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Autism is a neurodevelopmental disorder characterized by impaired social interaction, verbal andnon-verbal communication, and restricted and repetitive behavior. Parents usually notice signs in the first two years of their child's life.[1] These signs often develop gradually, though some children with autism reach their developmental milestones at a normal pace and then regress.[2] The diagnostic criteria require that symptoms become apparent in early childhood, typically before age three.[3]
Autism is due to a combination of genetic and environmental factors.[4] Some cases are strongly associated with certain infections during pregnancy including rubella and use of alcohol or cocaine.[5]Controversies surround other proposed environmental causes;[6] for example, the vaccine hypotheses, which have since been disproven. Autism affects information processing in the brain by altering how nerve cells and their synapses connect and organize; how this occurs is not well understood.[7] In the DSM V, autism is included within the autism spectrum (ASDs), as is Asperger syndrome, which lacks delays in cognitive development and language, and pervasive developmental disorder, not otherwise specified (commonly abbreviated as PDD-NOS), which was diagnosed when the full set of criteria for autism or Asperger syndrome were not met.[8][3]
Early speech or behavioral interventions can help children with autism gain self-care, social, and communication skills.[9] Although there is no known cure,[9] there have been reported cases of children who recovered.[10] Not many children with autism live independently after reaching adulthood, though some become successful.[11] An autistic culture has developed, with some individuals seeking a cure and others believing autism should be accepted as a difference and not treated as a disorder.[12]
Globally, autism is estimated to affect 21.7 million people as of 2013.[13] As of 2010, the number of people affected is estimated at about 1–2 per 1,000 worldwide. It occurs four to five times more often in boys than girls. About 1.5% of children in the United States (one in 68) are diagnosed with ASD as of 2014, a 30% increase from one in 88 in 2012.[14][15][16] The rate of autism among adults aged 18 years and over in the United Kingdom is 1.1%.[17] The number of people diagnosed has been increasing dramatically since the 1980s, partly due to changes in diagnostic practice and government-subsidized financial incentives for named diagnoses;[16] the question of whether actual rates have increased is unresolved.[18]
Autism is a highly variable neurodevelopmental disorder[19] that first appears during infancy or childhood, and generally follows a steady course without remission.[20] People with autism may be severely impaired in some respects but normal, or even superior, in others.[21] Overt symptoms gradually begin after the age of six months, become established by age two or three years,[22] and tend to continue through adulthood, although often in more muted form.[23] 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.[24] Autism's individual symptoms occur in the general population and appear not to associate highly, without a sharp line separating pathologically severe from common traits.[25]
Social development
Social deficits distinguish autism and the related autism spectrum disorders (ASD; see Classification) from other developmental disorders.[23] 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".[26]
Unusual social development becomes 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 differ more strikingly from social norms; for example, they have less eye contact and turn-taking, and do not have the ability to use simple movements to express themselves, such as pointing at things.[27] Three- to five-year-old children with autism 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.[28] Most children with autism display moderately less attachment security than neurotypical children, although this difference disappears in children with higher mental development or less severe ASD.[29] Older children and adults with ASD perform worse on tests of face and emotion recognition[30] although this may be partly due to a lower ability to define a person's own emotions.[31]
Children with high-functioning autism suffer from more intense and frequent loneliness compared to non-autistic peers, despite the common belief that children with autism 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. Functional friendships, such as those resulting in invitations to parties, may affect the quality of life more deeply.[32]
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 intellectual disability, autism is associated with aggression, destruction of property, and tantrums.[33]
About a third to a half of individuals with autism do not develop enough natural speech to meet their daily communication needs.[34] 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, children with autism have less frequent and less diverse babbling, consonants, words, and word combinations; their gestures are less often integrated with words. Children with autism are less likely to make requests or share experiences, and are more likely to simply repeat others' words (echolalia)[35][36] or reverse pronouns.[37] Joint attention seems to be necessary for functional speech, and deficits in joint attention seem to distinguish infants with ASD:[8] for example, they may look at a pointing hand instead of the pointed-at object,[27][36] and they consistently fail to point at objects in order to comment on or share an experience.[8] Children with autism may have difficulty with imaginative play and with developing symbols into language.[35][36]
In a pair of studies, high-functioning children with autism aged 8–15 performed equally well as, 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.[38]
Repetitive behavior
Autistic individuals can display many forms of repetitive or restricted behavior, which the Repetitive Behavior Scale-Revised (RBS-R) categorizes as follows.[39]

  • Stereotyped behaviors: Repetitive movements, such as hand flapping, head rolling, or body rocking.
  • Compulsive behaviors: Time-consuming behaviors intended to reduce anxiety that an individual feels compelled to perform repeatedly or according to rigid rules, such as placing objects in a specific order, checking things, or hand washing.
  • Sameness: Resistance to change; for example, insisting that the furniture not be moved or refusing to be interrupted.
  • Ritualistic behavior: Unvarying pattern of daily activities, such as an unchanging menu or a dressing ritual. This is closely associated with sameness and an independent validation has suggested combining the two factors.[39]
  • Restricted interests: Interests or fixations that are abnormal in theme or intensity of focus, such as preoccupation with a single television program, toy, or game.
  • Self-injury: Behaviors such as eye-poking, skin-picking, hand-biting and head-banging.[8]

No single repetitive or self-injurious behavior seems to be specific to autism, but autism appears to have an elevated pattern of occurrence and severity of these behaviors.[40]
Other symptoms
Autistic individuals may have symptoms that are independent of the diagnosis, but that can affect the individual or the family.[24] 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.[41] Many individuals with ASD show superior skills in perception and attention, relative to the general population.[42] Sensoryabnormalities are found in over 90% of those with autism, and are considered core features by some,[43] although there is no good evidence that sensory symptoms differentiate autism from other developmental disorders.[44] Differences are greater for under-responsivity (for example, walking into things) than for over-responsivity (for example, distress from loud noises) or for sensation seeking (for example, rhythmic movements).[45] An estimated 60%–80% of autistic people have motor signs that include poor muscle tone, poor motor planning, and toe walking;[43] deficits in motor coordination are pervasive across ASD and are greater in autism proper.[46]
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;[47] this does not appear to result in malnutrition. Although some children with autism also have gastrointestinal symptoms, there is a lack of published rigorous data to support the theory that children with autism have more or different gastrointestinal symptoms than usual;[48] studies report conflicting results, and the relationship between gastrointestinal problems and ASD is unclear.[49]
Parents of children with ASD have higher levels of stress.[27] Siblings of children with ASD report greater admiration of and less conflict with the affected sibling than siblings of unaffected children and were similar to siblings of children with Down syndrome in these aspects of the sibling relationship. However, they reported lower levels of closeness and intimacy than siblings of children with Down syndrome; siblings of individuals with ASD have greater risk of negative well-being and poorer sibling relationships as adults.[50]
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.[51]However, there is increasing suspicion that autism is instead a complex disorder whose core aspects have distinct causes that often co-occur.[51][52]
Three diagrams of chromosome pairs A, B that are nearly identical. 1: B is missing a segment of A. 2: B has two adjacent copies of a segment of A. 3: B's copy of A's segment is in reverse order.Three diagrams of chromosome pairs A, B that are nearly identical. 1: B is missing a segment of A. 2: B has two adjacent copies of a segment of A. 3: B's copy of A's segment is in reverse order.
Deletion (1), duplication (2) and inversion (3) are all chromosome abnormalities that have been implicated in autism.[53]
Autism has a strong genetic basis, although the genetics of autism are complex and it is unclear whether ASD is explained more by rare mutations with major effects, or by rare multigene interactions of common genetic variants.[54][55] Complexity arises due to interactions among multiple genes, the environment, and epigeneticfactors which do not change DNA sequencing but are heritable and influence gene expression.[23] Many genes have been associated with autism through sequencing the genomes of affected individuals and their parents.[56]
Studies of twins suggest that heritability is 0.7 for autism and as high as 0.9 for ASD, and siblings of those with autism are about 25 times more likely to be autistic than the general population.[43] 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, and none of the genetic syndromes associated with ASDs have been shown to selectively cause ASD.[54] Numerous candidate genes have been located, with only small effects attributable to any particular gene.[54] Most loci individually explain less than 1% of cases of autism.[57] The large number of autistic individuals with unaffected family members may result from spontaneousstructural variation — such as deletions, duplications or inversions in genetic material during meiosis.[58][59] 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.[53]
Several lines of evidence point to synaptic dysfunction as a cause of autism.[7] Some rare mutations may lead to autism by disrupting some synaptic pathways, such as those involved with cell adhesion.[60] 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.[61] 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, there is strong evidence that autism arises very early in development.[62]
Exposure to air pollution during pregnancy, especially heavy metals and particulates, may increase the risk of autism.[63] Environmental factors that have been claimed without evidence to contribute to or exacerbate autism include certain foods, infectious diseases, solvents, diesel exhaust, PCBs, phthalatesand phenols used in plastic products, pesticides, brominated flame retardants, alcohol, smoking, illicit drugs, vaccines,[18] and prenatal stress. No evidence has been found for these claims, and some such as the MMR vaccine have been completely disproven.[64]
Parents may first become aware of autistic symptoms in their child around the time of a routine vaccination. This has led to unsupported theories blamingvaccine "overload", a vaccine preservative, or the MMR vaccine for causing autism.[65] The latter theory was supported by a litigation-funded study that has since been shown to have been "an elaborate fraud".[66] Although these theories lack convincing scientific evidence and are biologically implausible,[65] parental concern about a potential vaccine link with autism has led to lower rates of childhood immunizations, outbreaks of previously controlled childhood diseases in some countries, and the preventable deaths of several children.[67][68]
Autism's symptoms result from maturation-related changes in various systems of the brain. 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.[69] The behaviors appear to have multiple pathophysiologies.[25]
Unlike many other brain disorders, such as Parkinson's, autism does not have a clear unifying mechanism at either the molecular, cellular, or systems level; it is not known whether autism is a few disorders caused by mutations converging on a few common molecular pathways, or is (like intellectual disability) a large set of disorders with diverse mechanisms.[19] Autism appears to result from developmental factors that affect many or all functional brain systems,[71] and to disturb the timing of brain development more than the final product.[70]Neuroanatomical studies and the associations with teratogens strongly suggest that autism's mechanism includes alteration of brain development soon after conception.[62] This anomaly appears to start a cascade of pathological events in the brain that are significantly influenced by environmental factors.[72] Just after birth, the brains of children with autism tend to grow faster than usual, followed by normal or relatively slower growth in childhood. It is not known whether early overgrowth occurs in all children with autism. It seems to be most prominent in brain areas underlying the development of higher cognitive specialization.[43] Hypotheses for the cellular and molecular bases of pathological early overgrowth include the following:

The immune system is thought to play an important role in autism. Children with autism have been found by researchers to have inflammation of both the peripheral and central immune systems as indicated by increased levels of pro-inflammatory cytokines and significant activation of microglia.[80][81][82]Biomarkers of abnormal immune function have also been associated with increased impairments in behaviors that are characteristic of the core features of autism such as deficits in social interactions and communication.[81] 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. It is thought that activation of a pregnant mother's immune system such as from environmental toxicants or infection can contribute to causing autism through causing a disruption of brain development.[83][84][85] This is supported by recent studies that have found that infection during pregnancy is associated with an increased risk of autism.[86][87]
The relationship of neurochemicals to autism is not well understood; several have been investigated, with the most evidence for the role of serotonin and of genetic differences in its transport.[7] The role of group I metabotropic glutamate receptors (mGluR) in the pathogenesis of fragile X syndrome, the most common identified genetic cause of autism, has led to interest in the possible implications for future autism research into this pathway.[88] Some data suggests neuronal overgrowth potentially related to an increase in several growth hormones[89] or to impaired regulation of growth factor receptors. Also, some inborn errors of metabolism are associated with autism, but probably account for less than 5% of cases.[90]
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 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.[91] 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 syndrome, and a correlation between reduced MNS activity and severity of the syndrome in children with ASD.[92] However, individuals with autism also have abnormal brain activation in many circuits outside the MNS[93] and the MNS theory does not explain the normal performance of children with autism on imitation tasks that involve a goal or object.[94]
ASD-related patterns of low function and aberrant activation in the brain differ depending on whether the brain is doing social or nonsocial tasks.[96] 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[//clarification needed//]. In people with autism the two networks are not negatively correlated in time, suggesting an imbalance in toggling between the two networks, possibly reflecting a disturbance of self-referential thought.[97]
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.[98] Evidence for this theory has been found in functional neuroimaging studies on autistic individuals[38] and by a brainwave 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.[99] Other evidence suggests the underconnectivity is mainly within each hemisphere of the cortex and that autism is a disorder of the association cortex.[100]
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, orientation to auditory and visual stimuli, novelty detection, language and face processing, and information storage; several studies have found a preference for nonsocial stimuli.[101] For example, magnetoencephalography studies have found evidence in children with autism of delayed responses in the brain's processing of auditory signals.[102]
In the genetic area, relations have been found between autism and schizophrenia based on duplications and deletions of chromosomes; research showed that schizophrenia and autism are significantly more common in combination with 1q21.1 deletion syndrome. Research on autism/schizophrenia relations for chromosome 15 (15q13.3), chromosome 16 (16p13.1) and chromosome 17 (17p12) are inconclusive.[103]
Functional connectivity studies have found both hypo- and hyper-connectivity in brains of people with autism. Hypo-connectivity seems to dominate, especially for interhemispheric and cortico-cortical functional connectivity.[104]
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. Simon Baron-Cohen's empathizing–systemizing theory postulates that autistic individuals can systemize—that is, they can develop internal rules of operation to handle events inside the brain—but are less effective at empathizing by handling events generated by other agents. An extension, the extreme male brain theory, hypothesizes that autism is an extreme case of the male brain, defined psychometrically as individuals in whom systemizing is better than empathizing.[105] These theories are somewhat related to Baron-Cohen's earlier theory of mind approach, which hypothesizes that autistic behavior arises from an inability to ascribe mental states to oneself and others. The theory of mind hypothesis is supported by the atypical responses of children with autism to the Sally–Anne test for reasoning about others' motivations,[105] and the mirror neuron system theory of autism described in //Pathophysiology// maps well to the hypothesis.[92] However, most studies have found no evidence of impairment in autistic individuals' ability to understand other people's basic intentions or goals; instead, data suggests that impairments are found in understanding more complex social emotions or in considering others' viewpoints.[106]
The second category focuses on nonsocial or general processing: the executive functions such as working memory, planning, inhibition. In his review, Kenworthy states that "the claim of executive dysfunction as a causal factor in autism is controversial", however, "it is clear that executive dysfunction plays a role in the social and cognitive deficits observed in individuals with autism".[107] Tests of core executive processes such as eye movement tasks indicate improvement from late childhood to adolescence, but performance never reaches typical adult levels.[108] A strength of the theory is predicting stereotyped behavior and narrow interests;[109] two weaknesses are that executive function is hard to measure[107] and that executive function deficits have not been found in young children with autism.[30]
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.[110] A related theory—enhanced perceptual functioning—focuses more on the superiority of locally oriented and perceptual operations in autistic individuals.[111] 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.[52] A combined theory based on multiple deficits may prove to be more useful.[112]
Diagnosis is based on behavior, not cause or mechanism.[25][113] Under the DSM-5, autism is characterized by persistent deficits in social communication and interaction across multiple contexts, as well as restricted, repetitive patterns of behavior, interests, or activities. These deficits are present in early childhood, typically before age three, and lead to clinically significant functional impairment. Sample symptoms include lack of social or emotional reciprocity, stereotyped and repetitive use of language or idiosyncratic language, and persistent preoccupation with unusual objects. The disturbance must not be better accounted for by Rett syndrome, intellectual disability or global developmental delay.[3] ICD-10 uses essentially the same definition.[20]
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)[114] uses observation and interaction with the child. TheChildhood Autism Rating Scale (CARS) is used widely in clinical environments to assess severity of autism based on observation of children.[27] The Diagnostic interview for social and communication disorders (DISCO) may also be used.[115]
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.[116] A pediatric neuropsychologist is often asked to assess behavior and cognitive skills, both to aid diagnosis and to help recommend educational interventions.[117] A differential diagnosis for ASD at this stage might also consider intellectual disability, hearing impairment, and a specific language impairment[116] such as Landau–Kleffner syndrome.[118] The presence of autism can make it harder to diagnose coexisting psychiatric disorders such as depression.[119]
Clinical genetics evaluations are often done once ASD is diagnosed, particularly when other symptoms already suggest a genetic cause.[120] Although genetic technology allows clinical geneticists to link an estimated 40% of cases to genetic causes,[121] consensus guidelines in the US and UK are limited to high-resolution chromosome and fragile X testing.[120] A genotype-first model of diagnosis has been proposed, which would routinely assess the genome's copy number variations.[122] 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.[123] Metabolic and neuroimaging tests are sometimes helpful, but are not routine.[120]
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.[1] 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.[116] Although the symptoms of autism and ASD begin early in childhood, they are sometimes missed; years later, 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.[124] 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 or blindisms.[125]
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.[20] These symptoms do not imply sickness, fragility, or emotional disturbance.[23]
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.[126] Unlike with autism, people with Asperger syndrome have no substantial delay in language development.[127] The terminology of autism can be bewildering, with autism, Asperger syndrome and PDD-NOS often called the autism spectrum disorders (ASD)[9] or sometimes the autistic disorders,[128] 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.[120] ASD, in turn, is a subset of the broader autism phenotype, which describes individuals who may not have ASD but do have autistic-like traits, such as avoiding eye contact.[129]
The manifestations of autism cover a wide spectrum, ranging from individuals with severe impairments—who may be silent, developmentally 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.[130] Because the behavior spectrum is continuous, boundaries between diagnostic categories are necessarily somewhat arbitrary.[43] Sometimes the syndrome is divided into low-, medium- or high-functioning autism (LFA, MFA, and HFA), based on IQthresholds,[131] 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; the syndromal autism is associated with severe or profound intellectual disability or a congenital syndrome with physical symptoms, such as tuberous sclerosis.[132] Although individuals with Asperger syndrome tend to perform better cognitively than those with autism, the extent of the overlap between Asperger syndrome, HFA, and non-syndromal autism is unclear.[133]
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,[2][35][1][134] or that there is a continuum of behaviors between autism with and without regression.[135]
Research into causes has been hampered by the inability to identify biologically meaningful subgroups within the autistic population[136] and by the traditional boundaries between the disciplines of psychiatry, psychology, neurology and pediatrics.[137] Newer technologies such as fMRI and diffusion tensor imaging can help identify biologically relevant phenotypes (observable traits) that can be viewed on brain scans, to help further neurogeneticstudies of autism;[138] one example is lowered activity in the fusiform face area of the brain, which is associated with impaired perception of people versus objects.[7] It has been proposed to classify autism using genetics as well as behavior.[139]
About half of parents of children with ASD notice their child's unusual behaviors by age 18 months, and about four-fifths notice by age 24 months.[1]According to an article failure to meet any of the following milestones "is an absolute indication to proceed with further evaluations. Delay in referral for such testing may delay early diagnosis and treatment and affect the long-term outcome".[24]

  • No babbling by 12 months.
  • No gesturing (pointing, waving, etc.) by 12 months.
  • No single words by 16 months.
  • No two-word (spontaneous, not just echolalic) phrases by 24 months.
  • Any loss of any language or social skills, at any age.

The United States Preventive Services Task Force in 2016 found it was unclear if screening was beneficial or harmful among children in whom there is no concerns.[140] The Japanese practice is to screen all children for ASD at 18 and 24 months, using autism-specific formal screening tests. In contrast, in the UK, children whose families or doctors recognize possible signs of autism are screened. It is not known which approach is more effective.[7] 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, the Checklist for Autism in Toddlers (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).[1] It may be more accurate to precede these tests with a broadband screener that does not distinguish ASD from other developmental disorders.[141] Screening tools designed for one culture's norms for behaviors like eye contact may be inappropriate for a different culture.[142] Although genetic screening for autism is generally still impractical, it can be considered in some cases, such as children with neurological symptoms and dysmorphic features.[143]
Infection with rubella during pregnancy causes fewer than 1% of cases of autism;[144] vaccination against rubella can prevent many of those cases.[145]
The main goals when treating children with autism are to lessen associated deficits and family distress, and to increase quality of life and functional independence. In general, higher IQs are correlated with greater responsiveness to treatment and improved treatment outcomes.[146][147] No single treatment is best and treatment is typically tailored to the child's needs.[9] Families and the educational system are the main resources for treatment.[7] Studies of interventions have methodological problems that prevent definitive conclusions aboutefficacy,[148] however the development of evidence-based interventions has advanced in recent years.[146]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.[149] Intensive, sustained special education programs and behavior therapy early in life can help children acquire self-care, social, and job skills,[9] and often improve functioning and decrease symptom severity and maladaptive behaviors;[150] claims that intervention by around age three years is crucial are not substantiated.[151] Available approaches include applied behavior analysis (ABA), developmental models,structured teaching, speech and language therapy, social skills therapy, and occupational therapy.[9] Among these approaches, interventions either treat autistic features comprehensively, or focalize treatment on a specific area of deficit.[146] There is some evidence that early intensive behavioral intervention (EIBI), an early intervention model based on ABA for 20 to 40 hours a week for multiple years, is an effective treatment for some children with ASD.[152] Two theoretical frameworks outlined for early childhood intervention include applied behavioral analysis (ABA) and developmental social pragmatic models (DSP).[146] One interventional strategy utilizes a parent training model, which teaches parents how to implement various ABA and DSP techniques, allowing for parents to disseminate interventions themselves.[146] Various DSP programs have been developed to explicitly deliver intervention systems through at-home parent implementation. Despite the recent development of parent training models, these interventions have demonstrated effectiveness in numerous studies, being evaluated as a probable efficacious mode of treatment.[146]
Educational interventions can be effective to varying degrees in most children: intensive ABA treatment has demonstrated effectiveness in enhancing global functioning in preschool children[153] and is well-established for improving intellectual performance of young children.[150] Similarly, teacher-implemented intervention that utilizes an ABA combined with a developmental social pragmatic approach has been found to be a well-established treatment in improving social-communication skills in young children, although there is less evidence in its treatment of global symptoms.[146]Neuropsychological reports are often poorly communicated to educators, resulting in a gap between what a report recommends and what education is provided.[117] It is not known whether treatment programs for children lead to significant improvements after the children grow up,[150] and the limited research on the effectiveness of adult residential programs shows mixed results.[154] The appropriateness of including children with varying severity of autism spectrum disorders in the general education population is a subject of current debate among educators and researchers.[155]
Many medications are used to treat ASD symptoms that interfere with integrating a child into home or school when behavioral treatment fails.[23][156] More than half of US children diagnosed with ASD are prescribed psychoactive drugs or anticonvulsants, with the most common drug classes beingantidepressants, stimulants, and antipsychotics.[157] Antipsychotics, such as risperidone and aripiprazole, have been found to be useful for treating irritability, repetitive behavior, and sleeplessness that often occurs with autism, however their side effects must be weighed against their potential benefits, and people with autism may respond atypically.[158] There is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD.[159] No known medication relieves autism's core symptoms of social and communication impairments.[160] Experiments in mice have reversed or reduced some symptoms related to autism by replacing or modulating gene function,[61][88] suggesting the possibility of targeting therapies to specific rare mutations known to cause autism.[60][161]
Alternative medicine
Although many alternative therapies and interventions are available, few are supported by scientific studies.[30][162] 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.[32]Scientific evidence appears to matter less to service providers than program marketing, training availability, and parent requests.[163] Some alternative treatments 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;[164] in 2005, botched chelation therapy killed a five-year-old child with autism.[165] There has been early research looking at hyperbaric treatmentsin children with autism.[166]
Although popularly used as an alternative treatment for people with autism, there is no good evidence that a gluten-free diet is of benefit.[167][168][169] In the subset of people who have gluten sensitivity there is limited evidence that suggests that a gluten free diet may improve some autistic behaviors.[167][170][171][172]
Treatment is expensive; indirect costs are more so. For someone born in 2000, a US study estimated an average lifetime cost of $4.11 million (net present value in 2017 dollars, inflation-adjusted from 2003 estimate),[173] with about 10% medical care, 30% extra education and other care, and 60% lost economic productivity.[174] 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;[175] one 2008 US study found a 14% average loss of annual income in families of children with ASD,[176] and a related study found that ASD is associated with higher probability that child care problems will greatly affect parental employment.[177] US states increasingly require private health insurance to cover autism services, shifting costs from publicly funded education programs to privately funded health insurance.[178] After childhood, key treatment issues include residential care, job training and placement, sexuality, social skills, and estate planning.[179]
Society and culture
The emergence of the autism rights movement has served as an attempt to encourage people to be more tolerant of those with autism.[180] Through this movement, people hope to cause others to think of autism as a difference instead of a disease. Proponents of this movement wish to seek "acceptance, not cures."[181] There have also been many worldwide events promoting autism awareness such as World Autism Awareness Day, Light It Up Blue,Autism Sunday, Autistic Pride Day, Autreat, and others.[182][183][184][185][186] There have also been many organizations dedicated to increasing the awareness of autism and the effects that autism has on someone’s life. These organizations include Autism Speaks, Autism National Committee, Autism Society of America, and many others.[187] Social-science scholars have had an increased focused on studying those with autism in hopes to learn more about "autism as a culture, transcultural comparisons… and research on social movements."[188] Media has had an influence on how the public perceives those with autism. //Rain Man//, a film that won 4 Oscars including Best Picture, depicts a character with autism who has incredible talents and abilities.[189] While many autistics don't have these special abilities, there are some autistic individuals who have been successful in their fields.[190][191][192]
There is no known cure.[9][7] Children recover occasionally, so that they lose their diagnosis of ASD;[10] this occurs sometimes after intensive treatment and sometimes not. It is not known how often recovery happens;[150] reported rates in unselected samples of children with ASD have ranged from 3% to 25%.[10] Most children with autism acquire language by age five or younger, though a few have developed communication skills in later years.[193] Most children with autism lack social support, meaningful relationships, future employment opportunities or self-determination.[32] Although core difficulties tend to persist, symptoms often become less severe with age.[23]
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.[194] 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.[195] Most people with autism face significant obstacles in transitioning to adulthood.[196]
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,[18] and 11 per 1,000 children in the United States for ASD as of 2008;[15][144] because of inadequate data, these numbers may underestimate ASD's true rate.[120] Globally, autism affects an estimated 21.7 million people as of 2013, while Asperger syndrome affects a further 31.1 million.[13] In 2012, the NHS estimated that the overall prevalence of autism among adults aged 18 years and over in the UK was 1.1%.[17] Rates of PDD-NOS's has been estimated at 3.7 per 1,000, Asperger syndrome at roughly 0.6 per 1,000, and childhood disintegrative disorder at 0.02 per 1,000.[197] CDC's most recent estimate is that 1 out of every 68 children, or 14.7 per 1,000, has an ASD as of 2010.[198]
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,[197][199] though unidentified environmental risk factors cannot be ruled out.[6] The available evidence does not rule out the possibility that autism's true prevalence has increased;[197] a real increase would suggest directing more attention and funding toward changing environmental factors instead of continuing to focus on genetics.[200]
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 intellectual disability and more than 5.5:1 without.[18] Several theories about the higher prevalence in males have been investigated, but the cause of the difference is unconfirmed;[84] one theory is that females are underdiagnosed.[201]
Although the evidence does not implicate any single pregnancy-related risk factor as a cause of autism, the risk of autism is associated with advanced age in either parent, and with diabetes, bleeding, and use of psychiatric drugs in the mother during pregnancy.[84][202] The risk is greater with older fathers than with older mothers; two potential explanations are the known increase in mutation burden in older sperm, and the hypothesis that men marry later if they carry genetic liability and show some signs of autism.[43] Most professionals believe that race, ethnicity, and socioeconomic background do not affect the occurrence of autism.[203]
Several other conditions are common in children with autism.[7] They include:

