parents sought secretin treatment and a black market for the hormone developed quickly. However, later studies found secretin ineffective in treating autism.

Leaky gut syndrome theories inspired several dietary treatments, including gluten-free diets, casein-free diets, antifungal diets, low-sugar diets, as well as supplements that include nystatin, B12, and probiotics. Parents are more likely to get advice about these diets from other parents, the media, and the Internet than from medical experts. There is no solid research evidence that autistic children are more likely to have GI symptoms than typical children. In particular, design flaws in studies of elimination diets mean that the currently available data are inadequate to guide treatment recommendations. A 2008 study found that children with autism had no more peptides in their urine than typical children, casting doubt on the proposed mechanism underlying the leaky-gut theory.

Many studies have presented evidence for and against association of autism with viral infection after birth. Laboratory rats infected with Borna disease virus show some symptoms similar to those of autism but blood studies of autistic children show no evidence of infection by this virus. Members of the herpes virus family may have a role in autism, but the evidence so far is anecdotal. Viruses have long been suspected as triggers for immune-mediated diseases such as multiple sclerosis but showing a direct role for viral causation is difficult in those diseases, and mechanisms whereby viral infections could lead to autism are speculative.

The hygiene hypothesis is to some extent the inverse of the viral infection hypothesis: it states that a lack of early childhood exposure to microbes or parasites contributes to autism. This hypothesis relies on some similarities between autism and asthma and other autoimmune disorders which are already hypothesized to be affected by hygiene: for example, autism and asthma affect more boys than girls, affect more urban than rural children, and are associated with increased head circumference. This hypothesis has not been tested scientifically.

This theory hypothesizes that toxicity and oxidative stress may cause autism in some cases. Evidence includes genetic effects on metabolic pathways, reduced antioxidant capacity, enzyme changes, and enhanced biomarkers for oxidative stress; however, the overall evidence is weaker than it is for involvement oxidative stress with disorders such as schizophrenia. One theory is that stress damages Purkinje cells in the cerebellum after birth, and it is possible that glutathione is involved.

This theory hypothesizes that an early developmental failure involving the amygdala cascades on the development of cortical areas that mediate social perception in the visual domain. The fusiform face area of the ventral stream is implicated. The idea is that it is involved in social knowledge and social cognition, and that the deficits in this network are instrumental in causing autism.

This theory hypothesizes that autism is caused by vitamin D deficiency, and that recent increases in diagnosed cases of autism are due to medical advice to avoid the sun. The theory has not been studied scientifically.

Lead poisoning has been suggested as a possible risk factor for autism, as the lead blood levels of autistic children has been reported to be significantly higher than typical. The atypical eating behaviors of autistic children, along with habitual mouthing and pica, make it hard to determine whether increased lead levels are a cause or a consequence of autism.

This theory hypothesizes that autism is associated with mercury poisoning, based on perceived similarity of symptoms and reports of mercury or its biomarkers in some autistic children. The principal source of human exposure to organic mercury is via fish consumption and for inorganic mercury is dental amalgams. Other forms of exposure, such as in cosmetics and vaccines, also occur. The evidence so far is indirect for the association between autism and mercury exposure after birth, as no direct test has been reported, and there is no evidence of an association between autism and postnatal exposure to any neurotoxicant.

There is little evidence of an increased body burden of mercury in autistic children. A 2003 study reported that mercury measurements of hair samples from autistic children's first haircuts were significantly lower than a matched group of normal children, declining as measures of severity increased, but a later meta-analysis based on two studies found that there was not enough evidence to conclude that hair mercury level is lower in autistic children. A 2006 study found a slight association between autism and environmental releases of mercury, primarily from coal power plants; this study used Texas county-wide data and did not distinguish between prenatal and postnatal exposure. A 2009 followup study found a similar slight association between autism rates and distance to industrial and power plant mercury sources in Texas.

Perhaps the best-known theory involving mercury and autism involves the use of the mercury-based compound thiomersal, a preservative that has been phased out from most childhood vaccinations in developed countries. Parents may first become aware of autistic symptoms in their child around the time of a routine vaccination. There is no convincing scientific evidence for a causal connection between thiomersal and autism, but parental concern about the thiomersal controversy has led to decreasing uptake of childhood immunizations and increasing likelihood of disease outbreaks.

The MMR vaccine theory of autism is one of the most extensively debated theories regarding the origins of autism. A controversial 1998 paper by Andrew Wakefield et al. reported a study of 12 children who had autism and bowel symptoms, in some cases reportedly with onset after MMR. Though the paper concluded "We did not prove an association between measles, mumps, and rubella vaccine and the syndrome described," Wakefield nevertheless suggested during a 1998 press conference that giving children the vaccines in three separate doses would be safer than a single jab. This suggestion has been heavily criticized, both on scientific grounds and for triggering a decline in vaccination rates. Using separate, single vaccines in place of MMR is widely believed to put children at increased risk since the combined vaccine reduces the risk of them catching the diseases while they are waiting for full immunization cover. Numerous peer-reviewed studies have also since failed to show any association between MMR vaccine and autism.

In 2004, the interpretation of a causal link between MMR vaccine and autism was formally retracted by ten of Wakefield's twelve co-authors. The retraction followed an investigation by The Sunday Times. The Centers for Disease Control and Prevention, the Institute of Medicine of the National Academy of Sciences, and the U.K. National Health Service have all concluded that there is no evidence of a link between the MMR vaccine and autism.

In July 2007 Andrew Wakefield and coauthors John Walker-Smith and Simon Murch faced charges of serious professional misconduct at the General Medical Council. It is alleged that the trio acted unethically in preparing the research into safety of the MMR vaccine. Wakefield denies the charges. In February 2009 The Sunday Times reported that Wakefield had manipulated patient data and misreported results in his 1998 paper, creating the appearance of a link with autism.

A 2008 preliminary case-control study based on a parent survey presented evidence that paracetamol (acetaminophen) following MMR vaccine is apparently associated with development of autism in children aged 1–5 years. The effect has not been independently confirmed.

It has been hypothesized that rain, or some environmental trigger positively associated with rain, acts together with an underlying genetic predisposition to cause autism. A 2008 study found that precipitation was associated with autism by examining county-level autism data for California, Oregon, and Washington. It is possible that nonprofessionals will misinterpret this result, and that it may well not lead to insights about the causes of autism.

Bruno Bettelheim believed that autism was linked to early childhood trauma, and his work was highly influential for decades both in the medical and popular spheres. Parents, especially mothers, of individuals with autism were blamed for having caused their child's condition through the withholding of affection. Leo Kanner, who first described autism, suggested that parental coldness might contribute to autism. Although Kanner eventually renounced the theory, Bettelheim put an almost exclusive emphasis on it in both his medical and his popular books. Treatments based on these theories failed to help children with autism, and after Bettelheim's death it came out that his reported rates of cure (around 85%) were found to be fraudulent.

Psychogenic theories in general have become increasingly unpopular, particularly since twin studies have shown that autism is highly heritable. Nevertheless, some case reports have found that deep institutional privation can result in "quasi-autistic" features without the neuroanatomical differences. Other case reports have suggested that children predisposed genetically to autism can develop "autistic devices" in response to traumatic events such as the birth of a sibling.

Like ADHD, which has a similar social construct theory, a spectral disorder such as autism may be understood as a cultural or social construct. The theory says that the boundary between normal and abnormal is subjective and arbitrary, so autism does not exist as an objective entity, but only as a social construct. It further argues that autistic individuals themselves have a way of being that is partly socially constructed. This theory does not say that there are no neurological or quality-of-life differences between groups deemed "autistic" and "non-autistic". To falsify this theory it would need to be shown that an objective characteristic can clearly separate both groups. For example, a genetic test that can fully substitute for a psychiatric diagnosis would undermine this theory.