  • **Genetic disorders**. About 10–15% of autism cases have an identifiable Mendelian (single-gene) condition, chromosome abnormality, or other genetic syndrome,[204] and ASD is associated with several genetic disorders.[205]
  • **Intellectual disability**. The percentage of autistic individuals who also meet criteria for intellectual disability has been reported as anywhere from 25% to 70%, a wide variation illustrating the difficulty of assessing autistic intelligence.[206] In comparison, for PDD-NOS the association with intellectual disability is much weaker,[207] and by definition, the diagnosis of Asperger's excludes intellectual disability.[208]
  • **Anxiety disorders** are common among children with ASD; there are no firm data, but studies have reported prevalences ranging from 11% to 84%. Many anxiety disorders have symptoms that are better explained by ASD itself, or are hard to distinguish from ASD's symptoms.[209]
  • **Epilepsy**, with variations in risk of epilepsy due to age, cognitive level, and type of language disorder.[210]
  • Several **metabolic defects**, such as phenylketonuria, are associated with autistic symptoms.[90]
  • **Minor physical anomalies** are significantly increased in the autistic population.[211]
  • Preempted diagnoses. Although the DSM-IV rules out concurrent diagnosis of many other conditions along with autism, the full criteria for Attention deficit hyperactivity disorder (ADHD), Tourette syndrome, and other of these conditions are often present and these comorbid diagnoses are increasingly accepted.[212]
  • Sleep problems affect about two-thirds of individuals with ASD at some point in childhood. These most commonly include symptoms of insomnia such as difficulty in falling asleep, frequent nocturnal awakenings, and early morning awakenings. Sleep problems are associated with difficult behaviors and family stress, and are often a focus of clinical attention over and above the primary ASD diagnosis.[213]

A few examples of autistic symptoms and treatments were described long before autism was named. The //Table Talk// ofMartin Luther, compiled by his notetaker, Mathesius, contains the story of a 12-year-old boy who may have been severely autistic.[214] Luther reportedly thought the boy was a soulless mass of flesh possessed by the devil, and suggested that he be suffocated, although a later critic has cast doubt on the veracity of this report.[215] The earliest well-documented case of autism is that of Hugh Blair of Borgue, as detailed in a 1747 court case in which his brother successfully petitioned to annul Blair's marriage to gain Blair's inheritance.[216] 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.[217]
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 autós (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".[218]
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.[219] Asperger was investigating an ASD now known as Asperger syndrome, though for various reasons it was not widely recognized as a separate diagnosis until 1981.[217] 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.[37] 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.[52] It is not known whether Kanner derived the term independently of Asperger.[220]
Kanner's reuse of autism led to decades of confused terminology like infantile schizophrenia, and child psychiatry's focus on maternal deprivation 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 intellectual disability and schizophrenia and from other developmental disorders, and demonstrating the benefits of involving parents in active programs of therapy.[221] 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.[222] Although the rise of parent organizations and the destigmatization of childhood ASD have deeply affected how we view ASD,[217] parents continue to feel social stigma in situations where their child's autistic behavior is perceived negatively by others,[223] and many primary care physicians and medical specialists still express some beliefs consistent with outdated autism research.[224]
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.[225] 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.[12][226]
Kilde til ovenstående:
Many causes of autism have been proposed, but understanding of the theory of causation of autismand the other autism spectrum disorders (ASD) is incomplete.[1] Research indicates that genetic factors predominate. The heritability of autism, however, is complex, and it is typically unclear which genes are responsible.[2] In rare cases, autism is strongly associated with agents that cause birth defects.[3] Many other causes have been proposed, such as childhood immunizations, but numerous epidemiological studies have shown no scientific evidence supporting any link between vaccinations and autism.[4]

Autism involves atypical brain development which often becomes apparent in behavior and social development before a child is three years old. It can be characterized by impairments in social interaction and communication, as well as restricted interests and stereotyped behavior, and the characterization is independent of any underlying neurological defects.[5][6] Other characteristics include repetitive-like tasks seen in their behavior and sensory interests.[7] This article uses the terms autism and ASD to denote classical autism and the wider dispersion of symptoms and manifestations of autism, respectively.
Autism's theory of causation is incomplete.[1] 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.[8] 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.[8][9] Different underlying brain dysfunctions have been hypothesized to result in the common symptoms of autism, just as completely different brain problems result in intellectual disability. The terms autism or ASDs capture the wide range of disease processes at work.[10] Although these distinct causes have been hypothesized to often co-occur,[9] it has also been suggested that the correlation between the causes has been exaggerated.[11] 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.[12]
The consensus among mainstream autism researchers is that genetic factors predominate. Environmental factors that have been claimed to contribute to autism or exacerbate its symptoms, or that may be important to consider in future research, include certain foods,[13] 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.[12] 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, there is overwhelming scientific evidence showing no causal association between the measles-mumps-rubella (MMR) vaccine and autism, and there is no scientific evidence that the vaccine preservative thiomersal causes autism.[4][14]

Genetic factors may be the most significant cause for autism spectrum disorders. Early studies of twins had estimated heritability to be over 90%, meaning that genetics explains over 90% of whether a child will develop autism.[15] However, this may be an overestimation, as new twin studies estimate the heritability at between 60-90%.[16][17] 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%.[18]
However, in spite of the strong heritability, most cases of ASD occur sporadically with no recent evidence of family history. It has been hypothesized that spontaneous //de novo// mutations in the father's sperm or mother's egg contribute to the likelihood of developing autism.[19]There are two lines of evidence that support this hypothesis. Firstly, individuals with autism have significantly reduced fecundity, they are 20 times less likely to have children than average, thus curtailing the persistence of mutations in ASD genes over multiple generations in a family.[20]Secondly, the likelihood of having a child develop autism increases with advancing paternal age,[21] and mutations in sperm gradually accumulate throughout a man's life.[22]
The first genes to be definitively shown to contribute to risk for autism were found in the early 1990s by researchers looking at gender-specific forms of autism caused by mutations on the X chromosome. An expansion of the CGG trinucleotide repeat in the promoter of the gene //FMR1// in boys causes fragile X syndrome, and at least 20% of boys with this mutation have behaviors consistent with autism spectrum disorder.[23]Mutations that inactivate the gene //MECP2// cause Rett syndrome, which is associated with autistic behaviors in girls, and in boys the mutation is embryonic lethal.[24]
Besides these early examples, the role of de novo mutations in ASD first became evident when DNA microarray technologies reached sufficient resolution to allow the detection of copy number variation (CNV) in the human genome.[25][26] CNVs are the most common type of structural variation in the genome, consisting of deletions and duplications of DNA that range in size from a kilobase to a few megabases. Microarray analysis has shown that de novo CNVs occur at a significantly higher rate in sporadic cases of autism as compared to the rate in their typically developing siblings and unrelated controls. A series of studies have shown that gene disrupting de novo CNVs occur approximately four times more frequently in ASD than in controls and contribute to approximately 5-10% of cases.[19][27][28][29] Based on these studies, there are predicted to be 130-234 ASD-related CNV loci.[29] The first whole genome sequencing study to comprehensively catalog de novo structural variation at a much higher resolution than DNA microarray studies has shown that the mutation rate is approximately 20% and not elevated in autism compared to sibling controls.[30] However, structural variants in individuals with autism are much larger and four times more likely to disrupt genes, mirroring findings from CNV studies.[30]
CNV studies were closely followed by exome sequencing studies, which sequence the 1-2% of the genome that codes for proteins (the "exome"). These studies found that de novo gene inactivating mutations were observed in approximately 20% of individuals with autism, compared to 10% of unaffected siblings, suggesting the etiology of ASD is driven by these mutations in around 10% of cases.[31][32][33][34][35][36] There are predicted to be 350-450 genes that significantly increase susceptibility to ASDs when impacted by inactivating de novo mutations.[37] A further 12% of cases are predicted to be caused by protein altering missense mutations that change an amino acid but do not inactivate a gene.[33] Therefore approximately 30% of individuals with autism have a spontaneous de novo large CNV that deletes or duplicates genes, or mutation that changes the amino acid code of an individual gene. A further 5-10% of cases have inherited structural variation at loci known to be associated with autism, and these known structural variants may arise de novo in the parents of affected children.[30]
Tens of genes and CNVs have been definitively identified based on the observation of recurrent mutations in different individuals, and suggestive evidence has been found for over 100 others.[38] The Simons Foundation Autism Research Initiative (SFARI) details the evidence for each genetic locus associated with autism.[39]
These early gene and CNV findings have shown that the cognitive and behavioral features associated with each of the underlying mutations is variable. Each mutation is itself associated with a variety of clinical diagnoses, and can also be found in a small percentage of individuals with no clinical diagnosis.[40][41] Thus the genetic disorders that comprise autism are not autism-specific. The mutations themselves are characterized by considerable variability in clinical outcome and typically only a subset of mutation carriers meet criteria for autism. This variable expressivityresults in different individuals with the same mutation varying considerably in the severity of their observed particular trait.[42]
The conclusion of these recent studies of de novo mutation is that the spectrum of autism is breaking up into quanta of individual disorders defined by genetics.[42]


Epigenetic mechanisms may increase the risk of autism. Epigenetic changes occur as a result not of DNA sequence changes but of chromosomal histone modification or modification of the DNA bases. Such modifications are known to be affected by environmental factors, including nutrition, drugs, and mental stress.[43] Interest has been expressed in imprinted regions on chromosomes 15q and 7q.[44]
Prenatal environment[edit]
The risk of autism is associated with several prenatal risk factors, including advanced age in either parent, diabetes, bleeding, and use of psychiatric drugs in the mother during pregnancy.[45] Autism has been linked to birth defect agents acting during the first eight weeks fromconception, though these cases are rare.[46]
Infectious processes[edit]
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.[47] Congenital rubella syndrome is the most convincing environmental cause of autism.[48] Infection-associated immunological events in early pregnancy may affect neural development more than infections in late pregnancy, not only for autism, but also for psychiatric disorders of presumed neurodevelopmental origin, notably schizophrenia.[49]
Environmental agents[edit]
Teratogens are environmental agents that cause birth defects. Some agents that are theorized to cause birth defects have also been suggested as potential autism risk factors, although there is little to no scientific evidence to back such claims. These include exposure of the embryo tovalproic acid,[50] thalidomide or misoprostol.[51] These cases are rare.[52] Questions have also been raised whether ethanol (grain alcohol) increases autism risk, as part of fetal alcohol syndrome or alcohol-related birth defects.[51] 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.[3]
Other maternal conditions[edit]
Thyroid problems that lead to thyroxine deficiency in the mother in weeks 8–12 of pregnancy have 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 mostherbicides. This hypothesis has not been tested.[53]
Diabetes in the mother during pregnancy is a significant risk factor for autism; a 2009 meta-analysis found that gestational diabetes was associated with a twofold increased risk. A 2014 review also found that maternal diabetes was significantly associated with an increased risk of ASD.[54] Although diabetes causes metabolic and hormonal abnormalities and oxidative stress, no biological mechanism is known for the association between gestational diabetes and autism risk.[45]
Maternal obesity during pregnancy may also increase the risk of autism, although further study is needed.[55]
Other in utero[edit]
It has been hypothesized that folic acid taken during pregnancy could play a role in reducing cases of autism by modulating gene expressionthrough an epigenetic mechanism. This hypothesis is supported by multiple studies.[56]
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.[57]
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 E-S 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.[58]
Based in part on animal studies, diagnostic ultrasounds administered during pregnancy have been hypothesized to increase the child's risk of autism. This hypothesis is not supported by independently published research, and examination of children whose mothers received an ultrasound has failed to find evidence of harmful effects.[59]
Some research suggests that maternal exposure to selective serotonin reuptake inhibitors during pregnancy is associated with an increased risk of autism, but it remains unclear whether there is a causal link between the two.[60] There is evidence, for example, that this association may be an artifact of confounding by maternal mental illness.[61]
Perinatal environment[edit]
Autism is associated with some perinatal and obstetric conditions. A 2007 review of risk factors found associated obstetric conditions that includedlow birth weight and gestation duration, and hypoxia during childbirth. This association does not demonstrate a causal relationship. As a result, an underlying cause could explain both autism and these associated conditions.[62] There is growing evidence that perinatal exposure to air pollutionmay be a risk factor for autism,[63] although this evidence suffers from methodological limitations, including a small number of studies and failure to control for potential confounding factors.[64]
Postnatal environment[edit]
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.[65]
Amygdala neurons[edit]
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.[66]
Autoimmune disease[edit]
This theory hypothesizes that autoantibodies that target the brain or elements of brain metabolism may cause or exacerbate autism. It is related to the maternal infection 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.[67]
Interactions between the immune system and the nervous system begin early during embryogenesis, and successful neurodevelopment depends on a balanced immune response. It is possible that aberrant immune activity during critical periods of neurodevelopment is part of the mechanism of some forms of ASD.[68] A small percentage of autism cases are associated with infection, usually before birth. Results from immune studies have been contradictory. Some abnormalities have been found in specific subgroups, and some of these have been replicated. It is not known whether these abnormalities are relevant to the pathology of autism, for example, by infection or autoimmunity, or whether they are secondary to the disease processes.[69] As autoantibodies are found in diseases other than ASD, and are not always present in ASD,[70] the relationship between immune disturbances and autism remains unclear and controversial.[71] A 2015 systematic review and meta-analysis found that children with a family history of autoimmune diseases were at a greater risk of autism compared to children without such a history.[72]
When an underlying maternal autoimmune disease is present, antibodies circulating to the fetus could contribute to the development of autism spectrum disorders.[73]
Endogenous opiate precursor theory[edit]
Main article: //Opioid excess theory//
In 1979, Jaak Panksepp proposed a connection between autism and opiates, noting that injections of minute quantities of opiates in young laboratory animals induce symptoms similar to those observed among autistic children.[74] Opiate theory hypothesizes that autism is caused by a digestive disorder present from birth which causes gluten (present in wheat-derived foods) and casein (present in dairy products) to be converted to the opioid peptides gliadorphin (aka gluteomorphin) and casomorphin.
According to the theory, exposure to these opiate compounds in young children interferes with normal neurological development by dulling sensory input. Lacking sufficient sensory input, the developing brain attempts to artificially generate the auditory, vestibular, visual, and tactile input on its own. This attempt at generating input manifests itself as behaviors common to autism, such as grunting or screaming (auditory), spinning or rocking back and forth (vestibular), preoccupation with spinning objects or waving of the fingers in front of the eyes (visual), and hand flapping or self-injury (tactile).
The theory further states that removing opiate precursors from a child's diet may allow time for these behaviors to cease, and neurological development in very young children to resume normally.[75] The possibility of a relationship between autism and the consumption of gluten and casein was first articulated by Kalle Reichelt in 1991.[76] The scientific evidence is not yet adequate to make treatment recommendations regarding diets, such as the GFCF diet, which exclude these substances.[77]
Gastrointestinal connection[edit]
Parents have reported gastrointestinal (GI) disturbances in autistic children, and several studies have investigated possible associations between autism and the gut,[78] but the results so far are inconclusive.
There is some research evidence that autistic children are more likely to have GI symptoms than typical children.[79] Even so, design flaws in studies of elimination diets mean that the data are inadequate to guide treatment recommendations.[13]
After a preliminary 1998 study of three children with ASD treated with secretin infusion reported improved GI function and dramatic improvement in behavior, many parents sought secretin treatment and a black market for the hormone developed quickly.[78] Later studies found secretin clearly ineffective in treating autism.[80]
Lack of vitamin D[edit]
There is limited evidence for the hypothesis that vitamin D deficiency has a role in autism, and it may be biologically plausible,[81] but more research is needed.[82]
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.[83] 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.[83]
Locus coeruleus–noradrenergic system[edit]
This theory hypothesizes that autistic behaviors depend at least in part on a developmental dysregulation that results in impaired function of thelocus coeruleusnoradrenergic (LC-NA) system. The LC-NA system is heavily involved in arousal and attention; for example, it is related to the brain's acquisition and use of environmental cues.[84]
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.[85] This view has gained little traction in the scientific community as the typical symptoms of mercury toxicity are significantly different from symptoms seen in autism.[86] 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.[87] A meta-analysis published in 2007 concluded that there was no link between mercury and autism.[88]
Oxidative stress[edit]
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.[89] One theory is that stress damages Purkinje cells in thecerebellum after birth, and it is possible that glutathione is involved.[90] Autistic children have lower levels of total glutathione, and higher levels of oxidized glutathione.[91] Based on this theory, antioxidants may be a useful treatment for autism.[92]
Refrigerator mother[edit]
Main article: //Refrigerator mother//
Child psychologist 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.[93] Leo Kanner, who first described autism,[94] suggested that parental coldness might contribute to autism.[95] 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.[96]
Scientific studies have refuted a causal relationship between vaccinations and autism.[97][98][99] Despite this, some parents believe that vaccinations cause autism and therefore delay or avoid immunizing their children under the "vaccine overload" hypothesis that giving many vaccines at once may overwhelm a child's immune system and lead to autism,[100] even though this hypothesis has no scientific evidence and is biologically implausible.[101] Because diseases such as measles can cause severe disabilities and death, the risk of death or disability for an unvaccinated child is higher than the risk for a child who has been vaccinated.[102]
MMR vaccine[edit]
Main article: //MMR vaccine controversy//
The MMR vaccine hypothesis of autism is one of the most extensively debated hypothesies regarding the origins of autism. Andrew Wakefield et al. reported a study of 12 children who had autism and bowel symptoms, in some cases reportedly with onset after MMR.[103] Although the paper, which was later retracted by the journal,[103] concluded "We did not prove an association between measles, mumps, and rubella vaccine and the syndrome described,"[104] Wakefield nevertheless suggested during a 1998 press conference that giving children the vaccines in three separate doses would be safer than a single dose.
In 2004, the interpretation of a causal link between MMR vaccine and autism was formally retracted by ten of Wakefield's twelve co-authors.[105]The retraction followed an investigation by //The Sunday Times//, which stated that Wakefield "acted dishonestly and irresponsibly".[106] The Centers for Disease Control and Prevention,[107] the Institute of Medicine of the National Academy of Sciences,[108] and the U.K. National Health Service[109]have all concluded that there is no evidence of a link between the MMR vaccine and autism.
In February 2010, The Lancet, which published Wakefield's study, fully retracted it after an independent auditor found the study to be flawed.[103]In January 2011, an investigation published in the journal BMJ described the Wakefield study as the result of deliberate fraud and manipulation of data.[110][111][112][113]
Thiomersal (thimerosal)[edit]
Main article: //Thiomersal controversy//
Perhaps the best-known hypothesis 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 including US and the EU.[114] Parents may first become aware of autistic symptoms in their child around the time of a routine vaccination. There is no scientific evidence for a causal connection between thiomersal and autism, but parental concern about the thiomersal controversy has led to decreasing rates of childhood immunizations[4] and increasing likelihood of disease outbreaks.[115][116] Because of public concerns,[//citation needed//] thiomersal content was completely removed or dramatically reduced from childhood vaccines that contained it in the 1990s; despite this, autism rates continued to climb well into the late 2000s.
A causal link between thimerosal and autism has been rejected by international scientific and medical professional bodies including the American Medical Association,[117] the American Academy of Pediatrics,[118] the American College of Medical Toxicology,[119] the Canadian Paediatric Society,[120] the U.S. National Academy of Sciences,[108] the Food and Drug Administration,[121] Centers for Disease Control and Prevention,[107]the World Health Organization,[122] the Public Health Agency of Canada,[123] and the European Medicines Agency.[124]
Viral infection[edit]
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.[47]
Social construct[edit]
The social construct 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.[125]
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.[126]
See also[edit]

The heritability of autism is the proportion of differences in expression of autism that can be explained by genetic variation; if the heritability of a condition is high, then the condition is considered to be primarily genetic. Autism has a strong genetic basis, although the genetics of autism is complex and it is unclear whether autism spectrum disorder (ASD) is explained more by multigene interactions or by rare mutations with major effects.[1]
Early studies of twins estimated the heritability of autism to be more than 90%–meaning that 90% of the differences between autistic and non-autistic individuals was due to genetics.[2] This may be an overestimate: new twin data and models with structural genetic variation are needed.[3]When only one identical twin is autistic, the other often has learning or social disabilities.[4] For adult siblings, the risk of having one or more features of the broader autism phenotype might be as high as 30%,[5] much higher than the risk in controls.[6]
Genetic linkage analysis has been inconclusive; many association analyses have had inadequate power.[3] For each autistic individual, mutationsin more than one gene may be implicated. Mutations in different sets of genes may be involved in different autistic individuals. There may be significant interactions among mutations in several genes, or between the environment and mutated genes. By identifying genetic markers inherited with autism in family studies, numerous candidate genes have been located, most of which encode proteins involved in neural development and function.[7][8] However, for most of the candidate genes, the actual mutations that increase the risk for autism have not been identified. Typically, autism cannot be traced to a Mendelian (single-gene) mutation or to single chromosome abnormalities such as fragile X syndrome or 22q13 deletion syndrome.[9][10]
Deletion (1), duplication (2) and inversion (3) are all chromosome abnormalities that have been implicated in autism.[11]
The large number of autistic individuals with unaffected family members may result from copy number variations (CNVs)—spontaneous alterations in the genetic material during meiosis that delete or duplicategenetic material.[12][13] Sporadic (non-inherited) cases have been examined to identify candidate genetic loci involved in autism. 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.[11]
Although the fraction of autism traceable to a genetic cause may grow to 30–40% as the resolution of array CGH improves,[11] several results in this area have been described incautiously, possibly misleading the public into thinking that a large proportion of autism is caused by CNVs and is detectable via array CGH, or that detecting CNVs is tantamount to a genetic diagnosis.[14] The Autism Genome Projectdatabase contains genetic linkage and CNV data that connect autism to genetic loci and suggest that every human chromosome may be involved.[15] It may be that using autism-related subphenotypes instead of the diagnosis of autism per se may be more useful in identifying susceptible loci.[16]

2Sibling studies

5.5Genomic imprintingTwin studies[edit]
Twin studies are a helpful tool in determining the heritability of disorders and human traits in general. They involve determining concordance of characteristics between identical (monozygotic or MZ) twins and between fraternal (dizygotic or DZ) twins. Possible problems of twin studies are: (1) errors in diagnosis of monozygocity, and (2) the assumption that social environment sharing by DZ twins is equivalent to that of MZ twins.
A condition that is environmentally caused without genetic involvement would yield a concordance for MZ twins equal to the concordance found for DZ twins. In contrast, a condition that is completely genetic in origin would theoretically yield a concordance of 100% for MZ pairs and usually much less for DZ pairs depending on factors such as the number of genes involved and assortative mating.
An example of a condition that appears to have very little if any genetic influence is irritable bowel syndrome (IBS), with a concordance of 28% vs. 27% for MZ and DZ pairs respectively.[17] An example of a human characteristics that is extremely heritable is eye color, with a concordance of 98% for MZ pairs and 7–49% for DZ pairs depending on age.[18]
Identical twin studies put autism's heritability in a range between 36% and 95.7%, with concordance for a broader phenotype usually found at the higher end of the range.[19] Autism concordance in siblings and fraternal twins is anywhere between 0 and 23.5%. This is more likely 2–4% for classic autism and 10–20% for a broader spectrum. Assuming a general-population prevalence of 0.1%, the risk of classic autism in siblings is 20- to 40-fold that of the general population.
Notable twin studies have attempted to shed light on the heritability of autism.
A small scale study in 1977 was the first of its kind to look into the heritability of autism. It involved 10 DZ and 11 MZ pairs in which at least one twin in each pair showed infantile autism. It found a concordance of 36% in MZ twins compared to 0% for DZ twins. Concordance of "cognitive abnormalities" was 82% in MZ pairs and 10% for DZ pairs. In 12 of the 17 pairs discordant for autism, a biological hazard was believed to be associated with the condition.[20]
A 1979 case report discussed a pair of identical twins concordant for autism. The twins developed similarly until the age of 4, when one of them spontaneously improved. The other twin, who had suffered infrequent seizures, remained autistic. The report noted that genetic factors were not "all important" in the development of the twins.[21]
In 1985, a study of twins enrolled with the UCLA Registry for Genetic Studies found a concordance of 95.7% for autism in 23 pairs of MZ twins, and 23.5% for 17 DZ twins.[22]
In a 1989 study, Nordic countries were screened for cases of autism. Eleven pairs of MZ twins and 10 of DZ twins were examined. Concordance of autism was found to be 91% in MZ and 0% in DZ pairs. The concordances for "cognitive disorder" were 91% and 30% respectively. In most of the pairs discordant for autism, the autistic twin had more perinatal stress.[23]
A British twin sample was reexamined in 1995 and a 60% concordance was found for autism in MZ twins vs. 0% concordance for DZ. It also found 92% concordance for a broader spectrum in MZ vs. 10% for DZ. The study concluded that "obstetric hazards usually appear to be consequences of genetically influenced abnormal development, rather than independent aetiological factors."[24]
A 1999 study looked at social cognitive skills in general-population children and adolescents. It found "poorer social cognition in males", and a heritability of 0.68 with higher genetic influence in younger twins.[25]
In 2000, a study looked at reciprocal social behavior in general-population identical twins. It found a concordance of 73% for MZ, i.e. "highly heritable", and 37% for DZ pairs.[26]
A 2004 study looked at 16 MZ twins and found a concordance of 43.75% for "strictly defined autism". Neuroanatomical differences (discordant cerebellar white and grey matter volumes) between discordant twins were found. The abstract notes that in previous studies 75% of the non-autistic twins displayed the broader phenotype.[27]
Another 2004 study examined whether the characteristic symptoms of autism (impaired social interaction, communication deficits, and repetitive behaviors) show decreased variance of symptoms among monozygotic twins compared to siblings in a sample of 16 families. The study demonstrated significant aggregation of symptoms in twins. It also concluded that "the levels of clinical features seen in autism may be a result of mainly independent genetic traits."[28]
An English twin study in 2006 found high heritability for autistic traits in a large group of 3,400 pairs of twins.[29]
One critic of the pre-2006 twin studies said that they were too small and their results can be plausibly explained on non-genetic grounds.[30]
Sibling studies[edit]
A study of 99 autistic probands which found a 2.9% concordance for autism in siblings, and between 12.4% and 20.4% concordance for a "lesser variant" of autism.[6]
A study of 31 siblings of autistic children, 32 siblings of children with developmental delay, and 32 controls. It found that the siblings of autistic children, as a group, "showed superior spatial and verbal span, but a greater than expected number performed poorly on the set-shifting, planning, and verbal fluency tasks."[31]
A 2005 Danish study looked at "data from the Danish Psychiatric Central Register and the Danish Civil Registration System to study some risk factors of autism, including place of birth, parental place of birth, parental age, family history of psychiatric disorders, and paternal identity." It found an overall prevalence rate of roughly 0.08%. Prevalence of autism in siblings of autistic children was found to be 1.76%. Prevalence of autism among siblings of children with Asperger syndrome or PDD was found to be 1.04%. The risk was twice as high if the mother had been diagnosed with a psychiatric disorder. The study also found that "the risk of autism was associated with increasing degree of urbanisation of the child's place of birth and with increasing paternal, but not maternal, age."[32]
A study in 2007 looked at a database containing pedigrees of 86 families with two or more autistic children and found that 42 of the third-born male children showed autistic symptoms, suggesting that parents had a 50% chance of passing on a mutation to their offspring. The mathematical models suggest that about 50% of autistic cases are caused by spontaneous mutations. The simplest model was to divide parents into two risk classes depending on whether the parent carries a pre-existing mutation that causes autism; it suggested that about a quarter of autistic children have inherited a copy number variation from their parents.[33]
Other family studies[edit]
A 1994 study looked at the personalities of parents of autistic children, using parents of children with Down's syndrome as controls. Using standardized tests it was found that parents of autistic children were "more aloof, untactful and unresponsive" compared to parents whose children did not have autism.[34]
A 1997 study found higher rates of social and communication deficits and stereotyped behaviors in families with multiple-incidence autism.[35]
Autism was found to occur more often in families of physicists, engineers and scientists. 12.5% of the fathers and 21.2% of the grandfathers (both paternal and maternal) of children with autism were engineers, compared to 5% of the fathers and 2.5% of the grandfathers of children with other syndromes.[36] Other studies have yielded similar results.[37][38] Findings of this nature have led to the coinage of the term "geek syndrome".[39]
A 2001 study of brothers and parents of autistic boys looked into the phenotype in terms of one current cognitive theory of autism. The study raised the possibility that the broader autism phenotype may include a "cognitive style" (weak central coherence) that can confer information-processing advantages.[40]
A study in 2005 showed a positive correlation between repetitive behaviors in autistic individuals and obsessive-compulsive behaviors in parents.[41] Another 2005 study focused on sub-threshold autistic traits in the general population. It found that correlation for social impairment or competence between parents and their children and between spouses is about 0.4.[42]
A 2005 report examined the family psychiatric history of 58 subjects with Asperger syndrome (AS) diagnosed according to DSM-IV criteria. Three (5%) had first-degree relatives with AS. Nine (19%) had a family history of schizophrenia. Thirty five (60%) had a family history of depression. Out of 64 siblings, 4 (6.25%) were diagnosed with AS.[43]
Twinning risk[edit]
This section needs expansion.You can help by adding to it. (February 2014)
It has been suggested that the twinning process itself is a risk factor in the development of autism, presumably due to perinatal factors.[44]However, three large-scale epidemiological studies have refuted this idea.[2][45]
Proposed models[edit]
Twin and family studies show that autism is a highly heritable condition, but they have left many questions for researchers, most notably

  • Why is fraternal twin concordance so low considering that identical twin concordance is high?
  • Why are parents of autistic children typically non-autistic?
  • Which factors could be involved in the failure to find a 100% concordance in identical twins?
  • Is profound intellectual disability a characteristic of the genotype or something totally independent?

Clues to the first two questions come from studies that have shown that at least 30% of individuals with autism have spontaneous de novomutations that occurred in the father's sperm or mother's egg and disrupt genes important for brain development, these spontaneous mutations likely cause autism in families where there is no family history.[46] The concordance between identical twins isn't quite 100% for two reasons, because these mutations have variable 'expressivity' and their effects manifest differently due to chance effects, epigenetic, and environmental factors. Also spontaneous mutations can potentially occur specifically in one twin and not the other after conception.[47] The likelihood of developing intellectual disability is dependent on the importance the effect the gene or mutation has on brain development, and also the genetic and environmental background upon which a mutation occurs.[48] The recurrence of the same mutations in multiple individuals affected by autism has led Brandler and Sebat to suggest that the spectrum of autism is breaking up into quanta of many different genetic disorders.[48]
Single genes[edit]
The most parsimonious explanation for cases of autism where a single child is affected and there is no family history or affected siblings is that a single spontaneous mutation that impacts one or multiple genes is a significant contributing factor.[48][49] Tens of individual genes or mutations have been definitively identified and are cataloged by the Simons Foundation Autism Research Initiative.[50][51] Examples of autism that has arisen from a rare or de novo mutation in a single-gene or locus include the neurodevelopmental disorders fragile X syndrome, 22q13 deletion syndrome, and 16p11.2 deletion syndrome.[52]
These mutations themselves are characterized by considerable variability in clinical outcome and typically only a subset of mutation carriers meet criteria for autism. For example, carriers of the 16p11.2 deletion have a mean IQ 32 points lower than their first-degree relatives that do not carry the deletion, however only 20% are below the threshold IQ of 70 for intellectual disability, and only 20% have autism.[53][54] Around 85% have a neurobehavioral diagnosis, including autism, ADHD, anxiety disorders, mood disorders, gross motor delay, and epilepsy, while 15% have no diagnosis.[54] Alongside these neurobehavioral phenotypes, the 16p11.2 deletions / duplications have been associated with macrocephaly / microcephaly, body weight regulation, and the duplication in particular is associated with schizophrenia.[53][55][56] Controls that carry mutations associated with autism or schizophrenia typically present with intermediate cognitive phenotypes or fecundity compared to neurodevelopmental cases and population controls.[57] Therefore, a single mutation can have multiple different effects depending on other genetic and environmental factors.
Multigene interactions[edit]
In this model, autism often arises from a combination of common, functional variants of genes. Each gene contributes a relatively small effect in increasing the risk of autism. In this model, no single gene directly regulates any core symptom of autism such as social behavior. Instead, each gene encodes a protein that disrupts a cellular process, and the combination of these disruptions, possibly together with environmental influences,[58] affect key developmental processes such as synapse formation. For example, one model is that many mutations affect MET and other receptor tyrosine kinases, which in turn converge on disruption of ERK and PI3K signaling.[52]
Two family types[edit]
In this model most families fall into two types: in the majority, sons have a low risk of autism, but in a small minority their risk is near 50%. In the low-risk families, sporadic autism is mainly caused by spontaneous mutation with poor penetrance in daughters and high penetrance in sons. The high-risk families come from (mostly female) children who carry a new causative mutation but are unaffected and transmit the dominant mutation to grandchildren.[59]
Main article: //Epigenetics of autism//
Several epigenetic models of autism have been proposed.[60] These are suggested by the occurrence of autism in individuals with fragile X syndrome, which arises from epigenetic mutations, and with Rett syndrome, which involves epigenetic regulatory factors. An epigenetic model would help explain why standard genetic screening strategies have so much difficulty with autism.[61]
Genomic imprinting[edit]
Genomic imprinting models have been proposed; one of their strengths is explaining the high male-to-female ratio in ASD.[62] One hypothesis is that autism is in some sense diametrically opposite to schizophrenia and other psychotic-spectrum conditions, that alterations of genomic imprinting help to mediate the development of these two sets of conditions, and that ASD involves increased effects of paternally expressed genes, which regulate overgrowth in the brain, whereas schizophrenia involves maternally expressed genes and undergrowth.[63]
Environmental interactions[edit]
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.[64] 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. All known teratogens (agents that cause birth defects) related to the risk of autism appear to act during the first eight weeks from conception, strong evidence that autism arises very early in development.[65] Although evidence for other environmental causes is anecdotal and has not been confirmed by reliable studies,[66] extensive searches are underway.[67]
Candidate gene loci[edit]
Known genetic syndromes, mutations, and metabolic diseases account for up to 20% of autism cases.[68] A number of alleles have been shown to have strong linkage to the autism phenotype. In many cases the findings are inconclusive, with some studies showing no linkage. Alleles linked so far strongly support the assertion that there is a large number of genotypes that are manifested as the autism phenotype. At least some of the alleles associated with autism are fairly prevalent in the general population, which indicates they are not rare pathogenic mutations. This also presents some challenges in identifying all the rare allele combinations involved in the etiology of autism.
A 2008 study compared genes linked with autism to those of other neurological diseases, and found that more than half of known autism genes are implicated in other disorders, suggesting that the other disorders may share molecular mechanisms with autism.[69]

A 2009 pair of genome-wide association studies found an association between autism and six single-nucleotide polymorphisms in an intergenic region between CDH10 (cadherin 10) and CDH9 (cadherin 9). These genes encode neuronal cell-adhesion molecules, implicating these molecules in the mechanism of autism.[70]

A family based study identified a deletion of CDH8 that was transmitted to three out of three affected children and zero out of four unaffected siblings.[71] Further evidence for the role of CDH8 comes from a spontaneous 1.52 megabase inversion that disrupts the gene in an affected child.[72]

A 2008 study observed a de novo deletion of 593 kb on this chromosome in about 1% of persons with autism, and similarly for the reciprocal duplication of the region.[73] Another 2008 study also found duplications and deletions associated with ASD at this locus.[74] This gene encodes ERK1, one of the extracellular signal regulated kinase subfamily of mitogen-activated protein kinases which are central elements of an intracellular signaling pathways that transmits signals from cell surfaces to interiors. 1% of autistic children have been found to have either a loss or duplication in a region of chromosome 16 that encompasses the gene for ERK1. A similar disturbance in this pathway is also found in neuro-cardio-facial-cutaneous syndromes (NCFC), which are characterized by cranio-facial development disturbances that also can be found in some cases of autism.[75]

This gene locus has been associated with rigid-compulsive behaviors. Notably, it has also been associated with depression but only as a result of social adversity, although other studies have found no link.[76]Significant linkage in families with only affected males has been shown.[77][78] Researchers have also suggested that the gene contributes to hyperserotonemia.[79] However, a 2008 meta-analysis of family- and population-based studies found no significant overall association between autism and either the promoter insertion/deletion (5-HTTLPR) or the intron 2 VNTR (STin2 VNTR) polymorphisms.[80]

Markers within an interval containing this gene are associated with ASD at a locally significant level. The region likely harbors a combination of multiple rare and common alleles that contribute to genetic risk for ASD.[81]

GABA is the primary inhibitory neurotransmitter of the human brain. Ma et al. (2005) concluded thatGABRA4 is involved in the etiology of autism, and that it potentially increases autism risk through interaction with GABRB1.[82] The GABRB3 gene has been associated with savant skills.[83] The GABRB3 gene deficient mouse has been proposed as a model of ASD.[84]
Engrailed 2 (EN2)

Engrailed 2 is believed to be associated with cerebellar development. Benayed et al.. (2005) estimate that this gene contributes to as many as 40% of ASD cases, about twice the prevalence of the general population.[85] But at least one study has found no association.[86]

A number of studies have shown a significant linkage of autism and Asperger syndrome with this locus.[87][88] The most prominent markers are in the vicinity of D3S3715 and D3S3037.[89]

In adults, Reelin glycoprotein is believed to be involved in memory formation, neurotransmission, and synaptic plasticity. A number of studies have shown an association between the REELIN gene and autism,[90][91] but a couple of studies were unable to duplicate linkage findings.[92]

This gene encodes the mitochondrial aspartate/glutamate carrier (AGC1). It has been found to have a significant linkage to autism in some studies,[93][94][95] but linkage was not replicated in others,[96] and a 2007 study found no compelling evidence of an association of any mitochondrial haplogroup in autism.[97]

A link has been found between HOX genes and the development of the embryonic brain stem. In particular, two genes, HOXA1 and HOXB1, in transgenic 'knockout' mice, engineered so that these genes were absent from the genomes of the mice in question, exhibited very specific brain stem developmental differences from the norm, which were directly comparable to the brain stem differences discovered in a human brain stem originating from a diagnosed autistic patient.[98]
Conciatori et al.. (2004) found an association of HOXA1 with increased head circumference.[99] A number of studies have found no association with autism.[100][101][102] The possibility remains that single allelic variants of the HOXA1 gene are insufficient alone to trigger the developmental events in the embryo now associated with autistic spectrum conditions. Tischfield et al.. published a paper which suggests that because HOXA1 is implicated in a wide range of developmental mechanisms, a model involving multiple allelic variants of HOXA1 in particular may provide useful insights into the heritability mechanisms involved.[103] Additionally, Ingram et al.. alighted upon additional possibilities in this arena.[104] Transgenic mouse studies indicate that there is redundancy spread across HOX genes that complicate the issue, and that complex interactions between these genes could play a role in determining whether or not a person inheriting the requisite combinations manifests an autistic spectrum condition[105]—transgenic mice with mutations in both HOXA1 and HOXB1 exhibit far more profound developmental anomalies than those in which only one of the genes differs from the conserved 'norm'.
In Rodier's original work, teratogens are considered to play a part in addition, and that the possibility remains open for a range of teratogens to interact with the mechanisms controlled by these genes unfavourably (this has already been demonstrated using valproic acid, a known teratogen, in the mouse model).[106]

Philippi et al. (2005) found a strong association between this gene and autism. This is a recent finding that needs to be replicated.[107]
300496, AUTSX3

Mutations in this gene can give rise to autism spectrum disorders and related postnatal neurodevelopmental disorders.[108]

The maternally expressed imprinted gene UBE3A has been associated with Angelman syndrome. MeCP2 deficiency results in reduced expression of UBE3A in some studies.[109]

The gene called SHANK3 (also designated ProSAP2) regulates the structural organization of neurotransmitter receptors in post-synaptic dendritic spines making it a key element in chemical binding crucial to nerve cell communication.[110] SHANK3 is also a binding partner of chromosome 22q13 (i.e. a specific section of Chromosome 22) and neuroligin proteins; deletions and mutations of SHANK3, 22q13(i.e. a specific section of Chromosome 22) and genes encoding neuroligins have been found in some people with autism spectrum disorders.[111]
Mutations in the SHANK3 gene have been strongly associated with the autism spectrum disorders. If the SHANK3 gene is not adequately passed to a child from the parent (haploinsufficiency) there will possibly be significant neurological changes that are associated with yet another gene, 22q13, which interacts with SHANK3. Alteration or deletion of either will effect changes in the other.[111]
A deletion of a single copy of a gene on chromosome 22q13 has been correlated with global developmental delay, severely delayed speech or social communication disorders and moderate to profound delay of cognitive abilities. Behavior is described as "autistic-like" and includes high tolerance to pain and habitual chewing or mouthing[111] (see also 22q13 deletion syndrome). This appears to be connected to the fact that signal transmission between nerve cells is altered with the absence of 22q13.
SHANK3 proteins also interact with neuroligins at the synapses of the brain further complicating the widespread effects of changes at the genetic level and beyond.[112]
300425, AUTSX1
Neuroligin is a cell surface protein (homologous to acetylcholinesterase and other esterases) that binds tosynaptic membranes.[113] Neuroligins organize postsynaptic membranes that function to transmit nerve cell messages (excitatory) and stop those transmissions (inhibitory);[114] In this way, neuroligins help to ensure signal transitions between nerve cells. Neuroligins also regulate the maturation of synapses and ensure there are sufficient receptor proteins on the synaptic membrane.
Mice with a neuroligin-3 mutation exhibit poor social skills but increased intelligence.[115] Though not present in all individuals with autism, these mutations hold potential to illustrate some of the genetic components of spectrum disorders.[112] However, a 2008 study found no evidence for involvement of neuroligin-3 and neuroligin-4x with high-functioning ASD.[116]

The MET gene (MET receptor tyrosine kinase gene) linked to brain development, regulation of the immune system, and repair of the gastrointestinal system, has been linked to autism. This MET gene codes for aprotein that relays signals that turn on a cell's internal machinery. Impairing the receptor's signaling interferes with neuron migration and disrupts neuronal growth in the cerebral cortex and similarly shrinks the cerebellum—abnormalities also seen in autism.[117]
It is also known to play a key role in both normal and abnormal development, such as cancer metastases. A mutation of the gene, rendering it less active, has been found to be common amongst children with autism.[117] Mutation in the MET gene demonstrably raises risk of autism by 2.27 times.[118]
neurexin 1

In February 2007, researchers in the Autism Genome Project (an international research team composed of 137 scientists in 50 institutions) reported possible implications in aberrations of a brain-development gene called neurexin 1 as a cause of some cases of autism.[15] Linkage analysis was performed on DNA from 1,181 families in what was the largest-scale genome scan conducted in autism research at the time.
The objective of the study was to locate specific brain cells involved in autism to find regions in the genomelinked to autism susceptibility genes. The focus of the research was copy number variations (CNVs), extra or missing parts of genes. Each person does not actually have just an exact copy of genes from each parent. Each person also has occasional multiple copies of one or more genes or some genes are missing altogether. The research team attempted to locate CNVs when they scanned the DNA.
Neurexin 1 is one of the genes that may be involved in communication between nerve cells (neurons). Neurexin 1 and other genes like it are very important in determining how the brain is connected from cell to cell, and in the chemical transmission of information between nerve cells. These genes are particularly active very early in brain development, either in utero or in the first months or couple of years of life. In some families their autistic child had only one copy of the neurexin 1 gene.
Besides locating another possible genetic influence (the findings were statistically insignificant), the research also reinforced the theory that autism involves many forms of genetic variations.
A 2008 study implicated the neurexin 1 gene in two independent subjects with ASD, and suggested that subtle changes to the gene might contribute to susceptibility to ASD.[119]
A Neurexin 1 deletion has been observed occurring spontaneously in an unaffected mother and was passed on to an affected child, suggesting that the mutation has incomplete penetrance.[72]

Multiple 2008 studies have identified a series of functional variants in the CNTNAP2 gene, a member of the neurexin superfamily, that implicate it as contributing to autism.[58][120][121][122]

The FOXP2 gene is of interest because it is known to be associated with developmental language and speech deficits.[123][124] A 2008 study found that FOXP2 binds to and down-regulates CNTNAP2, and that the FOXP2-CNTNAP2 pathway links distinct syndromes involving disrupted language.[125]

A 2007 study suggested that the GSTP1*A haplotype of the glutathione S-transferase P1 gene (GSTP1) acts in the mother during pregnancy and increases the likelihood of autism in the child.[126]

A 2014 meta-analysis found significant associations between autism and several single-nucleotide polymorphisms in the OXTR gene.[127]
There is a large number of other candidate loci which either should be looked at or have been shown to be promising. Several genome-wide scans have been performed identifying markers across many chromosomes.[128][129][130]
A few examples of loci that have been studied are the 17q21 region,[131][132] the 3p24-26 locus,[128] PTEN,[133] 15q11.2–q13[109] and deletion in the 22q11.2 area.[134]
Homozygosity mapping in pedigrees with shared ancestry and autism incidence has recently implicated the following candidate genes: PCDH10, DIA1 (formerly known as C3ORF58), NHE9, CNTN3, SCN7A, and RNF8. Several of these genes appeared to be targets of MEF2,[135][136] one of the transcription factors known to be regulated by neuronal activity[137] and that itself has also recently been implicated as an autism-related disorder candidate gene.[138]

Kilde til ovenstående:
Autism spectrum disorder (ASD) includes autism, Asperger disorder, childhood disintegrative disorder and pervasive developmental disorder not otherwise specified. While the exact cause of ASD has remained somewhat of a mystery, it appears to be genetic in origin.[1] Most data supports apolygenic, epistatic model, meaning that the disorder is caused by two or more genes and that those genes are interacting in a complex manner. Several genes, between two and fifteen in number, have been identified and could potentially contribute to disease susceptibility.[2][3] However, an exact determination of the cause of ASD has yet to be discovered and there probably is not one single genetic cause of any particular set of disorders, leading many researchers to believe that epigenetic mechanisms, such as genomic imprinting or epimutations, may play a major role.[4][5]
Epigenetic mechanisms can contribute to disease phenotypes. Epigenetic modifications include DNA cytosine methylation and post-translational modifications to histones. These mechanisms contribute to regulating gene expression without changing the sequence of the DNA and may be influenced by exposure to environmental factors and may be heritable from parents.[1] Rett syndrome and Fragile X syndrome (FXS) are single gene disorders related to ASD with overlapping symptoms that include deficient neurological development, impaired language and communication, difficulties in social interactions, and stereotyped hand gestures. It is not uncommon for a patient to be diagnosed with both ASD and Rett syndrome and/or FXS. Epigenetic regulatory mechanisms play the central role in pathogenesis of these two diseases.[4][6][7] Rett syndrome is caused by a mutation in the gene that encodes methyl-CpG-binding protein (MECP2), one of the key epigenetic regulators of gene expression.[8] MeCP2 binds methylated cytosine residues in DNA and interacts with complexes that remodel chromatin into repressive structures.[9][10] On the other hand, FXS is caused by mutations that are both genetic and epigenetic. Expansion of the CGG repeat in the 5’-untranslated region of the FMR1 genes leads to susceptibility of epigenetic silencing, leading to loss of gene expression.[7]
Genomic imprinting may also contribute to ASD. Genomic imprinting is another example of epigenetic regulation of gene expression. In this instance, the epigenetic modification(s) causes the offspring to express the maternal copy of a gene or the paternal copy of a gene, but not both. The imprinted gene is silenced through epigenetic mechanisms. Candidate genes and susceptibility alleles for autism are identified using a combination of techniques, including genome-wide and targeted analyses of allele sharing in sib-pairs, using association studies and transmission disequilibrium testing (TDT) of functional and/or positional candidate genes and examination of novel and recurrent cytogenetic aberrations. Results from numerous studies have identified several genomic regions known to be subject to imprinting, candidate genes, and gene-environment interactions. Particularly, chromosomes 15q and 7q appear to be epigenetic hotspots in contributing to ASD. Also, genes on the X chromosome may play an important role, as in Rett Syndrome.[1]

Chromosome 15[edit]
In humans, chromosome 15q11-13 is the location of a number of mutations that have been associated with Autism spectrum disorders (ASD).
15q11-13 duplication[edit]
Duplications of 15q11-13 are associated with about 5% of patients with ASD[1] and about 1% of patients diagnosed with classical Autism.[11]15q11-13 in humans contains a cluster of genetically imprinted genes important for normal neurodevelopment. (Table 1) Like other genetically imprinted genes, the parent of origin determines the phenotypes associated with 15q11-13 duplications.[12] "Parent of origin effects" cause gene expression to occur only from one of the two copies of alleles that individuals receive from their parents. (For example, MKRN3 shows a parent of origin effect and is paternally imprinted. This means that only the MKRN3 allele received from the paternal side will be expressed.) Genes that are deficient in paternal or maternal 15q11-13 alleles result in Prader-Willi or Angelman syndromes, respectively, and duplications in the maternal copy lead to a distinct condition that often includes autism. Overexpression of maternally imprinted genes is predicted to cause autism, which focuses attention to the maternally expressed genes on 15q11-13, although it is still possible that alterations in the expression of both imprinted and bilallelically expressed genes contribute to these disorders.[13] The commonly duplicated region of chromosome 15 also includes paternally imprinted genes that can be considered candidates for ASD. (See Table 1)
Table 1
Parental Copy Imprinted (Pat/Mat)
Functional relevance to Autism or Autism Spectrum Disorders
Resides within the intron-exon of ZNF127AS that is transcribed from the antisense strand. Coding for a RING Zinc finger protein.
The antisense transcript of MKRN3 gene
Expressed in brain (especially in hypothalamus). Important in Prader-Willi syndrome.
Codes for a neural growth suppressor that promotes neurite outgrowth and GABAergicneuronal differentiation. Important in Prader-Willi syndrome.
Encodes the small nucleolar RNA-binding protein N as well as a group of snRNAs.
Encodes the E6-AP ubiquitin protein ligase. Candidate gene for Angelman syndrome. Dysregulation is associated with ASD. Linkage to this gene has been detected in ASD but no mutations identified in a small group of subjects.
Produces an aminophospholipid translocase. Expressed in hippocampus and olfactory bulb. Has been linked to ASD.
Conflicting data

Encodes the alpha 5 subunit of the GABAA receptor. GABRA5 containing receptors mediate tonic inhibition in hippocampal neurons. Knockout of this gene increases learning and memory in mice.

Encodes the beta 3 subunit of the GABAA receptor. Some conflicting results on its association with ASD. Has shown dysregulation in Rett, Autism and Angelman Disorders.[11]
Conflicting data

Codes for the gamma 3 subunit of the GABAA receptor. Conflicting results on its association with ASD but mostly negative. No significant phenotype alteration in knockouts.
Table 1- Modified from Schanen (2006)
Genes on 15q11-13 can be classified into three main categories:

  • GABAA receptor genes:

Members of the GABA receptor family, especially GABRB3, are attractive candidate genes for Autism because of their function in the nervous system. Gabrb3 null mice exhibit behaviors consistent with autism[9] and multiple genetic studies have found significant evidence for association.[10] Furthermore, a significant decrease in abundance of GABRB3 has been reported in the brain of AS, AUT and RTT patients.[2]Other GABA receptors residing on different chromosomes have also been associated with autism (e.g. GABRA4 and GABRB1 on chromosome 4p).[14]

  • Maternally imprinted genes:

There are two maternally imprinted genes in 15q11-13, UBE3A and ATP10A (Table 1) and both lie toward the centromeric end. Both these genes are important candidates for ASD. Significant decrease in UBE3A abundance has been observed in post mortem brain samples from patients with AUT, AS and RT.[11] Patients with autism have also shown abnormalities in methylation of the UBE3A CpG island.[5]

  • Paternally imprinted genes:

Most of the genes in 15q11-13 are paternally expressed. Gene expression analysis of paternally expressed imprinted genes has revealed that, in some cases excess of maternal 15q11-13 dosage can cause abnormal gene expression of the paternally expressed genes as well (even though the paternal 15q11-13 is normal).[15]

  • Regulation of gene expression in 15q11-13:

Regulation of gene expression in the 15q11-13 is rather complex and involves a variety of mechanisms such as DNA methylation, non-coding andanti-sense RNA.[16]
The imprinted genes of 15q11-13 are under the control of a common regulatory sequence, the imprinting control region (ICR). The ICR is a differentially methylated CpG island at the 5′ end of SNRPN. It is heavily methylated on the silent maternal allele and unmethylated on the active paternal allele.[15]
MeCP2, which is a candidate gene for Rett syndrome, has been shown to affect regulation of expression in 15q11-13. Altered (decreased) expression of UBE3A and GABRB3 is observed in MeCP2 deficient mice and ASD patients. This effect seems to happen without MeCP2 directly binding to the promoters of UBE3A and GABRB3. (Mechanism unknown)[2] However, chromatin immunoprecipitation and bisulfite sequencing have demonstrated that MeCP2 binds to methylated CpG sites within GABRB3 and the promoter of SNRPN/SNURF.[11]
Furthermore, homologous 15q11-13 pairing in neurons that is disrupted in RTT and autism patients, has been shown to depend on MeCP2.[17]Combined, these data suggest a role for MeCP2 in the regulation of imprinted and biallelic genes in 15q11-13. However, evidently it does not play a role in the maintenance of imprinting.[11]
Chromosome 7[edit]