Asperger syndrome and high-functioning autism are particular targets of the theory that social factors determine what it means to be autistic. The theory hypothesizes that individuals with these diagnoses inhabit the identities that have been ascribed to them, and promote their sense of well-being by resisting or appropriating autistic ascriptions.

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Autism rights movement

The puzzle piece ribbon is used by some autism societies.

The autism rights movement (ARM) (also neurodiversity movement or anti-cure movement or autistic culture movement) is a social movement that encourages autistic people, their caregivers and society to adopt a position of neurodiversity, accepting autism as a variation in functioning rather than a mental disorder to be cured. The ARM advocates a variety of goals including a greater acceptance of autistic behaviors; treatment that teaches autistic individuals coping skills rather than treatment focused on imitating behaviors of neurotypical peers, including extinguishing harmless stimming, forcing eye contact and breaking routines; the creation of social networks and events that allow autistics to socialize on their own terms; and the recognition of the autistic community as a minority group.

Autism rights or neurodiversity advocates believe that autism spectrum disorders are genetic and should be accepted as a natural expression of the human genome. This perspective is distinct from two wings of the autism cure movement: (1) the perspective that autism spectrum disorders are caused by a genetic defect and should be addressed by targeting the autism gene(s) and (2) the perspective that autism is caused by environmental factors like vaccines and pollution and could be cured by addressing environmental causes.

The movement is controversial and there are a wide variety of both supportive and critical opinions about the movement among people whose lives are affected by autism.

There are several organizations in the autism rights movement. Some, like the Autistic Self Advocacy Network have non-profit status while others like Autism Network International do not. Much organizing, communicating and advocacy is also done online on organizations’ websites and personal blogs.

Curing autism is a controversial and politicized issue. Doctors and scientists are not clear on the cause(s) of autism yet many organizations like Defeat Autism Now! and Autism Speaks advocate researching a cure. Members of the various autism rights organizations view autism as a way of life rather than as a disease and thus advocate acceptance over a search for a cure. Some advocates believe that common treatments for the behavioral and speech delays associated with autism, like ABA therapy, are not only misguided but also unethical.

The anti-cure perspective endorsed by the movement is a view that autism is not a disorder, but a normal occurrence -- an alternate variation in brain wiring or a less common expression of the human genome. Advocates of this perspective believe that autism is a unique way of being that should be validated, supported and appreciated rather than shunned, discriminated against or cured. They believe quirks and uniqueness of autistic individuals should be tolerated as the differences of any minority group should be tolerated and that efforts to cure autism should not be compared, for example, to curing cancer but instead to the antiquated notion of curing left-handedness.

Variations within the anti-cure movement are diverse. Jim Sinclair, a leader in the movement, argues that autism essential to a person, not a disease secondary to the person. He says that wishing that an autistic person be cured is equivalent to wishing that he disappear and another completely different person exist in his place. Visions for a future where autism has been eradicated, he believes, is the desire to end the autistic culture. Some movement members with Asperger Syndrome, who do not have the language delays typical of autistic individuals, believe their way of life should be respected and they should be left alone completely. Other members agree that autistics should not be made to act exactly like everyone else, but that they should receive therapy to help them learn to communicate in innovative ways or regulate emotions.

Jim Sinclair was the first individual to communicate the anti-cure or autism rights perspective in the late 1980s. In 1992 he co-founded the Autism Network International, an organization that publishes newsletters “written by and for autistic people.” Other individuals involved in the creation of the ANI were Dona Williams and Kathy Grant, two autistic individuals that knew Sinclair through pen pal lists and autism conferences. The first issue of the newsletter, “Our Voice,” was distributed online in November 1992 to an audience of mostly neuro-typical professionals and parents of young children with autism. The number of autistics in the organization grew slowly over the years and became a communication network for like-minded autistics.

The rise of the internet provided more opportunities for autistic individuals to connect and organize. Due to geographical distance, communication and speech patterns of autistic individuals and the domination of nuerotypical professionals and family members in established autism organizations, the internet provided an invaluable space for members of the movement to organize and communicate. Autistics.org was founded in 1998 and started Internet campaigns in 2000. The Real Voices of Autism is a social networking site for “autistics and their neurodiversity movement allies” and ACDate is an online dating site for autistics. Neurodiversity.com is a blog that provides information, news and opinions from the autism rights perspective. These sites all encourage the celebration of neurodiversity.