A genome-wide scan approach has revealed possible linkage of ASDs and autism to numerous chromosomes. These linkage studies initially implicated the long arm of chromosome 7, and sequence analyses specifically targeted two susceptibility loci at the regions of 7q21.3 and 7q32.2.[1] Parent-of-origin linkage modeling identified the imprinted gene cluster 7q21.3, which includes two paternally expressed genes, two maternally expressed genes, and one preliminarily determined maternally expressed gene, as summarized in the table below. (Table 2)
Table 2: Paternal/Maternal gene expression of the imprinted region on chromosome 7q21.3
Parental Copy Imprinted (Pat/Mat)
Functional relevance to Autism or Autism Spectrum Disorders
Paternal mutations are associated with myoclonus-dystonia syndrome, which is implicated in obsessive-compulsive disorder and panic attacks. A binding target of MECP2 (mouse).
Overlapping reading frames yield two proteins that can inhibit signaling from the transforming growth factor-β(TGF-β) Type I receptor and activin receptor-like kinase I (AlkI). This transcript is abundant in the brain. A binding target of MECP2 (mouse).
A protein phosphatase complex that associates with neurabin in dendritic development and maturation. Complex disruption alters surface expression of glutamate receptors in hippocampal neurons. Candidate ASD gene.
Encodes transcription factor DLX5, which acts as a critical mediator in the forebrain for the differentiation ofGABAergic neurons. Acts in tandem with the adjacent DLX6 gene, which is regulated via the Rett-associated gene,MECP2. Candidate ASD gene.
Mat(Preliminary data)
G-protein coupled receptor for calcitonin, involved in calcium metabolism
Table 2- Modified from Schanen (2006)
DLX5 and DLX2 directly regulate expression of glutamic acid decarboxylase, the enzyme that produces the neurotransmitter GABA. Conclusive evidence of autism susceptibility due to novel sequence variants of these genes has yet to be clearly identified, however. To date, these loci cannot be definitely associated with autism, though their connection with Mecp2 via regulation suggests the epigenetic effects should be re-evaluated.[1]
The second region on chromosome 7q32.2 encompasses another imprinted domain with one maternally expressed and four paternally expressed genes. (Table 3)
Table 3- Imprinted gene cluster on chromosome 7q32.2
Parental Copy Imprinted (Pat/Mat)
Functional relevance to Autism or Autism Spectrum Disorders
Transcript upregulated by histone deacetylase inhibitors. Not an obvious candidate autism gene.
Dysregulation of expression alters cell growth and female homozygous knockout mice have imprinted maternal behaviors.
Antisense intronic transcript expressed in testis.
The γ2 subunit has been shown to directly associate with dopamine receptors.
COPG2 intronic transcript
Table 3- Modified from Schanen (2006)
X Chromosome[edit]
There is a definite gender bias in the distribution of ASD. There are about four times as many affected males across the ASD population. Even when patients with mutations in X-linked genes (MECP2 and FMR1) are excluded, the gender bias remains. However, when only looking at patients with the most severe cognitive impairment, the gender bias is not as extreme. While the most obvious conclusion is that an X-linked gene of major effect is involved in contributing to ASD, the mechanism appears to be much more complex and perhaps epigenetic in origin.[1]
Based on the results of a study on females with Turner syndrome, a hypothesis involving epigenetic mechanisms was proposed to help describe the gender bias of ASD. Turner syndrome patients have only one X chromosome which can be either maternal or paternal in origin. When 80 females with monosomy X were tested for measures of social cognition, the patients with a paternally derived X chromosome performed better than those with a maternally derived X chromosome. Males have only one X chromosome, derived from their mother. If a gene on the paternal X chromosome confers improved social skills, males are deficient in the gene. This could explain why males are more likely to be diagnosed with ASD.[18]
In the proposed model, the candidate gene is silenced on the maternal copy of the X chromosome. Thus, males do not express this gene and are more susceptible to subsequent impairments in social and communication skills. Females, on the other hand, are more resistant to ASD.[19][20][21][22] Recently a cluster of imprinted genes on the mouse X chromosome was discovered; the paternal allele was expressed while the female copy was imprinted and silenced.[23][24] Further studies are aimed at discovering whether these genes contribute directly to behavior and whether the counterpart genes in humans are imprinted.[1]
The Link to Rett Syndrome[edit]
Epigenetic alterations of the methylation states of genes such as MECP2 and EGR2 have been shown to play a role in autism and autism spectrum disorders. MECP2 abnormalities have been shown to lead to a wide range of phenotypic variability and molecular complexities.[25]These variabilities have led to the exploration of the clinical and molecular convergence between Rett syndrome and autism.[25]
Sleeping and language impairments, seizures, and developmental timing are common in both autism and Rett syndrome (RTT). Because of these phenotypic similarities, there has been research into the specific genetic similarities between these two pervasive developmental disorders. MECP2 has been identified as the predominant gene involved in RTT. It has also been shown that the regulation of the MECP2 gene expression has been implicated in autism.[26] Rett syndrome brain samples and autism brain samples show immaturity of dendrite spines and reduction of cell-body size due to errors in coupled regulation between MECP2 and EGR2.[27] However, because of the multigene involvement in autism, the MECP2 gene has only been identified as a vulnerability factor in autism.[28] The most current model illustrating MECP2 is known as the transcriptional activator model.
Another potential molecular convergence involves the early growth response gene-2 (EGR2).[25] EGR2 is the only gene in the EGR family that is restricted to the central nervous system and is involved in cerebral development and synaptic plasticity.[25] EGR2 expression has been shown to decrease in the cortexes of individuals with both autism and RTT.[29] MECP2 expression has also been shown to decrease in individuals with RTT and autism. MECP2 and EGR2 have been shown to regulate each other during neuronal maturation.[29] A role for the dysregulation of the activity-dependent EGR2/MECP2 pathway in RTT and autism has been proposed.[29] Further molecular linkages are being examined; however, the exploration of MECP2 and EGR2 have provided a common link between RTT, autism, and similarities in phenotypic expression.

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The opioid excess theory is a theory which postulates that autism is the result of a metabolic disorder in which opioid peptides produced through metabolism of gluten and casein pass through an abnormally permeable intestinal membrane and then proceed to exert an effect on neurotransmission through binding with opioid receptors.[1] It is believed by advocates of this hypothesis that autistic children are unusually sensitive to gluten, which results in small bowel inflammation in these children, which in turn allows these opioid peptides to enter the brain.[2]
Early years[edit]
This hypothesis was first proposed by Jaak Panksepp in a 1979 paper, in which he speculated that autism might be "an emotional disturbance arising from an upset in the opiate systems in the brain."[3] Kalle Reichelt then emerged as one of the leading advocates of this theory, publishing papers alleging that "the patterns of peptides and associated proteins from urinary samples [from people with autism] differ considerably from each other and from normal controls." In addition, Reichelt's research has concluded that autistic individuals have increased levels of these peptides in their cerebrospinal fluid.[4] Additionally, in a 1991 paper, Reichelt argued that gluten and casein may play a causative role in autism, as the incomplete digestion thereof may produce certain opioid peptides.[5] Thus, those, such as Paul Shattock, who advocate this theory also advocate the use of a gluten-free, casein-free diet as a treatment for autism.[6]
Wakefield study[edit]
In 1998, a fraudulent paper was published in //The Lancet// by Andrew Wakefield presenting apparent evidence of a link between the MMR vaccine, gastrointestinal disease and autism. In this paper, which has since been retracted, Wakefield et al. speculated that food-derived peptides "may exert central-opioid effects, directly or through the formation of ligands with peptidase enzymes required for breakdown of endogenous central-nervous-system opioids, leading to disruption of normal neuroregulation and brain development by endogenous encephalins and endorphins."[7]
Later research[edit]
Reichelt has published a number of papers concluding that autistic children excrete higher levels of peptides in their urine,[8] as well as that such peptides may cause autistic gaze aversion; specifically, by interfering with corticothalamocortical processing of visual stimuli.[9] As a result of this theory, others, particularly Panksepp, have speculated that opioid antagonists such as naloxone and naltrexone may be useful in the treatment of autism.[10][11] In addition, Christopher Gillberg of Gothenburg University has published some studies showing that animals treated with opiates exhibit less clinging, in line with the behavior of autistic children, who, his research has also shown, "do not seem concerned when their parents are not near" and "exhibit less crying than infants without autism,"[12] and has also linked an excess of endogenous opioids to stereotypic (i.e. repetitive) behavior.[13] However, more recently, two studies were published which failed to find a difference in levels of peptides in the urine of autistic children as opposed to those without autism.[14][15] A 2009 review found that no evidence exists that urinary peptide levels are correlated with gut permeability.[16]
Possible implications for treatment[edit]
Several double blind studies experimented with low dose opioid antagonists, such as naltrexone, for treatment of autism. A recent systematic review, published in 2014[17] showed statistically significant improvement in symptoms of irritability and hyperactivity in 77% of children treated with naltrexone. Core autism symptoms were unaffected. Side effects were mild and the drug was generally well tolerated. The number of children undergoing such therapy in the 10 analysed studies was only 128, however.
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Autism therapies are interventions that attempt to lessen the deficits and problem behaviours associated with autism spectrum disorder (ASD) in order to increase the quality of life and functional independence of autistic individuals. Treatment is typically catered to person's needs. Treatments fall into two major categories: educational interventions and medical management. Training and support are also given to families of those with ASD.[2]
Studies of interventions have some methodological problems that prevent definitive conclusions about efficacy.[3] Although many psychosocial interventions have some positive evidence, suggesting that some form of treatment is preferable to no treatment, the systematic reviewshave reported that the quality 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.[4] Intensive, sustained special education programs and behavior therapy early in life can help children with ASD acquire self-care, social, and job skills,[2] and often can improve functioning, and decrease symptom severity and maladaptive behaviors;[5] claims that intervention by around age three years is crucial are not substantiated.[6] Available approaches include applied behavior analysis (ABA), developmental models, structured teaching, speech and language therapy, social skills therapy, and occupational therapy.[2]Educational interventions have some effectiveness in children: intensive ABA treatment has demonstrated effectiveness in enhancing global functioning in preschool children,[7] and is well established for improving intellectual performance of young children.[5] Neuropsychological reports are often poorly communicated to educators, resulting in a gap between what a report recommends and what education is provided.[8] The limited research on the effectiveness of adult residential programs shows mixed results.[9]
Many medications are used to treat problems associated with ASD.[10] More than half of U.S. children diagnosed with ASD are prescribedpsychoactive drugs or anticonvulsants, with the most common drug classes being antidepressants, stimulants, and antipsychotics.[11] Aside from antipsychotics,[12] there is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD.[13][14]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.[15]
Some newer treatments are geared towards children with ASD and focus on community-based education and living, and early intervention. The treatments that may have the most benefit focus on early behavioral development and have shown significant improvements in communication and language. These treatments include parental involvement as well as special educational methods. Further research will examine the long term outcome of these treatments and the details surrounding the process and execution of them.[16]
Many alternative therapies and interventions are available, ranging from elimination diets to chelation therapy. Few are supported by scientific studies.[17][18][19][20][21] Treatment approaches lack empirical support in quality-of-life contexts, and many programs focus on success measures that lack predictive validity and real-world relevance.[22] Scientific evidence appears to matter less to service providers than program marketing, training availability, and parent requests.[23] Even if they do not help, conservative treatments such as changes in diet are expected to be harmless aside from their bother and cost.[24] Dubious invasive treatments are a much more serious matter: for example, in 2005, botchedchelation therapy killed a five-year-old boy with autism.[25]
Treatment is expensive;[26] indirect costs are more so. For someone born in 2000, a U.S. study estimated an average discounted lifetime cost of $4.11 million (2017 dollars, inflation-adjusted from 2003 estimate[27]), with about 10% medical care, 30% extra education and other care, and 60% lost economic productivity.[28] A UK study estimated discounted lifetime costs at ₤1.61 million and ₤1.04 million for an autistic person with and without intellectual disability, respectively[29] (2017 pounds, inflation-adjusted from 2005/06 estimate[30]). Legal rights to treatment are complex, vary with location and age, and require advocacy by caregivers.[31] 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;[32] one 2008 U.S. study found a 14% average loss of annual income in families of children with ASD,[33] and a related study found that ASD is associated with higher probability that child care problems will greatly affect parental employment.[34] After childhood, key treatment issues include residential care, job training and placement, sexuality, social skills, and estate planning.[31
Educational interventions attempt to help children not only to learn academic subjects and gain traditional readiness skills, but also to improve functional communication and spontaneity, enhance social skills such as joint attention, gain cognitive skills such as symbolic play, reduce disruptive behavior, and generalize learned skills by applying them to new situations. Several model programs have been developed, which in practice often overlap and share many features, including:[2]

  • early intervention that does not wait for a definitive diagnosis;
  • intense intervention, at least 25 hours per week, 12 months per year;
  • low student/teacher ratio;
  • family involvement, including training of parents;
  • interaction with neurotypical peers;
  • social stories, ABA and other visually based training;[35]
  • structure that includes predictable routine and clear physical boundaries to lessen distraction; and
  • ongoing measurement of a systematically planned intervention, resulting in adjustments as needed.

Several educational intervention methods are available, as discussed below. They can take place at home, at school, or at a center devoted to autism treatment; they can be done by parents, teachers, speech and language therapists, and occupational therapists.[2][36] A 2007 study found that augmenting a center-based program with weekly home visits by a special education teacher improved cognitive development and behavior.[37]
Studies of interventions have methodological problems that prevent definitive conclusions about efficacy.[3] Although many psychosocialinterventions have some positive evidence, suggesting that some form of treatment is preferable to no treatment, the methodological quality ofsystematic 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.[4] Concerns about outcome measures, such as their inconsistent use, most greatly affect how the results of scientific studies are interpreted.[38] A 2009 Minnesota study found that parents follow behavioral treatment recommendations significantly less often than they follow medical recommendations, and that they adhere more often to reinforcement than to punishment recommendations.[39]Intensive, sustained special education programs and behavior therapy early in life can help children acquire self-care, social, and job skills,[2] and often improve functioning and decrease symptom severity and maladaptive behaviors;[5] claims that intervention by around age three years is crucial are not substantiated.[6]

Applied behavior analysis[edit]

Further information: //Applied behavior analysis//
Applied behavior analysis (ABA) is the applied research field of the science of behavior analysis, and it underpins a wide range of techniques used to treat autism and many other behaviors and diagnoses,[40] including those who are patients in rehab or who need to have their behavior changed. ABA-based interventions focus on teaching tasks one-on-one using the behaviorist principles of stimulus, response and reward,[41] and on reliable measurement and objective evaluation of observed behavior.[2] There is wide variation in the professional practice of behavior analysisand among the assessments and interventions used in school-based ABA programs.[42]

Discrete trial training[edit]

Further information: //Discrete trial training//
Developmental trajectories (as measured with IQ-tests) of children with autism receiving either early and intensive behavioral intervention (n=195) or control treatment (n = 135)[43]
Many intensive behavioral interventions rely heavily on discrete trial teaching (DTT) methods, which use stimulus-response-reward techniques to teach foundational skills such as attention, compliance, and imitation.[44] However, children have problems using DTT-taught skills in natural environments.[2] These students are also taught with naturalistic teaching procedures to help generalize these skills. In functional assessment, a common technique, a teacher formulates a clear description of a problem behavior, identifies antecedents, consequences, and other environmental factors that influence and maintain the behavior, develops hypotheses about what occasions and maintains the behavior, and collects observations to support the hypotheses.[2] A few more-comprehensive ABA programs use multiple assessment and intervention methods individually and dynamically.[42]
ABA-based techniques have demonstrated effectiveness in several controlled studies: children have been shown to make sustained gains in academic performance, adaptive behavior, and language, with outcomes significantly better than control groups.[2] A 2009 review of educational interventions for children, whose mean age was six years or less at intake, found that the higher-quality studies all assessed ABA, that ABA is well-established and no other educational treatment is considered probably efficacious, and that intensive ABA treatment, carried out by trained therapists, is demonstrated effective in enhancing global functioning in pre-school children.[7] These gains maybe complicated by initial IQ.[45] A 2008 evidence-based review of comprehensive treatment approaches found that ABA is well established for improving intellectual performance of young children with ASD.[5] A 2009 comprehensive synthesis of early intensive behavioral intervention (EIBI), a form of ABA treatment, found that EIBI produces strong effects, suggesting that it can be effective for some children with autism; it also found that the large effects might be an artifact of comparison groups with treatments that have yet to be empirically validated, and that no comparisons between EIBI and other widely recognized treatment programs have been published.[46] A 2009 systematic review came to the same principal conclusion that EIBI is effective for some but not all children, with wide variability in response to treatment; it also suggested that any gains are likely to be greatest in the first year of intervention.[6] A 2009 meta-analysis concluded that EIBI has a large effect on full-scale intelligence and a moderate effect on adaptive behavior.[47] However, a 2009 systematic review and meta-analysis found that applied behavior intervention (ABI), another name for EIBI, did not significantly improve outcomes compared with standard care of preschool children with ASD in the areas of cognitive outcome, expressive language, receptive language, and adaptive behavior.[48] Applied behavior analysis is cost effective for administrators [49]
Recently behavior analysts have built comprehensive models of child development (see Behavior analysis of child development) to generate models for prevention as well as treatment for autism.

Pivotal response training[edit]

Main article: //Pivotal response training//
Pivotal response treatment (PRT) is a naturalistic intervention derived from ABA principles. Instead of individual behaviors, it targets pivotal areas of a child's development, such as motivation, responsivity to multiple cues, self-management, and social initiations; it aims for widespread improvements in areas that are not specifically targeted. The child determines activities and objects that will be used in a PRT exchange. Intended attempts at the target behavior are rewarded with a natural reinforcer: for example, if a child attempts a request for a stuffed animal, the child receives the animal, not a piece of candy or other unrelated reinforcer.[50]

Aversive therapy[edit]

The Judge Rotenberg Educational Center uses aversion therapy, notably contingent shock (electric shock delivered to the skin for a few seconds), to control the behavior of its patients, many of whom are autistic. The practice is controversial[51] and has not been popular or used elsewhere since the 1990s.

Communication interventions[edit]

See also: //Speech therapy// and //Picture Exchange Communication System//
The inability to communicate, verbally or non-verbally, is a core deficit in Autism. Children with Autism are often engaged in repetitive activity or other behaviors because they cannot convey their intent any other way. They do not know how to communicate their ideas to caregivers or others. Helping a child with Autism learn to communicate their needs and ideas is absolutely core to any intervention. Communication can either be verbal or non-verbal. Children with Autism require intensive intervention to learn how to communicate their intent.
Communication interventions fall into two major categories. First, many autistic children do not speak, or have little speech, or have difficulties in effective use of language.[52] Social skills have been shown to be effective in treating children with autism.[52] Interventions that attempt to improve communication are commonly conducted by speech and language therapists, and work on joint attention, communicative intent, and alternative oraugmentative and alternative communication (AAC) methods such as visual methods.[53] AAC methods do not appear to impede speech and may result in modest gains.[54] A 2006 study reported benefits both for joint attention intervention and for symbolic play intervention,[55] and a 2007 study found that joint attention intervention is more likely than symbolic play intervention to cause children to engage later in shared interactions.[56]
Second, social skills treatment attempts to increase social and communicative skills of autistic individuals, addressing a core deficit of autism. A wide range of intervention approaches is available, including modeling and reinforcement, adult and peer mediation strategies, peer tutoring, social games and stories, self-management, pivotal response therapy, video modeling, direct instruction, visual cuing, Circle of Friends and social-skills groups.[57] A 2007 meta-analysis of 55 studies of school-based social skills intervention found that they were minimally effective for children and adolescents with ASD,[58] and a 2007 review found that social skills training has minimal empirical support for children with Asperger syndrome or high-functioning autism.[19]


The SCERTS model[59] is an educational model for working with children with autism spectrum disorder (ASD). It was designed to help families, educators and therapists work cooperatively together to maximize progress in supporting the child.
The acronym refers to the focus on:

  • SC – social communication – the development of functional communication and emotional expression.
  • ER – emotional regulation – the development of well-regulated emotions and ability to cope with stress.
  • TS – transactional support – the implementation of supports to help families, educators and therapists respond to children's needs, adapt the environment and provide tools to enhance learning.

Computer-assisted therapy for reasoning about communicative actions[edit]

Many remediation strategies have not taken into account that people with autism suffer from difficulties in learning social rules from examples. Computer-assisted autism therapy has been proposed to teach not simply via examples but to teach the rule along with it.[60] A reasoning rehabilitation strategy, based on playing with a computer based mental simulator that is capable of modeling mental and emotional states of the real world, has been subject to short-term and long-term evaluations.[61] The simulator performs the reasoning in the framework of belief-desire-intention model. Learning starts from the basic concepts of knowledge and intention and proceeds to more complex communicative actions such as explaining, agreeing, and pretending.

Relationship based, developmental models[edit]

Relationship based models give importance to the relationships that help children reach and master early developmental milestones. These are often missed or not mastered in children with ASD. Examples of these early milestones are engagement and interest in the world, intimacy with a caregiver, intentionality of action.

Relationship Development Intervention[edit]

Main article: //Relationship Development Intervention//
Relationship development intervention[62] is a family-based treatment program for children with autism spectrum disorder (ASD). This program is based on the belief that the development of dynamic intelligence (the ability to think flexibly, take different perspectives, cope with change and process information simultaneously) is key to improving the quality of life of children with autism.

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Main article: //Floortime//
The Floortime/DIR (Developmental, Individual Differences based, Relationship based ) approach is a developmental intervention to autism developed by Stanley Greenspan and Serena Weider. This approach is based on the idea that the core deficits in autism are individual differences in the sensory system, motor planning problems, difficulties in communication and relation to others, and the inability to connect ones desire to intentional action and communication. When addressed through a combination of sensory support and DIR/Floortime techniques, the facilitator is playfully obstructive to redirect the child to play and relate to their therapist. The primary goal of Floortime is to improve the child's cognitive, language, and social abilities.[63] However, these claims should be regarded with some scepticism, owing to a lack of independent scientific research into the efficacy of the floortime approach.
The DIR model is based on the model of a developmental 'tree', the central notion being that Autistic children have yet to master certain early developmental milestones, or 'branches' of the tree, which are as follows:

  • Stage One: Regulation and Interest in the World: Being calm and feeling well enough to attend to a caregiver and surroundings. Have shared attention.
  • Stage Two: Engagement and Relating: Interest in another person and in the world, developing a special bond with preferred caregivers. Distinguishing inanimate objects from people.
  • Stage Three: Two way intentional communication: Simple back and forth interactions between child and caregiver. Smiles, tickles, anticipatory play.
  • Stage Four: Social Problem solving: Using gestures, interaction, babble to indicate needs, wants, pleasure, upset. Get a caregiver to help with a problem. Using pre-language skills to show intention.
  • Stage Five: Symbolic Play: Using words, pictures, symbols to communicate an intention, idea. Communicate ideas and thoughts, not just wants and needs.
  • Stage Six: Bridging Ideas: This stage is the foundation of logic, reasoning, emotional thinking and a sense of reality.[64]

Exponents of the floortime approach argue that children with ASD struggle with or have missed some of these vital developmental stages. An introduction to DIR/Floortime can be found in the book – Engaging Autism: Using the Floortime Approach to Help Children Relate, Communicate, and Think, by Stanley Greenspan, M.D. and Serena Wieder, PhD.

The P.L.A.Y. Project (or PLAY Project)[edit]

Main article: //The P.L.A.Y. Project//
The P.L.A.Y. Project (or PLAY Project) [65](an acryonym for PLAY and Language for Autistic Youngsters) is a community-based, national autism training and early intervention program established in 2001 by Richard Solomon, MD.[66] Based on the DIR® (Developmental, Individualized, Relationship-based) theory of Stanley Greenspan MD, the program is designed to train parents and professionals to implement intensive, developmental interventions for young children (18 months to 6 years) with autism. The program is operating in nearly 100 agencies worldwide including 25 states and in 5 countries outside of the U.S. (Australia, Canada, England, Ireland and Switzerland). The PLAY Project has been operating since 2001 from its headquarters in Ann Arbor, MI.
In September 2009, The P.L.A.Y. Project received a $1.85 million grant [67] from the National Institute of Mental Health (NIMH) to conduct a three-year controlled, clinical study of the P.L.A.Y. Project model. Drawing participants from five Easter Seals autism service locations, the study compares the outcomes of 60 children who participate in The P.L.A.Y. Project with the outcomes of 60 children who receive standard community interventions, making it the largest study of its kind. Before and after the 12-month intervention, each child is assessed with a battery of tests to measure developmental level, speech and language, sensory-motor profile, and social skills.
The results of previous research on the program were published by the peer-reviewed British journal, Autism [68] (May, 2007).


Main article: //Son-Rise//
Son-Rise is a home-based program that emphasizes on implementing a color- and sensory-free playroom. Before implementing the home-based program, an institute trains the parents how to accept their child without judgment through a series of dialogue sessions. Like Floortime, parents join their child's ritualistic behavior for relationship-building. To gain the child's "willing engagement", the facilitator continues to join them only this time through parallel play. Proponents claim that children will become non-autistic after parents accept them for who they are and engage them in play. The program was started by the parents of Raun Kaufman, who is claimed to have gone from being autistic to normal via the treatment in the early 1970s.[69] No independent study has tested the efficacy of the program, but a 2003 study found that involvement with the program led to more drawbacks than benefits for the involved families over time,[70] and a 2006 study found that the program is not always implemented as it is typically described in the literature, which suggests it will be difficult to evaluate its efficacy.[71]


Main article: //Treatment and Education of Autistic and Related Communication Handicapped Children//
Treatment and Education of Autistic and Related Communication Handicapped Children (TEACCH), which has come to be called "structured teaching", emphasises structure by using organized physical environments, predictably sequenced activities, visual schedules and visually structured activities, and structured work/activity systems where each child can practice various tasks.[2] Parents are taught to implement the treatment at home. A 1998 controlled trial found that children treated with a TEACCH-based home program improved significantly more than a control group.[72] A 2013 meta-analysis compiling all the clinical trials of TEACCH indicated that it has small or no effects on perceptual, motor, verbal, cognitive, and motor functioning, communication skills, and activities of daily living. There were positive effects in social and maladaptive behavior, but these required further replication due to the methodological limitations of the pool of studies analysed.[73]

Sensory integration[edit]

Main article: //Sensory processing disorder//
Unusual responses to sensory stimuli are more common and prominent in children with autism, although there is not good evidence that sensory symptoms differentiate autism from other developmental disorders.[74] Several therapies have been developed to treat Sensory processing disorder.[75] Some of these treatments (for example, sensorimotor handling) have a questionable rationale and have no empirical evidence. Other treatments have been studied, with small positive outcomes, but few conclusions can be drawn due to methodological problems with the studies. These treatments include prism lenses, physical exercise, auditory integration training, and sensory stimulation or inhibition techniques such as "deep pressure"—firm touch pressure applied either manually or via an apparatus such as a hug machine or a pressure garment.[76] Weighted vests, a popular deep-pressure therapy, have only a limited amount of scientific research available, which on balance indicates that the therapy is ineffective.[77] Although replicable treatments have been described and valid outcome measures are known, gaps exist in knowledge related to Sensory processing disorder and therapy.[78] In a 2011 Cochrane review, no evidence was found to support the use of auditory integration training as an ASD treatment method.[79] Because empirical support is limited, systematic evaluation is needed if these interventions are used.[80]
The term Multisensory integration in simple terms means the ability to use all of ones senses to accomplish a task. Occupational Therapists sometimes prescribe sensory treatments for children with Autism however in general there has been little or no scientific evidence of effectiveness.[76]
A 2008 book My Stroke of Insight by Jill Bolte Taylor gives some insight, from a brain researcher's point of view, on what sensory processing disorder feels like. Other books on sensory integration include The Out of Sync Child – Recognizing and Coping with Sensory Processing Disorder by Carol Kranowitz and Lucy Jane Miller.