The essays of some individuals in the movement, including Amanda Baggs and Jim Sinclair, have been used as reading assignments in a class at the University of Wisconsin-Madison.

Some parents of autistic children are involved in the movement. Morton Ann Gernsbacher, who is a parent of an autistic child and a professor of psychology, said that autistics need acceptance and not a cure and has expressed opposition to the view of autism as a disorder. Estee Klar-Wolfond, the mother of an autistic son, founded The Autism Acceptance Project in support of autistic people. Autistics.org claims that parents can be the movement's strongest allies. In addition, some autistic people involved in the movement are also parents. Autism professionals Tony Attwood and Simon Baron-Cohen have sent supportive messages to the Aspies for Freedom organization.

The movement embraces a number of issues and goals that range from challenging the way autistic people are treated by others to challenging the way autism is portrayed. Not all supporters of the movement have the same opinions about the issues and there is controversy about the issues from within the movement.

Aspies For Freedom claims that the most common therapies for autism are unethical. They argue that ABA therapy and restriction of stimming "and other autistic coping mechanisms" are mentally harmful, that aversion therapy and the use of restraints are physically harmful, and that alternative treatments like chelation are dangerous. Michelle Dawson, a Canadian autism self advocate, testified in court against government funding of ABA therapy. An autistic person named Jane Meyerding criticized therapy which attempts to remove autistic behaviors because she says that the behaviors that the therapy tries to remove are attempts to communicate.

Since those in the autism rights movement see autism as a natural human variation and not a disorder, they are opposed to attempts to eliminate autism. In particular, there is opposition to prenatal genetic testing of autism in unborn fetuses, which some believe might be possible in the future (see Heritability of autism). Some worry that this can prevent autistic people from being born. On February 23, 2005 Joseph Buxbaum of the Autism Genome Project at the Mount Sinai School of Medicine said there could be a prenatal test for autism within 10 years. However, the genetics of autism have proven to be extremely complex. In any case, the Autistic Genocide Clock was started in response to this, which counts down to 10 years after Buxbaum made this announcement. The public has started to debate the ethics involved in the possible elimination of a genotype that has liabilities and advantages, which may be seen as tampering with natural selection.

Some people lament that professionals, such as social workers, may discourage autistics from having children. Some are concerned that the "ultimate cure will be a genetic test to prevent autistic children from being born" and that most fetuses with autism would be aborted if prenatal tests for autism are developed.

Autism has been compared to a disease, rather than the variation in functioning preferred by supporters of neurodiversity, with an attendant focus on the burden placed on society in caring for autistic individuals. Caring for individuals with autism has been compared to treating a patient with cancer, though extended over the duration of a normal lifespan. Autistic children have also been described as being held hostage to a psychiatric disorder. Others have used the term "mad child disease" to describe autism, which some autistic individuals and their parents have found highly offensive. Margaret Somerville, founding director of the McGill Centre for Medicine, Ethics and Law, said that with activism there is a direct goal and it is sometimes necessary to sacrifice complexity and nuance to make a point, but some autistic activists don't believe desperation justifies the rhetoric. Bennett L. Leventhal said he understands concern about comparing autistic children to victims of hostage but thinks the campaigns make the point that these are real diseases that will consume children if untreated. Autistic rights activists also reject terming the reported increase in the autistic population as an 'epidemic' since the word implies autism is a disease.

Attempts have also been made to place a figure on the financial 'cost' of autism, addressed to both scholarly and popular audiences. These efforts have been criticized by some autism rights advocates, comparing it to the now-reviled eugenics movement in the early 20th century. Michelle Dawson has pointed out that no effort has been made to examine the cost of 'eliminating the disease' to autistic individuals, and she, as well as others, have also pointed out the valuable contributions autistic individuals can, and have made to society.

Some autistic rights activists believe some characteristics described as being autistic traits are actually misconceptions. Michelle Dawson has disputed the belief that 75% of autistic people have low intelligence. Psychologist Laurent Mottron of Hôpital Rivière-des-Prairies in Montreal says that autistic people often score much higher on a nonverbal test of abstract reasoning than on a standard IQ test. Some people subscribe to the belief that autistic people lack a "theory of mind"; that is, they are unaware that others do not necessarily think or know the same things that they (autistics) do. Some autistics have claimed that non-autistics are insensitive to their perspectives, and write parodies based on this, addressing non-autism as a mental disorder characterized by lack of "theory of other minds".

Jim Sinclair, who has also been target of similar criticism from very early on, goes into detail about "the politics of opposition to self-advocacy".

The controversy has erupted on autism e-mail lists, where some parents are referred to derogatorily as "curebies" and "portrayed as slaves to conformity, so anxious for their children to appear normal that they cannot respect their way of communicating". These parents respond that this attitude shows "a typical autistic lack of empathy by suggesting that they should not try to help their children". Lenny Schafer said that the autism-like lack of empathy of anti-cure activists prevent them from seeing what is in the hearts of pro-cure advocates.

Some autistic activists say it is not easy to distinguish between high and low functioning. Some autistic individuals, in contrast, are supportive of the distinction between the low and high functioning labels as well as autism and Asperger's, and believe it is important in helping individuals get proper consultation and treatment.

One study said that approximately 78% of persons on the spectrum are high functioning. The research indicated that functional level is not a strong indicator of support services needed—in other words, being high functioning or even very high functioning did not ensure independent living. Two percent of low functioning autistics were found to have stable full-time paid employment, and only 12 percent of high functioning autistics have stable full-time paid employment. Rates of independent living amongst high functioning autistics is only four percent, with a further 13 percent able to live on their own with professional or family support. The impact on caregivers of low functioning autistics is enormous, but the impact on caregivers of high functioning autistics is, contrary to popular belief, almost as large. In a 2001 New Scientist interview about Asperger syndrome, Simon Baron-Cohen (an autism researcher) said that Asperger's differs from classic autism in terms of disability because, from the perspective of the person with AS, they may be different, but not disabled, while classic autism causes more difficulties.

A common theme expressed among autism rights activists and neurodiversity groups is that they are different from parent- and professional- led organizations and conferences that dominate the autism scene. Michelle Dawson criticizes the norm of allowing parents to speak on behalf of their autistic children at conferences to the exclusion of autistics. "With the happy and proud collaboration of governments, courts, researchers, service providers, and funding bodies," she says, "parents have succeeded in removing autistics from the vicinity of any important discussions or decisions." This exclusion results in policy and treatment decisions being made soley by individuals who do not directly experience autism.

Jim Sinclair notes that autism conferences are traditionally geared toward neurotypical parents and professionals. To an austic person they may be quite "hostile" in terms of sensory stimulation and rigidity. A key goal of events like Autreat and websites like neurodiversity.com and Real Voices of Autism is to provide a space where autistics are able to communicate in ways and at time that are comfortable to them.

Parents with the perspective of autism as a disorder (which is called the pro-cure perspective in the autism rights movement) believe that a cure for autism is in their children's best interests because they see a cure as something that will reduce suffering. According to The New York Times, these critics say ABA gives autistic children the best chance of success in adulthood. Some parents believe that intensive behavioral therapy is the only way to rescue autistic children. Some critics also fear that the movement will prevent other autistic children from receiving treatment. Kit Weintraub has responded to Michelle Dawson's claims that ABA is harmful by saying that it is harmful to deny medically necessary and appropriate treatment to autistic children who need it. Weintraub said she does not want ideology to triumph over the welfare of autistic children.

The movement has been criticized for its own failure to incorporate diversity, include certain subgroups within the autistic community and that some in the movement are insulting to neurotypical individuals.