Animal-assisted therapy[edit]

Animal-assisted therapy, where an animal such as a dog or a horse becomes a basic part of a person's treatment, is a controversial treatment for some symptoms. A 2007 meta-analysis found that animal-assisted therapy is associated with a moderate improvement in autism spectrum symptoms.[81] Reviews of published dolphin-assisted therapy (DAT) studies have found important methodological flaws and have concluded that there is no compelling scientific evidence that DAT is a legitimate therapy or that it affords any more than fleeting improvements in mood.[82]


Neurofeedback attempts to train individuals to regulate their brainwave patterns by letting them observe their brain activity more directly. In its most traditional form, the output of EEG electrodes is fed into a computer that controls a game-like audiovisual display. Neurofeedback has been evaluated with positive results for ASD, but studies have lacked random assignment to controls.[83]


Patterning is a set of exercises that attempts to improve the organization of a child's neurologic impairments. It has been used for decades to treat children with several unrelated neurologic disorders, including autism. The method, taught at The Institutes for the Achievement of Human Potential, is based on oversimplified theories and is not supported by carefully designed research studies.[84]


In packing, children are wrapped tightly for up to an hour in wet sheets that have been refrigerated, with only their heads left free. The treatment is repeated several times a week, and can continue for years. It is intended as treatment for autistic children who harm themselves; most of these children cannot speak. Similar envelopment techniques have been used for centuries, such as to calm violent patients in Germany in the 19th century; its modern use in France began in the 1960s, based on psychoanalytic theories such as the theory of the refrigerator mother. Packing is currently used in hundreds of French clinics. There is no scientific evidence for the effectiveness of packing, and some concern about risk of adverse health effects.[85]

Other methods[edit]

There are many simple methods such as priming, prompt delivery, picture schedules, peer tutoring, and cooperative learning, that have been proven to help autistic students to prepare for class and to understand the material better. Priming is done by allowing the students to see the assignment or material before they are shown in class. Prompt delivery consists of giving prompts to the autistic children in order to elicit a response to the academic material. Picture schedules are used to outline the progression of a class and are visual cues to allow autistic children to know when changes in the activity are coming up. This method has proven to be very useful in helping the students follow the activities. Peer tutoring and cooperative learning are ways in which an autistic student and a nonhandicapped student are paired together in the learning process. This has shown be very effective for “increasing both academic success and social interaction.”[86] There are more specific strategies that have been shown to improve an autistic’s education, such as LEAP, Treatment and Education of Autistic and Related Communication Handicapped Children, and Non-Model-Specific Special Education Programs for preschoolers. LEAP is “an intensive 12-month program that focuses on providing a highly structured and safe environment that helps students to participate in and derive benefit from educational programming” and focuses on children from 5-21 who are on the have a more severe case of autism.[87] The goal of the program is to develop functional independence through academic instruction, vocational/translational curriculum, speech/language services, and other services personalized for each student.[87] While LEAP, TEACCH, and Non-Model Specific Special Education Programs are all different strategies, there has been no evidence that one is more effective than the other.[88]

Societal aspects[edit]

Martha Nussbaum discusses how education is one of the fertile functions that is important for the development of a person and their ability to achieve a multitude of other capabilities within society.[89] Autism causes many symptoms that interfere with a child’s ability to receive a proper education such as deficits in imitation, observational learning, and receptive and expressive communication. Of all disabilities affecting the population, autism ranks third lowest in acceptance into a postsecondary education institution.[90] In a study funded by the National Institute of Health, Shattuck et al. found that only 35% of autistics are enrolled in a 2 or 4 year college within the first two years after leaving high school compared to 40% of children who have a learning disability.[91] Due to the growing need for a college education to obtain a job, this statistic shows how autistics are at a disadvantage in gaining many of the capabilities that Nussbaum discusses and makes education more than just a type of therapy for those with autism.[90] According to the study by Shattuck, only 55% of children with autism participated in any paid employment within the first two years after high school. Furthermore, those with autism that come from low income families tend to have lower success in postsecondary schooling.[91] Due to these issues, education has become more than just an issue of therapy for those with autism but also a social issue.


Oftentimes, schools simply lack the resources to create an optimal classroom setting for those in need of special education. In the United States, it can cost between $6595 to $10,421 extra to educate a child with autism.[92] In the 2011-2012 school year, the average cost of education for a public school student was $12,401. In some cases, the extra cost required to educate a child with autism nearly doubles the average cost to educate the average public school student.[93] As the range of those with autism can widely vary, it is very difficult to create an autism program that is well suited to the entire population of autistics as well as those with other disabilities. In the United States, many school districts are requiring schools to meet the needs of disabled students, regardless of the number of children with disabilities there are in the school.[94] This combined with a shortage of licensed special education teachers has created a deficiency in the special education system. The shortage has caused some states to give temporary special education licenses to teachers with the caveat that they receive a license within a few years.[95]


In the United States, there have been three major policies addressing special education in the United States. These policies were the Education for All Handicapped Children Act in 1975, the Individuals with Disabilities Education Act in 1997, and the No Child Left Behind in 2001. The development of these policies showed increased guidelines for special education and requirements; such as requiring states to fund special education, equality of opportunities, help with transitions after secondary schooling, requiring extra qualifications for special education teachers, and creating a more specific class setting for those with disabilities.[96][97][98] The Individuals with Disabilities Education Act, specifically had a large impact on special education as public schools were then required to employ high qualified staff. For one to be a Certified Autism Specialist, one must have a master's degree, two years of career experience working with the autism population, earn 14 continuing education hours in autism every two years, and register with the International Institute of Education.[99] In 1993, Mexico passed an education law that called for the inclusion of those with disabilities. This law was very important for Mexico education, however, there have been issues in implementing it due to a lack of resources.[100]
There have also been multiple international groups that have issued reports addressing issues in special education. The United Nations on “International Norms and Standards relating to Disability” in 1998. This report cites multiple conventions, statements, declarations, and other reports such as: The Universal Declaration of Human Rights, The Salamanca Statement, the Sundberg Declaration, the Copenhagen Declaration and Programme of Action, and many others. One main point that the report emphasizes is the necessity for education to be a human right. The report also states that the “quality of education should be equal to that of persons without disabilities.” The other main points brought up by the report discuss integrated education, special education classes as supplementary, teacher training, and equality for vocational education.[101] The United Nations also releases a report by the Special Rapporteur that has a focus on persons with disabilities. In 2015, a report titled “Report of the Special Rapporteur to the 52nd Session of the Commission for Social Development: Note by the Secretary-General on Monitoring of the implementation of the Standard Rules on the Equalization of Opportunities for Persons with Disabilities” was released. This report focused on looking at how the many countries involved, with a focus on Africa, have handled policy regarding persons with disabilities. In this discussion, the author also focuses on the importance of education for persons with disabilities as well as policies that could help improve the education system such as a move towards a more inclusive approach.[102] The World Health Organization has also published a report addressing people with disabilities and within this there is a discussion on education in their “World Report on Disability” in 201.[103] Other organizations that have issued reports discussing the topic are UNESCO, UNICEF, and the World Bank.[104]

Environmental enrichment[edit]

Environmental enrichment is concerned with how the brain is affected by the stimulation of its information processing provided by its surroundings (including the opportunity to interact socially). Brains in richer, more-stimulating environments, have increased numbers of synapses, and thedendrite arbors upon which they reside are more complex. This effect happens particularly during neurodevelopment, but also to a lesser degree in adulthood. With extra synapses there is also increased synapse activity and so increased size and number of glial energy-support cells.Capillary vasculation also is greater to provide the neurons and glial cells with extra energy. The neuropil (neurons, glial cells, capillaries, combined together) expands making the cortex thicker. There may also exist (at least in rodents) more neurons.
Research on nonhuman animals finds that more-stimulating environments could aid the treatment and recovery of a diverse variety of brain-related dysfunctions, including Alzheimer's disease and those connected to aging, whereas a lack of stimulation might impair cognitive development.
Research on humans suggests that lack of stimulation (deprivation—such as in old-style orphanages) delays and impairs cognitive development. Research also finds that higher levels of education (which is both cognitively stimulating in itself, and associates with people engaging in more challenging cognitive activities) results in greater resilience (cognitive reserve) to the effects of aging and dementia.

Massage therapy[edit]

A review of massage therapy as a symptomatic treatment of autism found limited evidence of benefit. There were few high quality studies, and due to the risk of bias found in the studies analyzed, no firm conclusions about the efficacy of massage therapy could be drawn.[105]


Music therapy uses the elements of music to let people express their feelings and communicate. A 2014 review found that music therapy may help in social interactions and communication.[106]
Music therapy can involve various techniques depending on where the subject is sitting on the ASD scale. Somebody who may be considered as 'low-functioning' would require vastly different treatment to somebody on the ASD scale who is 'high-functioning'. Examples of these types of therapeutic techniques include:[107]

  • Free improvisation – No boundaries or skills required
  • Structured improvisation – Some established parameters within the music
  • Performing or recreating music – Reproducing a pre-composed piece of music or song with associated activities
  • Composing music – Creating music that caters to the specific needs of that person using instruments or the voice
  • Listening – Engaging in specific musical listening base exercises

Improvisational Music Therapy (IMT), is increasing in popularity as a therapeutic technique being applied to children with ASD. The process of IMT occurs when the client and therapist make up music, through the use of various instruments, song and movement. The specific needs of each child or client need to be taken into consideration. Some children with ASD find their different environments chaotic and confusing, therefore, IMT sessions require the presence of a certain routine and be predictable in nature, within their interactions and surroundings.[108] Music can provide all of this, it can be very predicable, it is highly repetitious with its melodies and sounds, but easily varied with phrasing, rhythm and dynamics giving it a controlled flexibility. The allowance of parents or caregivers to sessions can put the child at ease and allow for activities to be incorporated into everyday life.[108]

Sensory enrichment therapy[edit]

Tentative evidence supports sensory enrichment.[109]

Parent mediated interventions[edit]

Parent mediated interventions offer support and practical advice to parents of autistic children.[53] A 2002 Cochrane Review found only two relevant studies, with small numbers of participants, and no clinical recommendations could be made due to these limitations.[110] A very small number of randomized and controlled studies suggest that parent training can lead to reduced maternal depression, improved maternal knowledge of autism and communication style, and improved child communicative behavior, but due to the design and number of studies available, definitive evidence of effectiveness is not available.[111]
Early detection of ASD in children can often occur before a child reaches the age of three years old. Methods that target early behavior can influence the quality of life for a child with ASD. Parents can learn methods of interaction and behavior management to best assist their child's development. A 2013 Cochrance review concluded that there were some improvements when parent intervention was used.[112]

Medical management[edit]

Drugs, supplements, or diets are often used to alter physiology in an attempt to relieve common autistic symptoms such as seizures, sleep disturbances, irritability, and hyperactivity that can interfere with education or social adaptation or (more rarely) cause autistic individuals to harm themselves or others.[113] There is plenty of anecdotal evidence to support medical treatment; many parents who try one or more therapies report some progress, and there are a few well-publicized reports of children who are able to return to mainstream education after treatment, with dramatic improvements in health and well-being. However, this evidence may be confounded by improvements seen in autistic children who grow up without treatment, by the difficulty of verifying reports of improvements, and by the lack of reporting of treatments' negative outcomes.[114] Only a very few medical treatments are well supported by scientific evidence using controlled experiments.[113]

Prescription medication[edit]

Many medications are used to treat problems associated with ASD.[10] More than half of U.S. children diagnosed with ASD are prescribedpsychoactive drugs or anticonvulsants, with the most common drug classes being antidepressants, stimulants, and antipsychotics.[11] Only the antipsychotics have clearly demonstrated efficacy.[12]
Research has focused on atypical antipsychotics, especially risperidone, which has the largest amount of evidence that consistently shows improvements in irritability, self-injury, aggression, and tantrums associated with ASD.[115] Risperidone is approved by the Food and Drug Administration (FDA) for treating symptomatic irritability in autistic children and adolescents.[12] In short-term trials (up to six months) most adverse events were mild to moderate, with weight gain, drowsiness, and high blood sugar requiring monitoring; long term efficacy and safety have not been fully determined.[116] It is unclear whether risperidone improves autism's core social and communication deficits.[12] The FDA's decision was based in part on a study of autistic children with severe and enduring problems of tantrums, aggression, and self-injury; risperidone is not recommended for autistic children with mild aggression and explosive behavior without an enduring pattern.[117]
Other drugs are prescribed off-label in the U.S., which means they have not been approved for treating ASD. Large placebo-controlled studies ofolanzapine and aripiprazole were underway in early 2008.[12] Aripiprazole may be effective for treating autism, but is also associated with side effects, such as weight gain and sedation.[118][//needs update//] Some selective serotonin reuptake inhibitors (SSRIs) and dopamine blockers can reduce some maladaptive behaviors associated with ASD.[119] Although SSRIs reduce levels of repetitive behavior in autistic adults,[120] a 2009 multisite randomized controlled study found no benefit and some adverse effects in children from the SSRI citalopram, raising doubts whether SSRIs are effective for treating repetitive behavior in autistic children.[121] A further study of related medical reviews determined that the prescription of SSRI antidepressants for treating autistic spectrum disorders in children lacked any evidence, and could not be recommended.[122][//needs update//] One study found that the psychostimulant methylphenidate was efficacious against hyperactivity associated with ASD, though with less response than in neurotypical children with ADHD.[13] Of the many medications studied for treatment of aggressive and self-injurious behavior in children and adolescents with autism, only risperidone and methylphenidate demonstrate results that have been replicated.[123] A 1998 study of the hormone secretin reported improved symptoms and generated tremendous interest, but several controlled studies since have found no benefit.[124] Oxytocin may play a role in autism and may be an effective treatment for repetitive and affiliative behaviors;[125] two related studies in adults found that oxytocin decreased repetitive behaviors and improved interpretation of emotions, but these preliminary results do not necessarily apply to children.[126] An experimental drug STX107 has stopped overproduction of metabotropic glutamate receptor 5 in rodents, and it has been hypothesized that this may help in about 5% of autism cases, but this hypothesis has not been tested in humans.[126]
Aside from antipsychotics,[12] there is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD.[13] Results of the handful of randomized controlled trials that have been performed suggest that risperidone, the SSRI fluvoxamine, and the typical antipsychotic haloperidol may be effective in reducing some behaviors, that haloperidol may be more effective than the tricyclic antidepressant clomipramine, and that the opioid antagonist naltrexone hydrochloride is not effective.[14] In small studies, memantine has been shown to significantly improve language function and social behavior in children with autism.[127][128] Research is underway on the effects of memantine in adults with autism spectrum disorders.[129] A person with ASD may respond atypically to medications and the medications can have adverse side effects.[15][130]

Dietary supplements[edit]

Many parents give their children dietary supplements in an attempt to treat autism or to alleviate its symptoms. The range of supplements given is wide; few are supported by scientific data, but most have relatively mild side effects.[18][113]
A review found some low-quality evidence to support the use of vitamin B6 in combination with magnesium at high doses, but the evidence was equivocal and the review noted the possible danger of fatal hypermagnesemia.[131] A Cochrane Review of the evidence for the use of B6 and magnesium found that "[d]ue to the small number of studies, the methodological quality of studies, and small sample sizes, no recommendation can be advanced regarding the use of B6-Mg as a treatment for autism."[132]
Dimethylglycine (DMG) is hypothesized to improve speech and reduce autistic behaviors,[18] and is a commonly used supplement.[113] Two double-blind, placebo-controlled studies found no statistically significant effect on autistic behaviors,[18] and reported few side effects. No peer-reviewed studies have addressed treatment with the related compound trimethylglycine.[113]
Vitamin C decreased stereotyped behavior in a small 1993 study.[133] The study has not been replicated, and vitamin C has limited popularity as an autism treatment. High doses might cause kidney stones or gastrointestinal upset such as diarrhea.[113]
Probiotics containing potentially beneficial bacteria are hypothesized to relieve some symptoms of autism by minimizing yeast overgrowth in thecolon. The hypothesized yeast overgrowth has not been confirmed by endoscopy, the mechanism connecting yeast overgrowth to autism is only hypothetical, and no clinical trials to date have been published in the peer-reviewed literature. No negative side effects have been reported.[113]
Melatonin is sometimes used to manage sleep problems in developmental disorders. Adverse effects are generally reported to be mild, including drowsiness, headache, dizziness, and nausea; however, an increase in seizure frequency is reported among susceptible children.[18] Several small RCTs have indicated that melatonin is effective in treating insomnia in autistic children, but further large studies are needed.[134] A 2013 literature review found 20 studies that reported improvements in sleep parameters as a result of melatonin supplementation, and concluded that "the administration of exogenous melatonin for abnormal sleep parameters in ASD is evidence-based."[135]
Although omega-3 fatty acids, which are polyunsaturated fatty acids (PUFA), are a popular treatment for children with ASD, there is very little high-quality scientific evidence supporting their effectiveness,[136][137] and further research is needed.[2]
Several other supplements have been hypothesized to relieve autism symptoms, including BDTH2,[138] carnosine, cholesterol,[139] cyproheptadine,D-cycloserine, folic acid, glutathione, metallothionein promoters, other PUFA such as omega-6 fatty acids, tryptophan, tyrosine, thiamine (seeChelation therapy), vitamin B12, and zinc. These lack reliable scientific evidence of efficacy or safety in treatment of autism.[18][113]


Further information: //Gluten-free, casein-free diet//
Atypical 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;[140] 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;[141] studies report conflicting results, and the relationship between GI problems and ASD is unclear.[2]
In the early 1990s, it was hypothesized that autism can be caused or aggravated by opioid peptides like casomorphine that are metabolic products of gluten and casein.[142] Based on this hypothesis, diets that eliminate foods containing either gluten or casein, or both, are widely promoted, and many testimonials can be found describing benefits in autism-related symptoms, notably social engagement and verbal skills. Studies supporting these claims have had significant flaws, so these data are inadequate to guide treatment recommendations.[24][143]
Other elimination diets have also been proposed, targeting salicylates, food dyes, yeast, and simple sugars. No scientific evidence has established the efficacy of such diets in treating autism in children. An elimination diet may create nutritional deficiencies that harm overall health unless care is taken to assure proper nutrition.[18] For example, a 2008 study found that autistic boys on casein-free diets have significantly thinner bones than usual, presumably because the diets contribute to calcium and vitamin D deficiencies.[144]

Chelation therapy[edit]

Based on the speculation that heavy metal poisoning may trigger the symptoms of autism, particularly in small subsets of individuals who cannot excrete toxins effectively, some parents have turned to alternative medicine practitioners who provide detoxification treatments via chelation therapy. However, evidence to support this practice has been anecdotal and not rigorous. Strong epidemiological evidence refutes links between environmental triggers, in particular thiomersal containing vaccines, and the onset of autistic symptoms. No scientific data supports the claim that the mercury in the vaccine preservative thiomersal causes autism[145] or its symptoms,[146] and there is no scientific support for chelation therapy as a treatment for autism.[147][148]
Thiamine tetrahydrofurfuryl disulfide (TTFD) is hypothesized to act as a chelating agent in children with autism. A 2002 pilot study administered TTFD rectally to ten autism spectrum children, and found beneficial clinical effect.[149] This study has not been replicated, and a 2006 review of thiamine by the same author did not mention thiamine's possible effect on autism.[150] There is not sufficient evidence to support the use of thiamine (vitamin B1) to treat autism.[18]


Chiropractic is an alternative medical practice whose main hypothesis is that mechanical disorders of the spine affect general health via the nervous system, and whose main treatment is spinal manipulation. A significant portion of the profession rejects vaccination, as traditional chiropractic philosophy equates vaccines to poison.[151] Most chiropractic writings on vaccination focus on its negative aspects,[152] claiming that it is hazardous, ineffective, and unnecessary,[151] and in some cases suggesting that vaccination causes autism[152] or that chiropractors should be the primary contact for treatment of autism and other neurodevelopmental disorders.[153] Chiropractic treatment has not been shown to be effective for medical conditions other than back pain,[154] and there is insufficient scientific evidence to make conclusions about chiropractic care for autism.[155]

Craniosacral therapy[edit]

Craniosacral therapy is an alternative medical practice whose main hypothesis is that restrictions at cranial sutures of the skull affect rhythmic impulses conveyed via cerebrospinal fluid, and that gentle pressure on external areas can improve the flow and balance of the supply of this fluid to the brain, relieving symptoms of many conditions.[156] There is no scientific support for major elements of the underlying model,[157] there is little scientific evidence to support the therapy, and research methods that could conclusively evaluate the therapy's effectiveness have not been applied.[156] No published studies are available on the use of this therapy for autism.[17]

Electroconvulsive therapy[edit]

Studies indicate that 12–17% of adolescents and young adults with autism satisfy diagnostic criteria for catatonia, which is loss of or hyperactive motor activity. Electroconvulsive therapy (ECT) has been used to treat cases of catatonia and related conditions in people with autism. However, no controlled trials have been performed of ECT in autism, and there are serious ethical and legal obstacles to its use.[158]

Hyperbaric oxygen therapy[edit]
A boy with ASD, and his father, in a hyperbaric oxygen chamber.
One small 2009 double-blind study of autistic children found that 40 hourly treatments of 24% oxygen at 1.3 atmospheres provided significant improvement in the children's behavior immediately after treatment sessions but this study has not been independently confirmed.[159] More recent, relatively large-scale controlled studies have also investigated HBOT using treatments of 24% oxygen at 1.3 atmospheres and have found less promising results. A 2010 double-blind study compared HBOT to a placebo treatment in children with autistic disorder. Both direct observational measures of behavioral symptoms and standardized psychological assessments were used to evaluate the treatment. No differences were found between the HBOT group and the placebo group on any of the outcome measures.[160] A second 2011 single-subject design study also investigated the effects of 40 HBOT treatments of 24% oxygen at 1.3 atmospheres on directly observed behaviors using multiple baselines across 16 participants. Again, no consistent outcomes were observed across any group and further, no significant improvements were observed within any individual participant.[161] Together these studies suggest that HBOT at 24% oxygen at 1.3 atmospheric pressure does not result in a clinically significant improvement of the behavioral symptoms of autistic disorder.
Nonetheless, news reports and related blogs indicate that HBOT is used for many cases of children with autism. HBOT can cost up to $150 per hour with individuals using anywhere from 40 to 120 hours as a part of their integrated treatment programs. In addition, purchasing (at $8,495–27,995) and renting ($1,395 per month) of the HBOT chambers is another option some families use.[161] When considering the financial and time investments required in order to participate in this treatment and the inconsistency of the present findings, HBOT seems to be a riskier and thus, often less favorable alternative treatment for autism. Further studies are needed in order for practitioners and families to make more conclusive and valid decisions concerning HBOT treatments.[162]


Unlike conventional neuromotor prostheses, neurocognitive prostheses would sense or modulate neural function in order to physically reconstitute cognitive processes such as executive function and language. No neurocognitive prostheses are currently available but the development of implantable neurocognitive brain-computer interfaces has been proposed to help treat conditions such as autism.[163]
Affective computing devices, typically with image or voice recognition capabilities, have been proposed to help autistic individuals improve their social communication skills.[164] These devices are still under development. Robots have also been proposed as educational aids for autistic children.[165]

Transcranial magnetic stimulation[edit]

Transcranial magnetic stimulation, which is a somewhat well established treatment for depression, has been proposed, and used, as a treatment for autism.[166] A review published in 2013 found insufficient evidence to support its widespread use for autism spectrum disorders.[167] A 2015 review found tentative but insufficient evidence to justify its us outside of clinical studies.[168]

Stem cell therapy[edit]

Mesenchymal stem cells and cord blood CD34+ cells have been proposed to treat autism, but this proposal has not been tested.[169] They may represent a future treatment.[170] Since immune system deregulation has been implicated in autism, mesenchymal stem cells show the greatest promise as treatment for the disorder. Changes in the innate and adaptive immune system have been observed. Those with autism show an imbalance in CD3+, CD4+, and CD8+ T cells, as well as in NK cells.[171] In addition, peripheral blood mononuclear cells (PBMCs) overproduce IL-1β.[171] MSC mediated immune suppressive activity could restore this immune imbalance.

Alternative medicine[edit]

Acupuncture has not been found to be helpful.[172]

Religious interventions[edit]

The //Table Talk// of Martin Luther contains the story of a twelve-year-old boy who some believe was severely autistic.[173] 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.[174] In 2003, an autistic boy in Wisconsin suffocated during an exorcism by an Evangelical minister in which he was wrapped in sheets.[175]
Ultraorthodox Jewish parents sometimes use spiritual and mystical interventions such as prayers, blessings, recitations of religious text, amulets, changing the child's name, and exorcism.[176]
One study has suggested that spirituality and not religious activities involving the mothers of autistic children were associated with better outcomes for the child.[177]

Anti-cure perspective[edit]

Further information: //Autism rights movement § Anti-cure perspective//
The exact cause of autism is unclear, yet some organizations advocate researching a cure. Some autism rights organizations view autism as a way of life rather than as a mental disorder and thus advocate acceptance over a search for a cure.[178][179]

Historical approach[edit]

Before autism was well understood, children in Britain and America would often be put in institutions on the instruction of doctors and the parents told to forget about them. Observer journalist Christopher Stevens, father of an autistic child, reports how a British doctor told him that after a child was admitted, usually "nature would take its course" and the child would die due to the prevalence of tuberculosis.[180]

Kilde til ovenstående:

The epidemiology of autism is the study of factors affecting autism spectrum disorders (ASD). A 2012 review of global prevalence estimates ofautism spectrum disorders found a median of 62 cases per 10,000 people.[1] There is a lack of evidence from low- and middle-income countries though.[1]
ASD averages a 4.3:1 male-to-female ratio.[2] The number of children known to have autism has increased dramatically since the 1980s, at least partly due to changes in diagnostic practice; it is unclear whether prevalence has actually increased;[2] and as-yet-unidentified environmental risk factors cannot be ruled out.[3] The risk of autism is associated with several prenatal factors, including advanced paternal age and diabetes in the mother during pregnancy.[4] ASD is associated with several genetic disorders[5] and with epilepsy.[6]
Autism is a complex neurodevelopmental disorder. Many causes have been proposed, but its theory of causation is still questionable and ultimately unknown.[2][7] Autism is believed to be largely inherited, although the genetics of autism are complex and it is unclear which genes are responsible.[8] Little evidence exists to support associations with specific environmental exposures.[2]
In rare cases, autism is strongly associated with agents that cause birth defects.[9] Other proposed causes, such as childhood vaccines, arecontroversial and the vaccine hypotheses lack any convincing scientific evidence.[3] Andrew Wakefield published a small study in 1998 in the United Kingdom suggesting a causal link between autism and the trivalent MMR vaccine. After data included in the report was shown to be deliberately falsified, the paper was retracted, and Wakefield's medical license revoked.[10][11]


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.[2]

Incidence and prevalence[edit]

Epidemiology defines several measures of the frequency of occurrence of a disease or condition:[12]

  • The incidence rate of a condition is the rate at which new cases occurred per person-year, for example, "2 new cases per 1,000 person-years".
  • The cumulative incidence is the proportion of a population that became new cases within a specified time period, for example, "1.5 per 1,000 people became new cases during 2006".
  • The point prevalence of a condition is the proportion of a population that had the condition at a single point in time, for example, "10 cases per 1,000 people at the start of 2006".
  • The period prevalence is the proportion that had the condition at any time within a stated period, for example, "15 per 1,000 people had cases during 2006".