There is also controversy about how well autistic people of different functioning levels are represented in the movement. Critics of the movement argue that the autistic spectrum people opposed to a cure are high functioning autistic or have Asperger syndrome and that they have the ability to communicate. Sue Rubin, an adult with autism who was the subject of the Oscar-nominated documentary Autism Is A World, is an example of an adult aligned with the cure group who says that the divide in the autism community is between high-functioning and low-functioning people; she says people with Asperger syndrome can communicate well and "pass for normal", while low-functioning people have severe disabilities. She says "low functioning people are just trying to get through the day without hurting, tapping, flailing, biting, screaming, etc. The thought of a gold pot of a potion with a cure really would be wonderful." Lenny Schafer argues that if one would change every use of autism to read Asperger syndrome the movement might "make sense".

A common complaint is that anti-cure advocates are clearly able to articulate complex opinions in writing, which is seen by some critics as inconsistent with a diagnosis of autism. Some autistic authors such as Amanda Baggs have claimed that this is not always the case that anti-cure autistics have mild difficulties. She says that when the critics assume that intelligent and articulate autistic people do not have difficulties like self-injurious behavior and difficulty with self-care, they affect the opinions of policy makers and make it more difficult for intelligent and articulate autistic people to get services. Baggs cites an example of an autistic person who was denied services based on having an IQ above 70.

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Epidemiology of autism

Reports of autism cases grew dramatically in the U.S. from 1996 to 2007. It is unknown how much, if any, growth came from changes in autism's prevalence.[16]

The epidemiology of autism is the study of factors affecting autism spectrum disorders (ASD). Most recent reviews estimate a prevalence of one to two cases per 1,000 people for autism, and about six per 1,000 for ASD; because of inadequate data, these numbers may underestimate ASD's true prevalence. ASD averages a 4.3:1 male-to-female ratio. The number of children known to have autism has increased dramatically since the 1980s, at least partly due to changes in diagnostic practice; the question of whether actual prevalence has increased is unresolved, and as-yet-unidentified contributing environmental risk factors cannot be ruled out. The risk of autism is associated with several prenatal and perinatal factors, including advanced parental age and low birth weight. ASD is associated with several genetic disorders and with epilepsy, and autism is associated with mental retardation.

Autism is a complex neurodevelopmental disorder. Many causes have been proposed, but its theory of causation is still incomplete. Autism is largely inherited, although the genetics of autism are complex and it is generally unclear which genes are responsible. Although a link between autism and environmental exposures is plausible, little evidence exists to support associations with specific environmental exposures. In rare cases, autism is strongly associated with agents that cause birth defects. Other proposed causes, such as childhood vaccines, are controversial and the vaccine hypotheses lack convincing scientific evidence.

Although incidence rates measure autism risk directly, most epidemiological studies report other frequency measures, typically point or period prevalence, or sometimes cumulative incidence. Attention is focused mostly on whether prevalence is increasing with time.

When studying how diseases are caused, incidence rates are the most appropriate measure of disease frequency as they assess risk directly. However, incidence can be difficult to measure with rarer chronic diseases such as autism. In autism epidemiology, point or period prevalence is more useful than incidence, as the disorder starts long before it is diagnosed, and the gap between initiation and diagnosis is influenced by many factors unrelated to risk. Research focuses mostly on whether point or period prevalence is increasing with time; cumulative incidence is sometimes used in studies of birth cohorts.

The three basic approaches used to estimate prevalence differ in cost and in quality of results. The simplest and cheapest method is to count known autism cases from sources such as schools and clinics, and divide by the population. This approach is likely to underestimate prevalence because it does not count children who have not been diagnosed yet, and it is likely to generate skewed statistics because some children have better access to treatment. The second method improves on the first by having investigators examine student or patient records looking for probable cases, to catch cases that have not been identified yet. The third method, which is arguably the best, screens a large sample of an entire community to identify possible cases, and then evaluates each possible case in more detail with standard diagnostic procedures. This last method typically produces the most reliable, and the highest, prevalence estimates.

Estimates of the prevalence of autism vary widely depending on diagnostic criteria, age of children screened, and geographical location. Most recent reviews tend to estimate a prevalence of 1–2 per 1,000 for autism and close to 6 per 1,000 for ASD; PDD-NOS is the vast majority of ASD, Asperger's is about 0.3 per 1,000 and the atypical forms childhood disintegrative disorder and Rett syndrome are much rarer. A 2006 study of nearly 57,000 British nine- and ten-year-olds reported a prevalence of 3.89 per 1,000 for autism and 11.61 per 1,000 for ASD; these higher figures could be associated with broadening diagnostic criteria. Studies based on more-detailed information, such as direct observation rather than examination of medical records, identify higher prevalence; this suggests that published figures may underestimate ASD's true prevalence.

Attention has been focused on whether the prevalence of autism is increasing with time. Earlier prevalence estimates were lower, centering at about 0.5 per 1,000 for autism during the 1960s and 1970s and about 1 per 1,000 in the 1980s, as opposed to today's 1–2 per 1,000.

The reported increase is largely attributable to changes in diagnostic practices, referral patterns, availability of services, age at diagnosis, and public awareness. A widely cited 2002 pilot study concluded that the observed increase in autism in California cannot be explained by changes in diagnostic criteria, but a 2006 analysis found that special education data poorly measured prevalence because so many cases were undiagnosed, and that the 1994–2003 U.S. increase was associated with declines in other diagnostic categories, indicating that diagnostic substitution had occurred. A 2007 study that modeled autism incidence found that broadened diagnostic criteria, diagnosis at a younger age, and improved efficiency of case ascertainment, can produce an increase in the frequency of autism ranging up to 29-fold depending on the frequency measure, suggesting that methodological factors may explain the observed increases in autism over time. A small 2008 study found that a significant number (40%) of people diagnosed with pragmatic language impairment as children in previous decades would now be given a diagnosis as autism. A study of all Danish children born in 1994–99 found that children born later were more likely to be diagnosed at a younger age, supporting the argument that apparent increases in autism prevalence were at least partly due to decreases in the age of diagnosis. A 2009 study of California data found that the reported incidence of autism rose 7- to 8-fold from the early 1990s to 2007, and that changes in diagnostic criteria, inclusion of milder cases, and earlier age of diagnosis probably explain only a 4.25-fold increase; the study did not quantify the effects of wider awareness of autism, increased funding, and expanding treatment options resulting in parents' greater motivation to seek services.

Several contributing environmental risk factors have been proposed to support the hypothesis that the actual frequency of autism has increased. These include certain foods, infectious disease, pesticides, MMR vaccine, and vaccines containing the preservative thiomersal, formerly used in several childhood vaccines in the U.S. Although there is overwhelming scientific evidence against the MMR hypothesis and no convincing evidence for the thiomersal hypothesis, other as-yet-unidentified contributing environmental risk factors cannot be ruled out. Although it is unknown whether autism's frequency has increased, any such increase would suggest directing more attention and funding toward changing environmental factors instead of continuing to focus on genetics.

The prevalence of autism in Africa is unknown.

A 2008 Australian study reported wide variation and inconsistent results in prevalence estimates; for example, national estimates for the prevalence of ASD in Australia ranged from 1.21 to 3.57 per 1,000 for children aged 6–12 years. The study concluded that the prevalence of ASD in Australian children cannot be estimated accurately from existing data.

A 2008 Hong Kong study reported an ASD incidence rate similar to those reported in Australia and North America, and lower than Europeans. It also reported a prevalence of 1.68 per 1,000 for children under 15 years.

A 2003 study reported that the cumulative incidence of autism in Denmark began a steep increase starting around 1990, and continued to grow until 2000, despite the withdrawal of thiomersal-containing vaccines in 1992. For example, for children aged 2–4 years, the cumulative incidence was about 0.5 new cases per 10,000 children in 1990 and about 4.5 new cases per 10,000 children in 2000.