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.[12] 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.[2]

Estimation methods[edit]

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.[13]
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.[13]

Frequency estimates[edit]

Estimates of the prevalence of autism vary widely depending on diagnostic criteria, age of children screened, and geographical location.[14] 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;[2] PDD-NOS is the vast majority of ASD, Asperger syndrome is about 0.3 per 1,000 and the atypical forms childhood disintegrative disorder and Rett syndrome are much rarer.[15]
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.[16] 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.[17] A 2009 study of the children in Cambridgeshire, England used different methods to measure prevalence, and estimated that 40% of ASD cases go undiagnosed, with the two least-biased estimates of true prevalence being 11.3 and 15.7 per 1,000.[18]
A 2009 U.S. study based on 2006 data estimated the prevalence of ASD in 8-year-old children to be 9.0 per 1,000 (approximate range 8.6–9.3).[19] A 2009 report based on the 2007 Adult Psychiatric Morbidity Survey by the National Health Service determined that the prevalence of ASD in adults was approximately 1% of the population, with a higher prevalence in males and no significant variation between age groups;[20]these results suggest that prevalence of ASD among adults is similar to that in children and rates of autism are not increasing.[21]

Changes with time[edit]

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 100.[2]
Bar chart versus time. The graph rises steadily from 1996 to 2007, from about 0.7 to about 5.3. The trend curves slightly upward.Bar chart versus time. The graph rises steadily from 1996 to 2007, from about 0.7 to about 5.3. The trend curves slightly upward.
Reports of autism cases per 1,000 children grew dramatically in the U.S. from 1996 to 2007. It is unknown how much, if any, growth came from changes in autism'sprevalence.[22]
The number of reported cases of autism increased dramatically in the 1990s and early 2000s, prompting investigations into several potential reasons:[23]

  • More children may have autism; that is, the true frequency of autism may have increased.
  • There may be more complete pickup of autism (case finding), as a result of increased awareness and funding. For example, attempts to sue vaccine companies may have increased case-reporting.
  • The diagnosis may be applied more broadly than before, as a result of the changing definition of the disorder, particularly changes in DSM-III-R and DSM-IV.
  • An editorial error in the description of the PDD-NOS category of Autism Spectrum Disorders in the DSM-IV, in 1994, inappropriately broadened the PDD-NOS construct. The error was corrected in the DSM-IV-TR, in 2000, reversing the PDD-NOS construct back to the more restrictive diagnostic criteria requirements from the DSM-III-R.[24]
  • Successively earlier diagnosis in each succeeding cohort of children, including recognition in nursery (preschool), may have affected apparent prevalence but not incidence.
  • A review of the "rising autism" figures compared to other disabilities in schools shows a corresponding drop in findings of mental retardation.[25]

The reported increase is largely attributable to changes in diagnostic practices, referral patterns, availability of services, age at diagnosis, and public awareness.[2][3][22] A widely cited 2002 pilot study concluded that the observed increase in autism in California cannot be explained by changes in diagnostic criteria,[26] 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.[27]
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.[28] 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.[29] 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.[30]
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.[31] Another 2009 California study found that the reported increases are unlikely to be explained by changes in how qualifying condition codes for autism were recorded.[32]
Several 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.[2] Although there is overwhelming scientific evidence against the MMR hypothesis and no convincing evidence for the thiomersal hypothesis, other as-yet-unidentified environmental risk factors cannot be ruled out.[3] 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.[33]

Geographical frequency[edit]


The prevalence of autism in Africa is unknown.[34]



The rate of autism diagnoses in Canada was 1 in 450 in 2003. However, preliminary results of an epidemiological study conducted at Montreal Children's Hospital in the 2003-2004 school year found a prevalence rate of 0.68% (or 1 per 147).[35]
A 2001 review of the medical research conducted by the Public Health Agency of Canada concluded that there was no link between MMR vaccine and either inflammatory bowel disease or autism.[36] The review noted, "An increase in cases of autism was noted by year of birth from 1979 to 1992; however, no incremental increase in cases was observed after the introduction of MMR vaccination." [36] After the introduction of MMR, "A time trend analysis found no correlation between prevalence of MMR vaccination and the incidence of autism in each birth cohort from 1988 to 1993."[36]

United States[**edit**]

CDC's most recent estimate is that 1 out of every 68 children, or 14.7 per 1,000, have some form of ASD as of 2010.[37] The number of diagnosed cases of autism grew dramatically in the U.S. in the 1990s and early 2000s. For the 2006 surveillance year, identified ASD cases were an estimated 9.0 per 1000 children aged 8 years (95% confidence interval [CI] = 8.6–9.3).[19] 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.[27] This prevalence estimate rose 57% (95% CI 27%–95%) from 2002 to 2006.[19]
The number of new cases of austism spectrum disorder (ASD) in Caucasian boys is roughly 50% higher than found in Hispanic children, and approximately 30% more likely to occur than in Non-Hispanic white children in the United States.[2][38]
A further study in 2006 concluded that the apparent rise in administrative prevalence was the result of diagnostic substitution, mostly for findings of mental retardation and learning disabilities.[27] "Many of the children now being counted in the autism category would probably have been counted in the mental retardation or learning disabilities categories if they were being labelled 10 years ago instead of today," said researcherPaul Shattuck of the Waisman Center at the University of Wisconsin–Madison, in a statement.[39]
A population-based study in Olmsted County, 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.[40] 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.[41]


A 2008 study in Venezuela reported a prevalence of 1.1 per 1000 for autism and 1.7 per 1000 for ASD.[42]


A journal reports that the median prevalence of ASD among 2–6-year-old children who are reported in China from 2000 upwards was 10.3/10,000.[43]

Hong Kong[**edit**]

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.[44]


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 the triple MMR vaccine dropped to near zero and was replaced with MR and M vaccine, the incidence rate grew to 97 and 161 cases per 10,000 children born in 1993 and 1994, respectively, indicating that the combined MMR vaccine did not cause autism.[45] A 2004 Japanese autism association reported that about 360.000 people have typical kanner type autism.

Middle East[edit]


A 2009 study reported that the annual incidence rate of Israeli children with a diagnosis of ASD receiving disability benefits rose from zero in 1982–1984 to 190 per million in 2004. It was not known whether these figures reflected true increases or other factors such as changes in diagnostic measures.[46]

Saudi Arabia[**edit**]

Studies of autism frequency have been particularly rare in the Middle East. One rough estimate is that the prevalence of autism in Saudi Arabia is 18 per 10,000, slightly higher than the 13 per 10,000 reported in developed countries. Estimates for ASD prevalence in Saudi Arabia are not available.[47]



A 2003 study reported that the cumulative incidence of autism in Denmark was stable until 1990. In 1992, thimerosal-containing vaccines were removed in Denmark. The incidence of autism increased after the removal of thimerosal-containing vaccines, during the interval from 1991 until 2000. 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. The study concluded that "ecological data do not support a correlation between thimerosal-containing vaccines and the incidence of autism".[48]


France made autism the national focus for the year 2012 and the Health Ministry now evaluates the rate of autism to be 67 per 10000 (1 out of 150).[49]
Eric Fombonne made some studies in the years 1992 and 1997. He found a prevalence of 16 per 10.000 for the global pervasive developmental disorder (PDD).[50][51] The INSERM found a prevalence of 27 per 10,000 for the ASD and a prevalence of 9 per 10,000 for the early infantile autism in 2003.[52] Those figures are considered as underrated as the WHO gives figures between 30 and 60 per 10,000.[53] The French Minister of Health gives a prevalence of 4.9 per 10,000 on its website but it counts only early infantile autism.[54]


A 2008 study in Germany 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%.[55]


A 2009 study in Norway reported prevalence rates for ASD ranging from 0.21% to 0.87%, depending on assessment method and assumptions about non-response, suggesting that methodological factors explain large variances in prevalence rates in different studies.[56]

United Kingdom[**edit**]

The incidence and changes in incidence with time are unclear in the United Kingdom.[57] The reported autism incidence in the UK rose starting before the first introduction of the MMR vaccine in 1989.[58] However, a perceived link between the two arising from the results of a fraudulent scientific study, has caused considerable controversy, despite being subsequently disproved.[59] 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.[60]


Further information: //Heritability of autism//
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.[61] The first studies of twins estimated heritability to be more than 90%; in other words, that genetics explains more than 90% of autism cases.[8] 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%,[62] much higher than the risk in controls.[63] About 10–15% of autism cases have an identifiable Mendelian (single-gene) condition, chromosome abnormality, or other genetic syndrome,[62] and ASD is associated with several genetic disorders.[5]
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;[2] new twin data and models with structural genetic variation are needed.[64]
Genetic linkage analysis has been inconclusive; many association analyses have had inadequate power.[64] 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.[2]

Risk factors[edit]

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.[2]
Autism is associated with several prenatal risk factors, including advanced age in either parent, diabetes, bleeding and use of psychiatric drugs in the mother during pregnancy.[4] Autism was found to be indirectly linked to prepregnancy obesity and low weight mothers.[65] 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.[66] However, recent studies have identified advancing paternal age as a significant risk factor for ASD.[67] Increased risk of autism has also been linked to rapid "catch-up" growth for children born to mothers who had unhealthy weight at conception.[65]
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.[68]
It is not known how many siblings of autistic individuals are themselves autistic. Several studies based on clinical samples have given quite different estimates, and these clinical samples differ in important ways from samples taken from the general community.[69]
Autism has also been shown to cluster in urban neighborhoods of high socioeconomic status. One study from California found a three to fourfold increased risk of autism in a small 30 by 40 km region centered on West Hollywood, Los Angeles.[70]

Comorbid conditions[edit]

Further information: //Conditions comorbid to autism spectrum disorders//
Autism is associated with several other conditions:

  • **Genetic disorders**. About 10–15% of autism cases have an identifiable Mendelian (single-gene) condition, chromosome abnormality, or other genetic syndrome,[62] and ASD is associated with several genetic disorders.[5]
  • **Intellectual disability**. The fraction of autistic individuals who also meet criteria for intellectual disability has been reported as anywhere from 25% to 70%, a wide variation illustrating the difficulty of assessing autistic intelligence.[71]
  • **Anxiety disorders** are common among children with ASD, although there are no firm data.[72] Symptoms include generalized anxiety andseparation anxiety,[73] and are likely affected by age, level of cognitive functioning, degree of social impairment, and ASD-specific difficulties. Many anxiety disorders, such as social phobia, are not commonly diagnosed in people with ASD because such symptoms are better explained by ASD itself, and it is often difficult to tell whether symptoms such as compulsive checking are part of ASD or a co-occurring anxiety problem. The prevalence of anxiety disorders in children with ASD has been reported to be anywhere between 11% and 84%.[72]
  • **Epilepsy**, with variations in risk of epilepsy due to age, cognitive level, and type of language disorder; 5–38% of children with autism have comorbid epilepsy, and only 16% of these have remission in adulthood.[6]
  • Several **metabolic defects**, such as phenylketonuria, are associated with autistic symptoms.[74]
  • **Minor physical anomalies** are significantly increased in the autistic population.[75]
  • Preempted diagnoses. Although the DSM-IV rules out concurrent diagnosis of many other conditions along with autism, the full criteria forADHD, Tourette syndrome, and other of these conditions are often present and these comorbid diagnoses are increasingly accepted.[76] A 2008 study found that nearly 70% of children with ASD had at least one psychiatric disorder, including nearly 30% with social anxiety disorderand similar proportions with ADHD and oppositional defiant disorder.[77] Childhood-onset schizophrenia, a rare and severe form, is another preempted diagnosis whose symptoms are often present along with the symptoms of autism.[78]

Kilde til ovenstående:

Autism spectrum or autism spectrum disorder describes a range of conditions classified asneurodevelopmental disorders in the DSM-5, published in 2013. Individuals diagnosed with autism spectrum disorder must present two types of symptoms:

  • Deficits in social communication and social interaction
  • Restricted, repetitive patterns of behavior, interests or activities

The DSM-5 redefined the autism spectrum disorders to encompass the previous (DSM-IV-TR) diagnoses of autism, Asperger syndrome, pervasive developmental disorder not otherwise specified(PDD-NOS), and childhood disintegrative disorder.[1]
Features of these disorders include social deficits and communication difficulties, stereotyped or repetitive behaviors and interests, sensory issues, and in some cases, cognitive delays.


Further information: //Autism § Classification//
File:Autism spectrum disorder video.webmFile:Autism spectrum disorder video.webm
Autism spectrum disorder video
In the United States, a revision to autism spectrum disorder (ASD) was presented in the Diagnostic and Statistical Manual of Mental Disorders version 5 (DSM-5), released May 2013.[2] The new diagnosis encompasses previous diagnoses of autistic disorder, Asperger's disorder, childhood disintegrative disorder, and PDD-NOS. Compared with the DSM-IV diagnosis of autistic disorder, the DSM-5 diagnosis of ASD no longer includes communication as a separate criterion, and has merged social interaction and communication into one category.[3] Slightly different diagnostic definitions are used in other countries. For example, the ICD-10 is the most commonly-used diagnostic manual in the UK.[4]
Rather than categorizing these diagnoses, the DSM-5 has adopted a dimensional approach to diagnosing disorders that fall underneath the autism spectrum umbrella. Some have proposed that individuals on the autism spectrum may be better represented as a single diagnostic category. Within this category, the DSM-5 has proposed a framework of differentiating each individual by dimensions of severity, as well as associated features (i.e., known genetic disorders, and intellectual disability).[//citation needed//]
Another change to the DSM includes collapsing social and communication deficits into one domain. Thus, an individual with an ASD diagnosis will be described in terms of severity of social communication symptoms, severity of fixated or restricted behaviors or interests, and associated features. The restricting of onset age has also been loosened from 3 years of age to "early developmental period", with a note that symptoms may manifest later when demands exceed capabilities.[//citation needed//][//clarification needed//]
Autism forms the core of the autism spectrum disorders. Asperger syndrome is closest to autism in signs and likely causes;[5] unlike autism, people with Asperger syndrome have no significant delay in language development, according to the older DSM-4 criteria.[6] PDD-NOS is diagnosed when the criteria are not met for a more specific disorder. Some sources also include Rett syndrome and childhood disintegrative disorder, which share several signs with autism but may have unrelated causes; other sources differentiate them from ASD, but group all of the above conditions into the pervasive developmental disorders.[5][7]
Autism, Asperger syndrome, and PDD-NOS are sometimes called the autistic disorders instead of ASD,[8] whereas autism itself is often calledautistic disorder, childhood autism, or infantile autism.[9] Although the older term pervasive developmental disorder and the newer term autism spectrum disorder largely or entirely overlap,[7] the earlier was intended to describe a specific set of diagnostic labels, whereas the latter refers to a postulated spectrum disorder linking various conditions.[10] ASD 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.[9]


Under the DSM-5, autism is characterized by persistent deficits in social communication and interaction across multiple contexts, as well as restricted, repetitive patterns of behavior, interests, or activities. These deficits are present in early childhood, and lead to clinically significant functional impairment.[11] There is also a unique form of autism called autistic savantism, where a child can display outstanding skills in music, art, and numbers with no practice.[12] Because of its relevance to different populations, self-Injurious behaviors (SIB) are not considered a core characteristic of the ASD population however approximately 50% of those with ASD take part in some type of SIB (head-banging, self-biting) and are more at risk than other groups with developmental disabilities.[13]
Some of the language behaviors typically seen in children with autism may include repetitive or rigid language, specific interests in conversation, atypical language development, or poor nonverbal communication skills, including lack of eye contact and meaningful gestures and facial expressions.[14]
Asperger syndrome was distinguished from autism in the DSM-IV by the lack of delay or deviance in early language development.[15] Additionally, individuals diagnosed with Asperger syndrome did not have significant cognitive delays.[16] PDD-NOS was considered "subthreshold autism" and "atypical autism" because it was often characterized by milder symptoms of autism or symptoms in only one domain (such as social difficulties).[17]The DSM-5 eliminated the four separate diagnosis: Asperger Syndrome, Pervasive Developmental Disorder Not Otherwise Specified (PDD-NOS), Childhood Degenerative Disorder, and Autistic Disorder and combined them under the diagnosis of Autism Spectrum Disorder.[11]

Developmental course[edit]

Autism spectrum disorders are thought to follow two possible developmental courses, although most parents report that symptom onset occurred within the first year of life.[18][19] One course of development is more gradual in nature, in which parents report concerns in development over the first two years of life and diagnosis is made around 3–4 years of age. Some of the early signs of ASDs in this course include decreased looking at faces, failure to turn when name is called, failure to show interests by showing or pointing, and delayed pretend play.[20]
A second course of development is characterized by normal or near-normal development followed by loss of skills or regression in the first 2–3 years. Regression may occur in a variety of domains, including communication, social, cognitive, and self-help skills; however, the most common regression is loss of language.[21][22]
There continues to be a debate over the differential outcomes based on these two developmental courses. Some studies suggest that regression is associated with poorer outcomes and others report no differences between those with early gradual onset and those who experience a regression period.[23] While there is conflicting evidence surrounding language outcomes in ASD, some studies have shown that cognitive and language abilities at age  2 1⁄2 may help predict language proficiency and production after age 5.[24] Overall, the literature stresses the importance of early intervention in achieving positive longitudinal outcomes.[25]


Main article: //Causes of autism//
While specific causes of autism spectrum disorders have yet to be found, many risk factors have been identified in the research literature that may contribute to their development. These risk factors include genetics, prenatal and perinatal factors, neuroanatomical abnormalities, and environmental factors. It is possible to identify general risk factors, but much more difficult to pinpoint specific factors. In the current state of knowledge, prediction can only be of a global nature and therefore requires the use of general markers.[26]

Genetic risk factors[edit]

The results of family and twin studies suggest that genetic factors play a role in the etiology of autism and other pervasive developmental disorders.[27] Studies have consistently found that the prevalence of autism in siblings of autistic children is approximately 15 to 30 times greater than the rate in the general population.[28] In addition, research suggests that there is a much higher concordance rate among monozygotic twins compared to dizygotic twins.[29] It appears that there is no single gene that can account for autism. Instead, there seem to be multiple genes involved, each of which is a risk factor for components of the autism spectrum disorders.[30][31][32]

Prenatal and perinatal risk factors[edit]

Several prenatal and perinatal complications have been reported as possible risk factors for autism. These risk factors include maternalgestational diabetes, maternal and paternal age over 30, bleeding after first trimester, use of prescription medication (e.g. valproate) during pregnancy, and meconium in the amniotic fluid. While research is not conclusive on the relation of these factors to autism, each of these factors has been identified more frequently in autistic children compared to their non-autistic siblings and other normally developing youth.[33]
Low vitamin D levels in early development has been hypothesized as a risk factor for autism.[34]

Vaccine controversy[edit]

Main article: //MMR vaccine controversy//
Perhaps the most controversial claim regarding autism etiology was the "vaccine controversy".[35] This conjecture, arising from a case of scientific misconduct,[36] suggested that autism results from brain damage caused either by (1) the measles, mumps, rubella (MMR) vaccine itself, or by (2)thimerosal, a vaccine preservative.[37] No convincing scientific evidence supports these claims, and further evidence continues to refute them, including the observation that the rate of autism continues to climb despite elimination of thimerosal from routine childhood vaccines.[38] A 2014 meta-analysis examined ten major studies on autism and vaccines involving 1.25 million children worldwide; it concluded that neither the MMR vaccine, which has never contained thimerosal,[39] nor the vaccine components thimerosal or mercury, lead to the development of ASDs.[40]


Main article: //Autism § Mechanism//
In general, neuroanatomical studies support the concept that autism may involve a combination of brain enlargement in some areas and reduction in others.[41] These studies suggest that autism may be caused by abnormal neuronal growth and pruning during the early stages of prenatal and postnatal brain development, leaving some areas of the brain with too many neurons and other areas with too few neurons.[42] Some research has reported an overall brain enlargement in autism, while others suggest abnormalities in several areas of the brain, including the frontal lobe, the mirror neuron system, the limbic system, the temporal lobe, and the corpus callosum.[43][44]
In neuroanatomical studies, when performing theory of mind and facial emotion response tasks, the median person on the autism spectrum exhibits less activation in the primary and secondary somatosensory cortices of the brain than the median member of a properly sampled control population. This finding coincides with reports demonstrating abnormal patterns of cortical thickness and grey matter volume in those regions of autistic persons' brains.[45]

Mirror neuron system[edit]

Main article: //Mirror neuron//
The mirror neuron system (MNS) consists of a network of brain areas that have been associated with empathy processes in humans.[46] In humans, the MNS has been identified in the inferior frontal gyrus (IFG) and the inferior parietal lobule (IPL) and is thought to be activated during imitation or observation of behaviors.[47] The connection between mirror neuron dysfunction and autism is tentative, and it remains to be seen how mirror neurons may be related to many of the important characteristics of autism.[48][49]

Temporal lobe[edit]

Functions of the temporal lobe are related to many of the deficits observed in individuals with ASDs, such as receptive language, social cognition,joint attention, action observation, and empathy. The temporal lobe also contains the superior temporal sulcus (STS) and the fusiform face area(FFA), which may mediate facial processing. It has been argued that dysfunction in the STS underlies the social deficits that characterize autism. Compared to typically developing individuals, one fMRI study found that individuals with high-functioning autism had reduced activity in the FFA when viewing pictures of faces.[50]

Mitochondrial dysfunction[edit]

It has been suggested that ASD could be linked to mitochondrial disease (MD), a basic cellular abnormality with the potential to cause disturbances in a wide range of body systems.[51] A recent meta-analysis study, as well as other population studies have shown that approximately 5% of children with ASD meet the criteria for classical MD.[52] It is unclear why the MD occurs considering that only 23% of children with both ASD and MD present with mitochondrial DNA (mtDNA) abnormalities.[52]


It has been hypothesized that increased activity of serotonin in the developing brain may facilitate the onset of autism spectrum disorder, with an association found in six out of eight studies between the use of selective serotonin reuptake inhibitors (SSRIs) by the pregnant mother and the development of ASD by the child exposed to SSRI in the antenatal environment. The study could not definitively conclude SSRIs caused the increased risk for ASDs due to the biases found in those studies, and the authors called for more definitive, better conducted studies.[53]


Evidence-based assessment[edit]

ASD can be detected as early as eighteen months or even younger in some cases.[54] A reliable diagnosis can usually be made by the age of two.[55] The diverse expressions of ASD symptoms pose diagnostic challenges to clinicians. Individuals with an ASD may present at various times of development (e.g., toddler, child, or adolescent), and symptom expression may vary over the course of development.[56] Furthermore, clinicians must differentiate among the different pervasive developmental disorders, and may also consider similar conditions, including intellectual disabilitynot associated with a pervasive developmental disorder, specific language disorders, ADHD, anxiety, and psychotic disorders.[57]
Considering the unique challenges in diagnosing ASD, specific practice parameters for its assessment have been published by the American Academy of Neurology,[58] the American Academy of Child and Adolescent Psychiatry,[56] and a consensus panel with representation from various professional societies.[59] The practice parameters outlined by these societies include an initial screening of children by general practitioners (i.e., "Level 1 screening") and for children who fail the initial screening, a comprehensive diagnostic assessment by experienced clinicians (i.e. "Level 2 evaluation"). Furthermore, it has been suggested that assessments of children with suspected ASD be evaluated within a developmental framework, include multiple informants (e.g., parents and teachers) from diverse contexts (e.g., home and school), and employ a multidisciplinary team of professionals (e.g., clinical psychologists, neuropsychologists, and psychiatrists).[60]
After a child shows initial evidence of ASD tendencies, psychologists administer various psychological assessment tools to assess for ASD.[60]Among these measurements, the Autism Diagnostic Interview-Revised (ADI-R) and the Autism Diagnostic Observation Schedule (ADOS) are considered the "gold standards" for assessing autistic children.[61][62] The ADI-R is a semi-structured parent interview that probes for symptoms of autism by evaluating a child's current behavior and developmental history. The ADOS is a semistructured interactive evaluation of ASD symptoms that is used to measure social and communication abilities by eliciting several opportunities (or "presses") for spontaneous behaviors (e.g., eye contact) in standardized context. Various other questionnaires (e.g., The Childhood Autism Rating Scale, Autism Treatment Evaluation Checklist) and tests of cognitive functioning (e.g., The Peabody Picture Vocabulary Test) are typically included in an ASD assessment battery.[//citation needed//]
In the UK, there is some diagnostic use of the Diagnostic Interview for Social and Communication Disorders (DISCO)[63] was which was developed for use at The Centre for Social and Communication Disorders, by Lorna Wing and Judith Gould, as both a clinical and a research instrument for use with children and adults of any age. The DISCO is designed to elicit a picture of the whole person through the story of their development and behaviour. In clinical work, the primary purpose is to facilitate understanding of the pattern over time of the specific skills and impairments that underlie the overt behaviour. If no information is available, the clinician has to obtain as much information as possible concerning the details of current skills and pattern of behaviour of the person. This type of dimensional approach to clinical description is useful for prescribing treatment.[64]


Main article: //Conditions comorbid to autism spectrum disorders//
Autism spectrum disorders tend to be highly comorbid with other disorders. Comorbidity may increase with age and may worsen the course of youth with ASDs and make intervention/treatment more difficult. Distinguishing between ASDs and other diagnoses can be challenging, because the traits of ASDs often overlap with symptoms of other disorders, and the characteristics of ASDs make traditional diagnostic procedures difficult.[65][66]
The most common medical condition occurring in individuals with autism spectrum disorders is seizure disorder or epilepsy, which occurs in 11-39% of individuals with ASD.[67] Tuberous sclerosis, a medical condition in which non-malignant tumors grow in the brain and on other vital organs, occurs in 1-4% of individuals with ASDs.[68]
Intellectual disabilities are some of the most common comorbid disorders with ASDs. Recent estimates suggest that 40-69% of individuals with ASD have some degree of an intellectual disability,[23] with females more likely to be in the severe range of an intellectual disability. A number of genetic syndromes causing intellectual disability may also be comorbid with ASD, including fragile X syndrome, Down syndrome, Prader-Willi andAngelman syndromes, and Williams syndrome.[69]
Learning disabilities are also highly comorbid in individuals with an ASD. Approximately 25-75% of individuals with an ASD also have some degree of a learning disability.[70]
Various anxiety disorders tend to co-occur with autism spectrum disorders, with overall comorbidity rates of 7-84%.[23] Rates of comorbiddepression in individuals with an ASD range from 4–58%.[71] The relationship between ASD and schizophrenia remains a controversial subject under continued investigation, and recent meta-analyses have examined genetic, environmental, infectious, and immune risk factors that may be shared between the two conditions.[72][73][74]
Deficits in ASD are often linked to behavior problems, such as difficulties following directions, being cooperative, and doing things on other people's terms.[75] Symptoms similar to those of attention deficit hyperactivity disorder (ADHD) can be part of an ASD diagnosis.[76]
Sensory processing disorder is also comorbid with ASD, with comorbidity rates of 42–88%.[77]


Main article: //Autism therapies//
There is no known cure for autism, although those with Asperger syndrome and those who have autism and require little-to-no support are more likely to experience a lessening of symptoms over time.[78][79][80] The main goals of treatment are to lessen associated deficits and family distress, and to increase quality of life and functional independence. In general, higher IQs are correlated with greater responsiveness to treatment and improved treatment outcomes.[81][82] Although evidence-based interventions for autistic children vary in their methods, many adopt a psychoeducational approach to enhancing cognitive, communication, and social skills while minimizing problem behaviors. It has been argued that no single treatment is best and treatment is typically tailored to the child's needs.[83]
Intensive, sustained special education programs and behavior therapy early in life can help children acquire self-care, social, and job skills. Available approaches include applied behavior analysis, developmental models, structured teaching, speech and language therapy, social skillstherapy, and occupational therapy.[83] Among these approaches, interventions either treat autistic features comprehensively, or focus treatment on a specific area of deficit.[82]
There has been increasing attention to the development of evidence-based interventions for young children with ASD. Two theoretical frameworks outlined for early childhood intervention include applied behavioral analysis (ABA) and the developmental social-pragmatic model(DSP).[82] Although ABA therapy has a strong evidence base, particularly in regard to early intensive home-based therapy. ABA's effectiveness may be limited by diagnostic severity and IQ of the person effected by ASD.[84] The Journal of Clinical Child and Adolescent Psychology has deemed two early childhood interventions as “well-established”: individual comprehensive ABA, and focused teacher-implemented ABA combined with DSP.[82]
Another evidence-based intervention that has demonstrated efficacy is a parent training model, which teaches parents how to implement variousABA and DSP techniques themselves.[82] Various DSP programs have been developed to explicitly deliver intervention systems through at-home parent implementation.
A multitude of unresearched alternative therapies have also been implemented. Many have resulted in harm to autistic people and should not employed unless proven to be safe.[//citation needed//]
In October 2015, the American Academy of Pediatrics (AAP) proposed new evidence-based recommendations[85] for early interventions in ASD for children under 3. These recommendations emphasize early involvement with both developmental and behavioral methods, support by and for parents and caregivers, and a focus on both the core and associated symptoms of ASD.[//citation needed//]


Main article: //Epidemiology of autism//
The U.S. Center for Disease Control's most recent estimate is that 1 out of every 68 children, or 14.7 per 1,000, have some form of ASD as of 2010.[86] Reviews tend to estimate a prevalence of 6 per 1,000 for autism spectrum disorders as a whole,[87] although prevalence rates vary for each of the developmental disorders in the spectrum. Autism prevalence has been estimated at 1-2 per 1,000, Asperger syndrome at roughly 0.6 per 1,000, childhood disintegrative disorder at 0.02 per 1,000, and PDD-NOS at 3.7 per 1,000.[87] These rates are consistent across cultures and ethnic groups, as autism is considered a universal disorder.[23]
While rates of autism spectrum disorders are consistent across cultures, they vary greatly by gender, with boys affected far more frequently than girls. The average male-to-female ratio for ASDs is 4.2:1,[88] affecting 1 in 70 males, but only 1 in 315 females.[89] Females, however, are more likely to have associated cognitive impairment. Among those with an ASD and intellectual disability, the sex ratio may be closer to 2:1.[90]Prevalence differences may be a result of gender differences in expression of clinical symptoms, with autistic females showing less atypical behaviors and, therefore, less likely to receive an ASD diagnosis.[91]


Further information: //Autism § History//
Controversies have surrounded various claims regarding the etiology of autism spectrum disorders. In the 1950s, the "refrigerator mother theory" emerged as an explanation for autism. The hypothesis was based on the idea that autistic behaviors stem from the emotional frigidity, lack of warmth, and cold, distant, rejecting demeanor of a child's mother.[92] Naturally, parents of children with an autism spectrum disorder suffered from blame, guilt, and self-doubt, especially as the theory was embraced by the medical establishment and went largely unchallenged into the mid-1960s. The "refrigerator mother" theory has since continued to be refuted in scientific literature, including a 2015 systematic review which showed no association between caregiver interaction and language outcomes in ASD.[93]
Another controversial claim suggests that watching extensive amounts of television may cause autism. This hypothesis was largely based on research suggesting that the increasing rates of autism in the 1970s and 1980s were linked to the growth of cable television at this time.[38]

Society and culture[edit]

Autism rainbow infinityAutism rainbow infinity
The rainbow-colored infinity symbol represents the diversity of the autism spectrum as well as the greaterneurodiversity movement.