A 2008 study found that inpatient admission rates for children with ASD increased 30% from 2000 to 2005, with the largest rise between 2000 and 2001 and a decline between 2001 and 2003. Inpatient rates for all mental disorders also rose for ages up to 15 years, so that the ratio of ASD to all admissions rose from 1.3% to 1.4%.

A 2005 study of a part of Yokohama with a stable population of about 300,000 reported a cumulative incidence to age 7 years of 48 cases of ASD per 10,000 children in 1989, and 86 in 1990. After the vaccination rate of MMR vaccine dropped to near zero, the incidence rate grew to 97 and 161 cases per 10,000 children in 1993 and 1994, respectively, indicating that MMR vaccine did not cause autism.

The incidence and changes in incidence with time are unclear in the UK. The reported autism incidence in the UK rose starting before the first introduction of the MMR vaccine in 1989. A 2004 study found that the reported incidence of pervasive developmental disorders in a general practice research database in England and Wales grew steadily during 1988–2001 from 0.11 to 2.98 per 10,000 person-years, and concluded that much of this increase may be due to changes in diagnostic practice.

The number of diagnosed cases of autism grew dramatically in the U.S. in the 1990s and early 2000s. For example, in 1996, 21,669 children and students aged 6–11 years diagnosed with autism were served under Part B of the Individuals with Disabilities Education Act (IDEA) in the U.S. and outlying areas; by 2001 this number had risen to 64,094, and by 2005 to 110,529. These numbers measure what is sometimes called "administrative prevalence", that is, the number of known cases per unit of population, as opposed to the true number of cases.

A population-based study of one Minnesota county found that the cumulative incidence of autism grew eightfold from the 1980–83 period to the 1995–97 period. The increase occurred after the introduction of broader, more-precise diagnostic criteria, increased service availability, and increased awareness of autism. During the same period, the reported number of autism cases grew 22-fold in the same location, suggesting that counts reported by clinics or schools provide misleading estimates of the true incidence of autism.

A 2008 study reported a prevalence of 1.1 per 1000 for autism and 1.7 per 1000 for ASD.

As late as the mid-1970s there was little evidence of a genetic role in autism; evidence from genetic epidemiology studies now suggests that it is one of the most heritable of all psychiatric conditions. The first studies of twins estimated heritability to be more than 90%; in other words, that genetics explains more than 90% of autism cases. When only one identical twin is autistic, the other often has learning or social disabilities. For adult siblings, the risk of having one or more features of the broader autism phenotype might be as high as 30%, much higher than the risk in controls. About 10–15% of autism cases have an identifiable Mendelian (single-gene) condition, chromosome abnormality, or other genetic syndrome, and ASD is associated with several genetic disorders.

Since heritability is less than 100% and symptoms vary markedly among identical twins with autism, environmental factors are most likely a significant cause as well. If some of the risk is due to gene-environment interaction the 90% heritability estimate may be too high; new twin data and models with structural genetic variation are needed.

Genetic linkage analysis has been inconclusive; many association analyses have had inadequate power. Studies have examined more than 100 candidate genes; many genes must be examined because more than a third of genes are expressed in the brain and there are few clues on which are relevant to autism.

Boys are at higher risk for autism than girls. The ASD sex ratio averages 4.3:1 and is greatly modified by cognitive impairment: it may be close to 2:1 with mental retardation and more than 5.5:1 without. Recent studies have found no association with socioeconomic status, and have reported inconsistent results about associations with race or ethnicity.

The risk of autism is associated with several prenatal and perinatal risk factors. A 2007 review of risk factors found associated parental characteristics that included advanced maternal age, advanced paternal age, and maternal place of birth outside Europe or North America, and also found associated obstetric conditions that included low birth weight and gestation duration, and hypoxia during childbirth. It is not known whether mutations that arise spontaneously in autism and other neuropsychiatric disorders come mainly from the mother or the father, or whether the mutations are associated with parental age.

A large 2008 population study of Swedish parents of children with autism found that the parents were more likely to have been hospitalized for a mental disorder, that schizophrenia was more common among the mothers and fathers, and that depression and personality disorders were more common among the mothers.

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