Families who care for an autistic child face added stress from a number of different causes. Parents may be shocked and dismayed by the diagnosis, and they may struggle to understand their child's diagnosis and find appropriate care options. They also struggle emotionally. In the words of a physician whose two children were both diagnosed with autism, “In the moment of diagnosis, it feels like the death of your hopes and dreams.”[94]
One study found that half of parents who had a child with any kind of developmental disability were still caring for their child by age 50[//clarification needed//], while only 17% of parents that age would typically be caring for children.[95]

Autism rights movement[edit]

Further information: //Autism rights movement// and //Neurodiversity//
The autism rights movement (ARM) is a social movement within the neurodiversity movement that encourages autistic people, their caregivers, and society to adopt a position of neurodiversity, and to accept autism as a variation in functioning rather than a mental disorder to be cured.[96]The ARM advocates for several goals, including a greater acceptance of autistic behaviors,[97] therapies that teach autistic individuals coping skills rather than therapies focused on imitating behaviors of neurotypical peers,[98] the creation of social networks and events that allow autistic people to socialize on their own terms,[99] and the recognition of the autistic community as a minority group.[100][//non-primary source needed//]
Autism rights and neurodiversity advocates believe that the autism spectrum is genetic and should be accepted as a natural expression of the human genome. This perspective is distinct from two other likewise distinct views:[96]

  • The perspective that autism is caused by a genetic defect and should be addressed by targeting the autism gene(s) is the most common or “mainstream” view.
  • The perspective that autism is caused by environmental factors, like vaccines and pollution, and could be cured by addressing environmental causes is a less common view, but is likewise contrary to neurodiversity.

The movement is controversial. A common criticism leveled against autistic activists is that many have Asperger syndrome or are otherwise high-functioning, and therefore do not represent the views of all autistic people.[101]

See also[edit]
Refrigerator mother theory is a widely discarded theory that autism is caused by a lack of maternal warmth. Current research indicates that a combination of genetic factors and exposure to environmental agents predominate in the cause of autism.[1]

The terms refrigerator mother and refrigerator parents were coined around 1950 as a label for mothers and parents of children diagnosed with autism or schizophrenia. When Leo Kanner first identified autism in 1943, he noted the lack of warmth among the parents of autistic children. Parents, particularly mothers, were often blamed for their children's atypical behavior, which included rigid rituals, speech difficulty, and self-isolation. Kanner later rejected the "refrigerator mother" theory, instead focusing on brain mechanisms.[2]
Origins of theory[edit]
In his 1943 paper that first identified autism, Leo Kanner called attention to what appeared to him as a lack of warmth among the fathers and mothers of autistic children.[3] In a 1949 paper, Kanner suggested autism may be related to a "genuine lack of maternal warmth", noted that fathers rarely stepped down to indulge in children's play, and observed that children were exposed from "the beginning to parental coldness, obsessiveness, and a mechanical type of attention to material needs only…. They were left neatly in refrigerators which did not defrost. Their withdrawal seems to be an act of turning away from such a situation to seek comfort in solitude."[4] In a 1960 interview, Kanner bluntly described parents of autistic children as "just happening to defrost enough to produce a child."[5] In Kanner's original paper, however, only one set of parents were described as "cold", with many family members appearing to be from one neurological minority or another upon close reading of the text.[6]
Although Kanner was instrumental in framing the refrigerator mother theory, it was Bruno Bettelheim, a University of Chicago professor and child development specialist, who facilitated its widespread acceptance both by the public and by the experts in the medical establishment in the 1950s and 1960s. In the absence of any biomedical explanation of autism's cause after the telltale symptoms were first described by scientists, Bettelheim and other leading psychoanalysts championed the notion that autism was the product of mothers who were cold, distant and rejecting, thus depriving their children of the chance to "bond properly". Bettelheim founded the Orthogenic School at the University of Chicago as a residential treatment milieu for such children, who he felt would benefit from a "parentectomy". This marked the apex of autism viewed as a disorder of parenting.[7]

The theory was embraced by the medical establishment and went largely unchallenged into the mid-1960s, but its effects have lingered into the 21st century. Many articles and books published in that era blamed autism on a maternal lack of affection, but by 1964, Bernard Rimland, apsychologist who had an autistic son, published a book that signaled the emergence of a counter-explanation to the established misconceptions about the causes of autism. His book, Infantile Autism: The Syndrome and its Implications for a Neural Theory of Behavior, attacked the refrigerator mother hypothesis directly.
Soon afterwards, Bettelheim wrote The Empty Fortress: Infantile Autism and the Birth of the Self, in which he compared autism to being a prisoner in a concentration camp:
"The difference between the plight of prisoners in a concentration camp and the conditions which lead to autism and schizophrenia in children is, of course, that the child has never had a previous chance to develop much of a personality."
Some authority was granted to this as well, because Bettelheim had himself been interned at the Dachau concentration camp before World War II. The book was immensely popular and he became a leading public figure on autism until his suicide in 1990. He became controversial after his death when it was learned that he had fabricated his credentials, and as former students at the Orthogenic School claimed he abused them.[8]There was a biography written 7 years after his death by the brother of a former patient, who interviewed some of the ex-patients who characterized him as a cruel tyrant.[9]
In 1969, Kanner addressed the refrigerator mother issue at the first annual meeting of what is now the Autism Society of America, stating:
From the very first publication until the last, I spoke of this condition in no uncertain terms as "innate." But because I described some of the characteristics of the parents as persons, I was misquoted often as having said that "it is all the parents' fault."[10]
Other notable psychiatrists[edit]
For Silvano Arieti, who wrote his major works from the 1950s through the 70s, the terms autistic thought and what he called paleologic thought are apparently the same phenomenon. Paleologic thought is a characteristic in both present-day schizophrenics and primitive men, a type of thinking that has its foundations in non-Aristotelian logic. An autistic child speaks of himself as "you" and not infrequently of the mother as "I". The "you" remains a "you" and is not transformed into "I".[11]
For Margaret Mahler and her colleagues, autism is a defense of children who cannot experience the mother as the living primary-object. According to them, autism is an attempt at dedifferentiation and deanimation.[12] The symbiotic autistic syndrome used to be called the "Mahler syndrome" because Mahler first described it: The child is unable to differentiate from the mother.
Arieti warned that an autistic tendency is a sign of a kind of disorder in the process of socialization, and that when autistic expressions appear it should be assumed that there is a sort of difficulty between the child and his parents, especially the schizogenic mother. Children who use autistic expressions, Arieti observes, are children who cannot bond socially.
In //Interpretation of Schizophrenia// Arieti maintained that for a normal process of socialization, it is necessary for the parent-child relations to be normal. Loving or non-anxiety parental attitudes favor socialization. Arieti not only maintained that the parent-child relations are the first social act and the major drive of socialization, but also a stimulus to either accept or reject society. The child's self in this view is a reflection of the sentiments, thoughts, and attitudes of the parents toward the child. Autistic children show an extreme socializing disorder and do not want any sort of relationship with people. They "eliminate" people from their consciousness. For Arieti the fear of the parents is extended to other adults: a tendency to cut off communication with human beings.
Persistence of the theory[edit]
According to Peter Breggin's 1991 book Toxic Psychiatry, the psychogenic theory of autism was abandoned for political pressure from parents' organizations, not for scientific reasons. For example, some case reports have shown that profound institutional privation can result in quasi-autistic symptoms.[13] Clinician Frances Tustin devoted her life to the theory. She wrote:
One must note that autism is one of a number of children's neurological disorders of psychogenic nature, i.e., caused by abusive and traumatic treatment of infants…. There is persistent denial by American society of the causes of damage to millions of children who are thus traumatized and brain damaged as a consequence of cruel treatment by parents who are otherwise too busy to love and care for their babies.[14]
Alice Miller, one of the best-known authors of the consequences of child abuse, has maintained that autism is psychogenic, and that fear of the truth about child abuse is the leitmotif of nearly all forms of autistic therapy known to her. When Miller visited several autism therapy centers in the United States, it became apparent to her that the stories of children "inspired fear in both doctors and mothers alike":
I spent a day observing what happened to the group. I also studied close-ups of children on video. What became clearer and clearer as the day went on was that all these children had a serious history of suffering behind them. This, however, was never referred to…. In my conversations with the therapists and mothers, I inquired about the life stories of individual children. The facts confirmed my hunch. No one, however, was willing to take these facts seriously.[15]
Like Arieti and Tustin, Miller believes that only empathetic parental attitudes lead to the complete blossoming of the child’s personality.
The refrigerator mother theory, widely discarded in the United States, still has some support in France[16] and Europe and is largely believed in South Korea to be the cause of autism.[17] The academic psychologist Tony Humphreys of University College Cork is a leading Irish proponent of the theory of frigid parenting, despite censure by the Psychological Society of Ireland.[18]
Modern alternatives[edit]
The modern consensus is that autism has a strong genetic basis, although the genetics of autism are complex and are not well understood.[19]Moreover, fetal and infant exposure to pesticides, viruses, and household chemicals have also been implicated as triggering the syndrome. [20]
Although recent studies have indicated that maternal warmth, praise, and quality of relationship are associated with reductions of behavior problems in autistic adolescents and adults, and that maternal criticisms are associated with maladaptive behaviors and symptoms, these ideas are distinct from the refrigerator mother hypothesis.[21]
Documentary film[edit]
In 2002, Kartemquin Films released //Refrigerator Mothers//, a documentary that takes a look at American mothers of the 1950s and 1960s and the blame leveled by the medical establishment for the mothers causing their children's autism. The premier was shown the Summer of 2002 by United States' PBS, which the PBS website has described as 'Though wholly discredited today, the “refrigerator mother” diagnosis condemned thousands of autistic children to questionable therapies, and their mothers to a long nightmare of self-doubt and guilt. In Refrigerator Mothers, the new film by David E. Simpson, J.J.Hanley and Gordon Quinn, and a Kartemquin Educational Films production, these mothers tell their story for the first time.'[22][23][24]
See also[edit]

Kilde til ovenstående:

The medical model of autism encourages continual research into the causes of autism, with the primary goal of finding a way to prevent or cure autism. This is a subset of the medical model of disability in general. The model advocates a variety of goals including increased awareness of autism prevalence, earlier and more accessible diagnosis, elimination of autistic behaviors through therapies such as applied behavior analysis, identification of environmental factors that may cause autism in infancy, and identification of a genetic marker to allow testing for autism in utero.
Advocates for the medical model believe that autism is a disorder caused by genetic defects or environmental harm, that the value of talents attributed to autism does not outweigh the deficits, and that autistic people would be better off if they were not autistic.
Many organizations subscribe to the medical model, most of which have non-profit status. The autism rights and neurodiversity movements are critics of the medical view.

Medical definition[edit]

Main article: //Autism//
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.[1]


The medical model has been the most popular stance on autism ever since the condition was identified by Leo Kanner and Hans Asperger in 1943. Researchers at the time believed that autism was similar to schizophrenia but with the patients being more self-involved.
In 1965, the National Society for Autistic Children, later renamed the Autism Society of America, was founded by Bernard Rimland and Ruth C. Sullivan, along with a small group of other parents.[2] The Autism Society does not advocate explicitly to cure autism.
In 1995, the Autism Research Institute (ARI) began hosting its annual Defeat Autism Now! (DAN!) conference to discuss the latest developments in research. Beginning with the 2011 conference, ARI renamed it the ARI conference and suspended the list of DAN! doctors.[3]
In 2005, Autism Speaks was founded by Bob Wright and Suzanne Wright, a year after their grandson Christian was diagnosed as autistic.[4]Autism Speaks has since become the most recognized autism-related organization worldwide. Other celebrity endorsements of the medical model have included Ed Asner, Toni Braxton, Jim Carrey, Byron Dafoe, Sarah Gardner, Robert F. Kennedy, Jr., Olaf Kölzig, Scott Mellanby, Zack Peter,AJ Rafael, and Mike Rio.
In 2008, the first World Autism Awareness Day was celebrated after a United Nations General Assembly resolution recognizing the day passed in December 2007.[5][6][7][8]

Current groups promoting the medical model[edit]

  • Athletes Against Autism is an association of athletes founded by three NHL players, which leverages the celebrity status of athletes to promote awareness and fundraising.
  • Autism Research Institute (ARI) is an information resource advocating various methods of autism treatment, some of which have been medically discredited. ARI hosted an annual conference called Defeat Autism Now! between 1995 and 2011.
  • Autism Speaks is an organization dedicated to awareness, research, and public policy advocacy. Autism Speaks has merged with the National Alliance for Autism Research and with Cure Autism Now.
  • Center for Autism and Related Disorders (CARD) is a therapy service that primarily provides families with applied behavior analysis.
  • In 2002, Autism Awareness Campaign UK initiated Autism Sunday, an international day of prayer observed on the second Sunday of February.
  • April is designated as Autism Awareness Month (called Autism Acceptance Month in the autism rights movement) to promote media coverage and fundraising for autism-related organizations. In 2008, a United Nations General Assembly resolution recognized April 2 as World Autism Awareness Day.[5][6][7][8]
  • In 2010, Autism Speaks launched Light It Up Blue, an awareness and fundraising campaign urging homeowners and businesses to replace their light bulbs with specialty blue light bulbs on April 2. Autism Speaks also benefits from blue autism- and puzzle-coded merchandise year-round.

Events and activities[edit]


Cure and prevention[edit]

The pro-cure perspective is a view of autism as a disorder characterized by various impairments, mostly in communication and social interaction. Although positive traits such as savant syndrome may be recognized, they are not seen as outweighing the negatives. Pro-cure organizations generally favor the medical model of disability with regards to autism. They believe that the atypical behaviors of autistic individuals are a detriment to those individuals' success, both socially and professional, and should therefore be reduced or eliminated through therapy. Autistic people's life experiences are viewed as sub-standard and a burden to their caretakers.
Autism Speaks co-founder Suzanne Wright published a "Call for Action" at the time of the organization's first national policy summit in Washington, D.C., explaining the urgency of what she called the autism crisis.[9] In this essay, she equates children being autistic to being "missing" and "gravely ill", and details the exhaustive experiences of their parents:

Each day across this country, those three million moms, dads and other care-takers I mentioned wake to the sounds of their son or daughter bounding through the house. That is – if they aren’t already awake. Truth be told, many of them barely sleep—or when they do – they somehow sleep with one ear towards their child’s room—always waiting. Wondering what they will get into next. Will they try to escape? Hurt themselves? Strip off their clothes? Climb the furniture? Raid the refrigerator? Sometimes – the silence is worse.
These families are not living.
They are existing. Breathing – yes. Eating – yes. Sleeping- maybe. Working- most definitely – 24/7.
This is autism.

The puzzle piece ribbon is the most recognized symbol for autism awareness.
Awareness campaigns by various organizations draw attention to the prevalence of autism, estimated by the year 2012 as 1 in 68 individuals (1 in 42 males, 1 in 189 females) by the United States Centers for Disease Control and Prevention (CDC).[10] This figure has risen from the estimated 1 in 150 in the year 2000. The prevalence statistic is used to describe the scope and size of the problem, and the increase over time is used to frame the issue as urgent. Some organizations and individuals even call it the autism //epidemic//.[11] Awareness campaigns educate people not only about the prevalence of autism but also how it is characterized. Almost every autism-related organization has a flyer or a section of their website describing what autism is, in a way that supports the organization's point of view. Descriptions used by the medical model are generally based on the facts and language used in medical journals.
Autism is classified as a disorder in the //Diagnostic and Statistical Manual of Mental Disorders// and International Statistical Classification of Diseases and Related Health Problems. Attempts have been made to place a figure on the financial cost of autism, addressed to both scholarly[12] and popular audiences.[13]


Main article: //Autism rights movement//
See also: //Folk epidemiology of autism//
Activists like Jim Sinclair and Donna Williams and Damon Matthew Wise, and organizations such as Aspies For Freedom and the Autistic Self Advocacy Network, contend that autism is not a disorder, but a normal variant within the neurological diversity of the human genome. Struggles faced by autistic people are attributed to discrimination rather than deficiencies. Proponents of the anti-cure perspective believe that quirks and uniqueness of autistic individuals should be accepted and that efforts to eliminate autism should not be compared, for example, to curing cancer but instead to the antiquated notion of curing left-handedness.[14][15] Therapies that attempt to restrict autistic behaviors, particularly applied behavior analysis (ABA), have been challenged on ethical grounds. Autism rights activists 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.[16] Michelle Dawson, a Canadian autism self-advocate, testified in court against government funding of ABA therapy.[15] 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.[14]


  1. 1. **Jump up****^** American Psychiatric Association. //Diagnostic and statistical manual of mental disorders: DSM-IV//. 4 ed. Washington, DC: American Psychiatric Association; 2000. ISBN 978-0-89042-025-6. OCLC 768475353. Diagnostic criteria for 299.00 Autistic Disorder.
  2. 2. **Jump up****^** //"Autism Society history"// (PDF). Autism Society. 2011.
  3. 3. **Jump up****^** Leitch, Kevin (2011-01-02). //"2011 – The Last Year For ARI's DAN!// //Doctors"//. Left Brain Right Brain.
  4. 4. **Jump up****^** Gross J, Strom S (2007-06-18). //"Autism debate strains a family and its charity"//. New York Times. //Archived// from the original on April 16, 2009. Retrieved 2007-10-09.
  5. 5. ^ Jump up to:**//a//** **//b//** //"Third Committee calls on Assembly to designate 2 April World Autism Day"// (Press release). UN General Assembly. 1 November 2007. Retrieved 29 October 2009.
  6. 6. ^ Jump up to:**//a//** **//b//** //"General Assembly Adopts Landmark Text Calling for Moratorium on Death Penalty, Adopts 54 Resolutions, 12 Decisions Recommended by Third Committee"// (Press release). UN General Assembly. 18 December 2007. Retrieved 29 October 2009.
  7. 7. ^ Jump up to:**//a//** **//b//** United Nations General Assembly Session 62 Resolution 139.**A/RES/62/139** page 2. 18 December 2007. Retrieved 29 October 2009.
  8. 8. ^ Jump up to:**//a//** **//b//** United Nations General Assembly Session 62 Verbatim Report76. **A/62/PV.76** 18 December 2007. Retrieved 29 October 2009.
  9. 9. **Jump up****^** Wright, Suzanne (2013-11-11). //"Autism Speaks to Washington – A Call for Action"//. Autism Speaks.
  10. 10. **Jump up****^** //"Autism Spectrum Disorder Data & Statistics"//. Centers for Disease Control and Prevention. 2014-03-24.
  11. 11. **Jump up****^** //"Autism Epidemic"//. The Autism Epidemic.
  12. 12. **Jump up****^** John L R Rubenstein; Moldin, Steven O. (2006). Understanding autism: from basic neuroscience to treatment. Boca Raton: Taylor & Frances. //ISBN// //0-8493-2732-6//.
  13. 13. **Jump up****^** //"Autism Clock"//. Archived from //the original// on 2007-07-21. Retrieved 2008-01-04.
  14. 14. ^ Jump up to:**//a//** **//b//** Harmon, Amy (2004-12-20). //"How About Not 'Curing' Us, Some Autistics Are Pleading"//. The New York Times. //Archived// from the original on December 2, 2011. Retrieved 2007-11-07.
  15. 15. ^ Jump up to:**//a//** **//b//** //"In Support of Michelle Dawson and Her Work"//. Retrieved 2012-03-21.
  16. 16. **Jump up****^** Mission Statement. Aspies for Freedom. Retrieved on 2008-11-24.

External links[edit]

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The autism rights movement (ARM), also known as the autistic culture movement, is a social movement within the neurodiversity and disability rights movements that encourages autistic people, their caregivers and society to adopt a position of neurodiversity, accepting autism as a variation in functioning rather than a disorder to be cured.[1] The ARM advocates a variety of goals including a greater acceptance of autistic behaviors;[2] therapies that teach autistic individuals coping skills rather than therapies focused on imitating behaviors of neurotypical peers;[3] the creation of social networks and events that allow autistic people to socialize on their own terms;[4] and the recognition of the autistic community as a minority group.[5]
Autism rights or neurodiversity advocates believe that the autism spectrum is genetic and should be accepted as a natural expression of the human genome. This perspective is distinct from two other likewise distinct views: (1) the mainstream perspective that autism is 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.[1]
The movement is controversial. There are a wide variety of both supportive and critical opinions about the movement among people who are autistic or associated with people with autism. A common criticism leveled against autistic activists is that the majority of them are high-functioning or have Asperger syndrome and do not represent the views of all autistic people,[6] although some prominent figures in the movement (such asAmy Sequenzia[7]) are nonverbal and have been labeled as low-functioning.


Jim Sinclair was the first individual to communicate the anti-cure or autism rights perspective in the late 1980s.[1] In 1992, Sinclair co-founded theAutism Network International, an organization that publishes newsletters "written by and for autistic people". Other individuals involved in the creation of the ANI were Donna Williams and Kathy Grant, two autistic individuals who knew Sinclair through pen pal lists and autism conferences. The first issue of the ANI newsletter, Our Voice, was distributed online in November 1992, to an audience of mostly neurotypical professionals and parents of young autistic children. The number of autistics in the organization grew slowly, over the years, and it eventually became a communication network for like-minded autistics.[8]
In 1996, a yearly retreat known as Autreat was established. Autreat is a United States retreat and conference hosted by the autism rights organization Autism Network International, specifically for autistic people.[9] As of 2012, Autreat has been held every year, except for 2001.
In 2004, Michelle Dawson challenged applied behavior analysis (ABA) on ethical grounds. She testified in //Auton v. British Columbia// against the required government funding of ABA.[10] That same year //The New York Times// covered the autism rights perspective by publishing Amy Harmon's article, "How about not curing us? Some autistics are pleading."[11]
Aspies For Freedom (AFF) was founded in 2004, and established June 18 as Autistic Pride Day starting in 2005. AFF was also instrumental in initiating protests against the National Alliance for Autism Research, Cure Autism Now, and the Judge Rotenberg Center.[11]
In 2006, the Autism Acceptance Project was founded by Estée Klar, the mother of an autistic child, with help from an autistic advisory and board.[12] The project affiliated with The Autistic Self Advocacy Network and other activist groups in North America and was one of the first to sign the petition against the New York Child Study Campaign. It is also recognized by ASAN in a letter to the United Nations of being one of the first autism organizations to promote autism acceptance. From 2005-8, TAAProject organized arts-based events to show the public an active autism rights movement that burgeoned online. In addition, it sponsored the controversial Joy of Autism: Redefining Ability and Quality of Life events and lectures in Toronto, featuring dozens of autistic artists and speakers including Jim Sinclair, Michelle Dawson, Phil Schwartz, Morton Ann Gernsbacher, Larry Bissonnette and more. In 2014, TAAProject worked with York University to bring non-verbal autistic self-advocates who type to communicate, Larry Bissonnette and Tracy Thresher to discuss autism and screen the film Wretches & Jabberers. Estee Klar continues her work also in Critical Disability Studies (PhD program) at York University in Toronto.
In 2008, the Autistic Self Advocacy Network (ASAN) succeeded in halting two ad campaigns it stated were demeaning to autistics. The first ads were a series published by the NYU Child Study Center that appeared in the form of ransom notes. One read, "We have your son. We will make sure he will no longer be able to care for himself or interact socially as long as he lives. This is only the beginning", and was signed, "Autism".[1]The second ads were published by PETA and featured a bowl of milk with the left over bits of cereal forming a frowning face. The text read, "Got autism?" and was meant to advertise what PETA claims is a link between autism and the casein in milk. Phone calls, letters and petitions organized by ASAN led to the removal of these ads.[13][14]
The rise of the Internet has provided more opportunities for autistic individuals to connect and organize. Considering the geographical distance, communication and speech patterns of autistic individuals, and the domination of neurotypical professionals and family members in established autism organizations, the Internet has provided an invaluable space for members of the movement to organize and communicate.[5][8]


The seven-colored heptagon of ASANThe seven-colored heptagon of ASAN
The Autistic Self-Advocacy Network (ASAN) uses a seven-coloredheptagonal symbol to represent both the autistic spectrum and the idea of diversity.
Some autistic rights activists believe some characteristics described as being autistic traits are actually misconceptions.[15] Michelle Dawson has disputed the belief that 75% of autistic people have low intelligence.[10]Psychiatrist 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.[16] Some autistics have claimed that non-autistics are insensitive to their perspectives, and write parodies based on this, addressing what they call allism(a lack of autism) as a mental disorder characterized by lack of "theory of other minds".[17][18]
Jim Sinclair, who has also been a target of similar criticism from very early on, goes into detail about "the politics of opposition to self-advocacy".[19]
The controversy has erupted on autism e-mail lists, where "curebie" is used as a derogatory term for parents who are portrayed as "slaves to conformity, so anxious for their children to appear normal that they cannot respect their way of communicating".[11] 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 empathyof anti-cure activists prevent them from seeing what is in the hearts of pro-cure advocates.[20]

Autism is not a disorder[edit]
Many autism rights activists object to the use of jigsaw pieces to represent autism, since they do not view autism as a problem to be solved.[21]
Autism is classified by psychologists as a disorder, 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 autistic individuals has been compared to treating a patient with cancer, though extended over the duration of a normal lifespan.[22] Autistic children have also been described as being held hostage to a psychiatric disorder.[23]Others have used the term "mad child disease" to describe autism,[24] which some autistic individuals and their parents have found highly offensive.[25] 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.[10] Bennett L. Leventhal said he understands concern about comparing autistic children to hostages but thinks the campaigns make the point that these are real diseases that will consume children if untreated.[23] Autistic rights activists also reject terming the reported increase in autism diagnoses as an 'epidemic' since the word implies autism is a disease.[26]
Attempts have been made to place a figure on the financial cost of autism, addressed to both scholarly[27] and popular audiences.[28] These efforts have been criticized by some autism rights advocates, who compare them to similar calculations about "persons with bad heredity" made by the eugenics movement in the early 20th century—a movement currently in disrepute.[29] Michelle Dawson has pointed out that no effort has been made to examine the cost of 'eliminating the disease' to autistic individuals,[30] and she, as well as others, have also pointed out the valuable contributions autistic individuals can, and have made to society.[30][31] Dr. Temple Grandin has speculated that an autistic caveman probably invented the first stone spear, and that if autism were eliminated, society would lose most of its scientists, musicians, and mathematicians.[32][33]
Some autistic activists say it is not easy to distinguish between high and low functioning.[11] Some autistic individuals, in contrast, are supportive of the distinction between the low and high functioning labels as well as autism and Asperger syndrome, and believe it is important in helping individuals get proper consultation and treatment.[34]

Autistic people have their own culture[edit]

Further information: //Autistic culture// and //Autistic art//
Some autistic activists suggest that life with autism is very much like being born among people who speak a different language, have a religion or philosophy one does not share and live a lifestyle that feels alien. To put it differently, Autists have an individual culture that's often very different from their environment.[//citation needed//]

Autistic people require inclusion in the autism debate[edit]

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 solely by individuals who do not directly experience autism.[22]
Jim Sinclair states that autism conferences are traditionally geared toward neurotypical parents and professionals, and that to an autistic person they may be quite "hostile" in terms of sensory stimulation and rigidity.[8]
In defiance of the common complaint that anti-cure advocates' ability to articulate complex opinions in writing—which some critics see as being impossible for autistic people[35]—autistic adults such as Amanda Baggs use their own writing and videos to demonstrate that it is possible for severely disabled autistics to be autism rights advocates.[36] 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 when it was discovered that she could type.[37]

Autism therapy is often unethical[edit]

Further information: //Autism therapies//
Aspies For Freedom stated that the most common therapies for autism are unethical, since they focus on extinguishing harmless stimming, forcingeye contact and breaking routines. AFF argued 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.[3]Michelle Dawson, a Canadian autism self-advocate, testified in court against government funding of ABA therapy.[35] 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.[11]

Autism genes should not be eliminated[edit]

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.[11] On February 23, 2005 Joseph Buxbaum of theAutism Genome Project at the Icahn School of Medicine at Mount Sinai said there could be a prenatal test for autism within 10 years.[38] However, the genetics of autism have proven to be extremely complex.[39] In any case, the Autistic Genocide Clock was started in response to this, which counts down to 10 years after Buxbaum made this announcement.[40] 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.[41]
Some people lament that professionals, such as social workers, may discourage autistics from having children.[42] Some are concerned that the "ultimate cure will be a genetic test to prevent autistic children from being born"[11] and that most autistic fetuses would be aborted if prenatal tests for autism are developed.[43]

Notion of "curing" autism is offensive[edit]

"Curing" or "treating" autism is a controversial and politicized issue. Doctors and scientists are not sure of the cause(s) of autism yet many organizations like Autism Research Institute 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.[11][43] Some advocates believe that common therapies for the behavioral and language differences associated with autism, like applied behavior analysis, are not only misguided but also unethical.[44]
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.[11] 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 eliminated.[11][45] They believe the quirks and uniqueness of autistic individuals should be tolerated as the differences of any minority group should be tolerated and that efforts to eliminate autism should not be compared, for example, to curing cancer but instead to the antiquated notion of curing left-handedness.[11][35] The ARM is a part of the larger disability rights movement, and as such acknowledges the social model of disability.[46] Within the model, struggles faced by autistic people are viewed as discrimination rather than deficiencies.
Jim Sinclair, a leader in the movement, argues that autism is essential to a person, not a disease secondary to the person. Sinclair says that wishing that an autistic person be cured is equivalent to wishing that they disappear and another completely different person exist in their place.[47] Visions for a future where autism has been eradicated, Sinclair believes, is the desire to end the autistic culture.[47]
Some movement members with Asperger syndrome, who do not have the language differences 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.[10][48] Simon Baron-Cohen, a professor of developmental psychology at Trinity College, Cambridge and an autism researcher, expressed the latter view.[49]Baron-Cohen said:[43]

I do think there is a benefit in trying to help people with autism-spectrum conditions with areas of difficulty such as emotion recognition. Nobody would dispute the place for interventions that alleviate areas of difficulty, while leaving the areas of strength untouched. But to talk about a 'cure for autism' is a sledge-hammer approach and the fear would be that in the process of alleviating the areas of difficulty, the qualities that are special – such as the remarkable attention to detail, and the ability to concentrate for long periods on a small topic in depth – would be lost. Autism is both a disability and a difference. We need to find ways of alleviating the disability while respecting and valuing the difference.

Autism Speaks boycott[edit]

Main article: //Autism Speaks § Controversies//
As the most recognized name in autism advocacy worldwide, Autism Speaks is seen as representative of autism, particularly advocacy of a cure.[50] As a result, Autism Speaks is implicated in perpetuating misconceptions, including inaccurate diagnostic criteria, functioning labels,"person"-first language, the medical model of disability, equation of communication and intelligence, promotion of ABA therapy, comparisons between autism and diseases, the view of rising autism diagnosis rates as an epidemic, the concept of autism as something separable from people with autism, the view of children with autism as trapped or broken, the belief that married couples who have children with autism are more likely to divorce, and the belief that parent-on-child murder is caused by lack of services.[51]
In addition to its cultural impact, Autism Speaks has been criticized for ignoring and excluding people with autism.[51] Until he resigned in 2013,John Elder Robison was the organization's only board member with autism. His resignation came two days after the release of an op-ed by the group's co-founder Suzanne Wright which, according to Robison, "is simply not defensible for someone who feels as I do, and I cannot continue to stand up for the public actions of an organization that makes the same mistakes over and over again by failing to connect to the community it purports to represent."[52] Simone Greggs, the mother of a child with autism, filed a lawsuit against Autism Speaks for disability discrimination after her job offer was rescinded. The suit alleges that she lost the job offer due to asking for an accommodation on behalf of her son.[53]
Autism Speaks has produced three major films, each met with strong opposition from the Autistic community. //Autism Every Day// is a documentary featuring interviews of parents with mostly negative opinions about autism and their situations. It has been criticized due to parents speaking about their children as if they are not there. In one interview, former board member Alison Singer, mother of a daughter with autism, reveals she contemplated murder-suicide with her daughter in the same room.[54] I Am Autism is a short video that personifies autism as a narrative voice, which compares itself to several diseases[55] and makes the false claim[56] of causing divorce.[57][58] //Sounding the Alarm// is a documentary exploring the transition to adulthood and the cost of lifetime care. It was criticized for being "full of dehumanizing rhetoric" and portraying ignorance of nonverbal communication.[59]
Because of the number of objections to the organization, Autism Speaks fundraising events have been the object of organized protest.[60][61]Many of these protests are organized by the Autistic Self Advocacy Network.[62] In 2013, the organization Boycott Autism Speaks published a list of companies that donate money to Autism Speaks along with their contact information, urging those in the Autistic community to pressure those companies into dropping their support via an active boycott, since direct appeals to Autism Speaks did not result in the desired changes.[63] A month later, ASAN published its 2014 Joint Letter to the Sponsors of Autism Speaks, signed by 26 different disability-related organizations, appealing to the moral responsibility of the sponsors, donors, and other supporters.[64]

Autism Rights groups[edit]

There are several organizations in the autism rights movement. Some like the Autistic Self Advocacy Network are led exclusively by Autistic people, while others such as Autism National Committee encourage cooperation between Autistic people and their non-autistic allies.
Year founded
Nonprofit status
National Autistic Society(NAS)
Charity supporting advocacy and education. NAS manages a number of schools throughout theUnited Kingdom.[65]
Registered charity
Vlaamse Vereniging Autisme(VVA)
Flanders based social network consisting of both Autistic individuals and family members. Autistic individuals and couples where one partner has Autism are frequent speakers or hosts at events intended to improve the understanding and collaboration between Autistic individuals and non-Autistic individuals and eliminate misconceptions about Autism.
vzw (equivalent to 501(c))
Autism National Committee(AutCom)
Advocacy organization with a specific focus on civil rights, dedicated to "Social Justice for All Citizens with Autism."[66]
Autism Network International(ANI)
Self-advocacy organization founded by Autistic individuals. ANI is the host of the annual Autreatconference.
Aspies For Freedom(AFF)
Web-based organization for the Autistic community that had more than 20,000 members. Aspies For Freedom has disbanded, but some of its former members have reorganized at the online communities of Autism Friends Network and ASDCommunity.

The Autism Acceptance Project(TAAProject)
Organization founded by mother to autistic son Estee Klar with a group of autistic advisory and board members. An arts-based organization with an online presence that conducts online and offline events to support autism acceptance and critical thinking about autism and disability. Based in Canada.
Canadian Registered Charity
Autistic Self Advocacy Network(ASAN)
Self-advocacy organization founded by Ari Ne'eman to represent the Autistic community and further the autism rights movement.
Don't Play Me, Pay Me
UK campaign focusing on Asperger syndrome, encouraging and supporting disabled actors.[67]
Autism Women's Network(AWN)
Self-advocacy organization founded by several Autistic women, focused on the intersection of the autism rights movement with feminism.[68]
Thinking Person's Guide To Autism(TPGA)
Collaborative online information resource and publisher of the book by the same name.
The I Can Network
The I Can Network is a movement dedicated to driving a rethink of the Autism Spectrum among young people and the community, away from ‘I Can’t’ to ‘I Can’.

Alternative Baseball Organization(ABO)
Adaptive baseball/softball organization formed by Taylor Duncan in 2016 to raise awareness and acceptance for teens and adults with autism through sport.[69]

Events and activities[edit]

  • The ANI annually hosts Autreat, a retreat-style conference developed to allow autistic individuals to meet, socialize and learn advocacy skills in an "autism friendly" environment. It was founded in 1996.[4]
  • In 2005, Aspies For Freedom founded Autistic Pride Day, which is now celebrated internationally, every year on June 18.
  • In 2005, The Autism Acceptance Project "" began its first arts-based events and lectures to support autistic individuals in response the negative portrayals of autism by the non-autistic community in Canada.
  • In 2008, Autistic Rights Movement UK founded. Name changed to Autistic UK, 2012.
  • In 2010, an initiative by Corina Lynn Becker created Autistics Speaking Day as a response to the then-upcoming first commemoration ofCommunication Shutdown.[70] The annual Communication Shutdown event encourages non-autistics to refrain from using social networking websites for one day as a perspective-taking exercise,[71] while Autistics Speaking Day encourages Autistic people to become more active on social media and to describe their experiences during a time when there are fewer neurotypical voices in the mix.
  • In 2011, the first Autism Acceptance Day celebrations were organized by Paula Durbin-Westby as a response to traditional "Autism Awareness" campaigns which the Autistic community found harmful and insufficient.[72][73] Autism Acceptance Day is now held every April.[72]
  • In 2013, Tone It Down Taupe was created as a parody of Light It Up Blue, asking people to "tone down the fear rhetoric [and] alarmism."[74]The campaign has successfully raised funds for multiple iPad giveaways to help autistic adults communicate.[75]
  • Advocates have implemented several experimental programs for alternative education for individuals on the spectrum. For instance, the School of ASPIE (Autistic Strength, Purpose and Independence in Education) in Boiceville, New York aims to help autistics cope with a non-autistic world, but stresses that it is acceptable and expected that they "act autistic".[11]
  • Autism rights activists organize protests against organizations they consider objectionable, most notably Autism Speaks and the Judge Rotenberg Center.

Criticisms and counter-movements[edit]

Main article: //Medical model of autism//
Parents with the perspective of autism as a disorder (which is called the "pro-cure perspective" in the autism rights movement) believe that therapy with the intent of extinguishing stereotypically autistic behavior is in their children's best interests; they see this as a treatment that will reduce their children's suffering.[76][77] These critics say ABA gives autistic children the best chance of success in adulthood, as they either do not believe it is possible that adult society could accommodate autistic people (who have not been trained by ABA to exhibit neurotypical behavior at all times) or they do not believe it is desirable to do so.
Some parents believe that intensive behavioral therapy is the only way to alleviate autistic children's disabilities.[11] Some critics also fear that the movement will prevent autistic children from receiving important therapies. Kit Weintraub has responded to Michelle Dawson's claims that ABA is harmful by insisting that it is medically necessary and appropriate treatment, and that it is harmful to deny it to autistic children who need it.[78]
There are also accusations about how well autistic people of different functioning levels are represented in the movement. Critics of the movement argue that anyone on the autism spectrum who is able to express their desire not to be cured must be high functioning autistic or have Asperger syndrome, Lenny Schafer argues that if every use of autism were changed to read Asperger syndrome, then the movement might make sense,[11] although the incorporation of Asperger syndrome into the autism diagnosis in the DSM-5 has been used as a counterargument by the autism rights movement.[79]
Sue Rubin, the subject of the Oscar-nominated documentary //Autism Is A World//, is an example of an autistic adult who is aligned with the cure group. In her opinion, people with Asperger syndrome can communicate well and "pass for normal", while "low-functioning" people have a severe disability; "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."[34]
Jonathan Mitchell, an autistic author and blogger who advocates for a cure for autism, has described autism as having "prevented me from making a living or ever having a girlfriend. It's given me bad fine motor coordination problems where I can hardly write. I have an impaired ability to relate to people. I can't concentrate or get things done."[80] He describes neurodiversity as a "tempting escape valve".[1]

Prominent figures[edit]

See also[edit]


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  68. 68. **Jump up****^** Cara Liebowitz (2013-12-17). //"DIVERgent: When Disability and Feminism Collide"//. Autism Women's Network.
  69. 69. **Jump up****^** Zachary Hansen (2016-11-08). //"For love of the game: a young man's dream for special needs baseball"//. The Atlanta Journal-Constitution.
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  71. 71. **Jump up****^** Social Media Users Challenged to Shutdown [sic] Networks | Scoop News
  72. 72. ^ Jump up to:**//a//** **//b//** //"Autism Acceptance Month is coming to a close. Thank you for your support! | Autism Acceptance Month"//. Archived from //the original// on 2013-05-04. Retrieved 2014-11-04.
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  74. 74. **Jump up****^** Kassiane Sibley (2013-04-02). //"Tone It Down Taupe for Autism Acceptance Day!"//. Thinking Person's Guide To Autism.
  75. 75. **Jump up****^** Paula C. Durbin-Westby (2014-03-25). //"Autism Acceptance: Tone it Down Taupe Sponsors iPad Giveaway in April"//. Autism Acceptance Day.
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External links[edit]
Wikiquote has quotations related to: **//Autism//**

Folk epidemiology of autism is derived from folk science, and refers to the popular beliefs about the origin of autism.[1] Using the rare occurrences or trends of autism in order to unify the complex disorder creates these epidemiologies.[1] The most popular folk epidemiologies for autism are influenced by anecdotal evidence.[1] This erroneous epidemiology has dominated over scientific evidence in society due to the miscommunication of scientific research.[2]


Folk epidemiologies of autism enter into the mass media before scientific evidence can support or disclaim the beliefs.[1][3] For example, in 1998Andrew Wakefield published an article in //The Lancet// containing a folk epidemiology that vaccines caused autism.[3] The anecdotal evidence for the folk epidemiology in this article entered into the mass media before the article could be retracted for the lack of scientific evidence.[1][3]


Folk epidemiology of autism is used by parents with autistic children in order to comprehend their child’s condition.[1] The physicians' and scientific research community's lack of communication and scientific evidence on autism leaves these parents browsing alternative media in search of answers to autism.[1][2] Most of the alternative media these parents come across are biased towards folk epidemiologies.[4] With little to no exposure of scientific evidence, parents ignorantly believe the folk epidemiologies of autism.[2][4]


The scientific researchers lack of explanation for why the studies on the origin of autism were unsuccessful, resulted in people questioning scientific evidence rather than anecdotal evidence.[5] For instance, scientific researchers are unsuccessful in clarifying the adverse effects and benefits of vaccines, causing parents to decide not to get their child vaccinated for fear of the negative side-effects.[3][5] The researchers’ neglect to be informative about their research allows folk epidemiologies to be more accepted in society.[5]

Sources and influences[edit]

Mass media[edit]

It is the responsibility of the mass media to entertain its audience.[3] The mass media has become biased towards using folk epidemiology of autism in order to create better entertainment.[3] The folk epidemiology of autism provides answers unlike the scientific evidence that only has disclaimed potential causes of autism.[4][5] The constant influence from the biased mass media has resulted in people being highly aware of false epidemiologies and unaware of the scientific research.[3] The media influence has merely strengthened the acceptance of folk epidemiologies for autism.[3][5]

Public figures[edit]

Public figures (see celebrity) address the issues of autism in a way that is easy to understand.[5] These simple explanations presented by public figures, such as Jenny McCarthy and Robert F. Kennedy Jr. are a greater influence on people's decisions than the scientific research presented by scientific researchers.[5] The scientific research on autism has little influence on people’s mindset since the scientific researchers give no explanations on the subject of autism.[2][5]


Until the retraction of Andrew Wakefield’s article there has been little opposition towards the folk epidemiologies of autism for many reasons.[5]Most people believe and are influenced by the evidence provided by the media, which causes large controversies when people or groups disagree with the media’s evidence.[5] Paul Offit is one of the few advocates who is publicly against the folk epidemiologies of autism.[5] He believes people need to be more informed about the scientific evidence.[5] Offit wants more money to go into the new scientific research on the cause of autism.[5] (also see Program for Appropriate Technology in Health and Immunization Alliance)


The false epidemiology of autism has caused new research for the origin of autism to suffer.[5] More resources are put into the research of folk epidemiologies than for the new scientific research for autism.[5] An example of this is illustrated in the vaccine controversy.[5] People and groups continue to push for more research on the link between vaccines and autism.[4][5] There have been thirteen studies that properly followed thescientific method and contained large numbers of participants that failed to connect autism to the measles-mumps-rubella vaccine.[4] There were seven well-constructed studies, which attempted to correlate autism to thiomersal in vaccines and were unsuccessful.[4]
As a result of folk epidemiology of autism, the knowledge of scientific breakthroughs on autism are not made publicly available.[4][5][6] The research for the root of autism is delayed due to the small amount of money going into the new research.[4][5] Researchers have started to investigate maternal and paternal ages as the root for autism.[6] (see causes of autism) The evidence found is promising, but needs to be investigated further with more monetary support and more support from the society.[6]

See also[edit]

Autism's False Prophets: Bad Science, Risky Medicine, and the Search for a Cure is a 2008 book by Paul Offit, a vaccine expert and chief of infectious diseases at Children's Hospital of Philadelphia. The book focuses on the controversy surrounding the now discredited link betweenvaccines and autism. The current scientific consensus is that no convincing scientific evidence supports these claims,[1][2] and a 2011 journal article described the vaccine-autism connection as "the most damaging medical hoax of the last 100 years".[3]


Offit describes the origins and development of claims regarding the MMR vaccine and the vaccine preservative thiomersal, as well as subsequentscientific evidence which has disproved a link with autism. The book discusses possible explanations for the persistence of these claims in the face of scientific evidence to the contrary, as well as the proliferation of potentially risky and unproven treatments for autism.[4] The author takes a critical view of several advocates of a vaccine–autism link, including Andrew Wakefield, David Kirby, Mark Geier, and Boyd Haley, raising scientific and, in some cases, ethical and legal concerns. The book also explores divisions within the autism community on the topic of vaccines, as some parents consider the ongoing narrow focus on vaccines a distraction from more scientifically promising avenues of research. In this vein, Offit interviews Kathleen Seidel, a mother of an autistic child who has published investigations critical of those who profit from promoting vaccine–autism claims.[5]
Offit also touches on the heated and bitter debate surrounding vaccine claims. He describes receiving death threats, hate mail, and threats against his children as a result of his advocacy for vaccination. Offit declined to do a book tour for Autism's False Prophets, citing concerns about his physical safety and comparing the intensity of hatred and threats directed at him to that experienced by abortion providers.[6] Author'sroyalties from the book are being donated to the Center for Autism Research at Children's Hospital of Philadelphia.[7]


The book was the nucleus of profiles of Offit in //Newsweek//[6] and //The Philadelphia Inquirer//.[8] The //New York Post// reviewed the book positively, concluding: "Although arguably the most courageous and most knowledgeable scientist about vaccines in the United States, Offit lives in fear for his life and that of his family."[4] //The Wall Street Journal// also praised the book as "an invaluable chronicle that relates some of the many ways in which the vulnerabilities of anxious parents have been exploited."[9]
The Philadelphia Inquirer wrote that the book "names names and calls nonsense nonsense", and provides "important insight into the fatal flaws of the key arguments of vaccine alarmists." The Inquirer applauded Offit's focus on slanted and sensationalist media coverage of the vaccine–autism issue, but faulted Offit for not holding scientists themselves sufficiently accountable for their failure to communicate the facts to the public.[10]
The //Rocky Mountain News// noted that the book "turned the tables" on those who see a pharmaceutical-industry conspiracy behind vaccination, by pointing out that the advocates of the autism–vaccine link receive large sums of money from lawyers and lobbyists. The News applauded the book's deconstruction of "misinformation" from Don Imus, Jenny McCarthy, Joseph Lieberman, and Robert F. Kennedy, Jr., among others, but found Offit's "sarcasm and brow-beating of those he disagrees with" to be "grating".[11]
//Salon// reviewed the book as an "enlightening, highly readable, and … timely" work which "deconstruct[s] the anti-vaccine movement as one driven by bad science, litigious greed, hype and ego."[5] Salon faulted Offit for minimizing the work that autism advocacy groups have done to raise awareness, create support networks, and obtain research funding; the review noted that Offit focuses instead on aggressive and scientifically "slanted" groups like Defeat Autism Now! and Generation Rescue. The review concluded that the book "effectively pulls back the curtain on the anti-vaccine movement to reveal a crusade grounded less in fact and more in greed and opportunism".[5]
//Science// called the book "forceful" and "an easy-to-read medical thriller about the consequences of greed, hubris, and intellectual sloppiness."[12]The review noted that Offit did not discuss the irrationality of human decision-making in the presence of relative risk and both anecdotal and empirical evidence, and mentioned that Offit did not carefully discuss the role of regression. In conclusion, the review observed that the book has emboldened the media to apply scientific principles, and called for using the book's momentum to shift resources from the autism–vaccination debate to research into causes and treatments.[12]
The Journal of Autism and Developmental Disorders said the book "makes an important contribution to popular debates about the etiology and treatment of autism spectrum disorders. The book is arguably the most detailed and thorough history available of the current anti-vaccine movement". The review noted one possible weakness: the book gives light coverage to the public's fundamental misunderstanding of theepidemiology of autism, in that the public fears an "autism epidemic" that may not in fact be occurring. The review concluded with a call to scientists and physicians to follow Offit's lead in communicating to the public even uncomfortable truths about autism.[13]
Four months after its release, the //New York Times// reported that the book had been endorsed widely by pediatricians, autism researchers, vaccine companies, and medical journalists, and was "galvanizing a backlash against the antivaccine movement in the United States." Many doctors are critical of "false equivalence" in media coverage of the vaccine issue, and now argue that reporters should treat the antivaccine lobby with the same level of indifference as AIDS denialism and other fringe theories.[14]
Later in 2009, the //New England Journal of Medicine// reported that the book effectively advocated for vaccines and refuted the vaccine–autism myth. It noted that a particular strength of the book is its outline of the scientific method and the basic principles of probability and causality, and its coverage of the difficulty of explaining science to the public, such as the difference between causality and coincidence. It noted as a weakness the book's several diversions into topics such as breast implants.[15]
Other largely favorable reviews appeared in //BioScience//,[16] in //Health Affairs//,[17] and in the Journal of Child Neurology.[18]
In a guest column for the //Atlanta Journal-Constitution//, neurologist Jon Poling panned Offit's book as "a novel of perceived good and evil". Poling, whose daughter was federally compensated for vaccine injuries, criticized Offit for attacking those with whom he disagrees: "In the story, Offit takes no prisoners, smearing characters in the vaccine-autism controversy as effortlessly as a rich cream cheese."[19]

See also[edit]

Autism Speaks is an autism advocacy organization in the United States that sponsors autism research and conducts awareness and outreach activities aimed at families, governments, and the public.[8] It was founded in February 2005 by Bob Wright, vice chairman of General Electric, and his wife Suzanne, a year after their grandson Christian was diagnosed with autism.[9]
In January 2008, child clinical psychologist Geraldine Dawson, PhD., became Autism Speaks's chief science officer. In April 2010, the organization named Yoko Ono its first "Global Autism Ambassador."[10] Since its founding, Autism Speaks has merged with three existing autism organizations raising millions of dollars for autism research.[9]
Since February 2009, Autism Speaks has used the "Wubbzy" character from //Wow!// //Wow! Wubbzy!//as a mascot.[11]
An Autism Rights advocate named Elizabeth Picciuto accused the organization of treating autism as a disease that needs to be cured, rather than a difference that needs to be understood and accepted.[12]
On May 1, 2015, Bob Wright resigned as chairman of the organization. He was succeeded by Brian Kelly who had served as Chair of the Audit and Family Services Committees for the organization, and is co-founder of Eastern Real Estate LLC. Bob Wright remains on the board as a co-founder.[6]
Suzanne Wright took a leave of absence on November 2, 2015 following a diagnosis of pancreatic cancer, due to which she fell gravely ill and died on July 29, 2016.[13]


Autism Speaks is an autism organization that, along with its predecessor organizations, has been a source of funding directed towards the causes and treatment of autism spectrum disorders; it also conducts awareness and outreach activities aimed at families, governments and the public.[8]In a 2006 press release, Autism Speaks stated its goal: "to accelerate and fund biomedical research into the causes, prevention, treatments and cure for autism spectrum disorders; to increase awareness of the disorder, and to improve the quality of life of affected individuals and their families".[14] In 2016, however, Autism Speaks removed curing autism from its mission statement.[15]


Autism Speaks and its predecessor organizations have raised public awareness for autism research, raised funds directly for research, and lobbied Congress to leverage the privately raised money with much greater public funds. From 1997 to 2006 their advocacy in the areas of treatment and environmental factors shifted research priorities in the U.S. from basic research to translational and clinical research, with less emphasis on the underlying biology and greater emphasis on putting what was known to practical use.[16]
Autism Speaks supports research in four main areas:[17]

  • Etiology includes genetic and environmental factors that may cause autism. This research includes searches for autism susceptibility genes, animal models for autism, environmental toxins, and maternal viral infections.
  • Biology studies cells, the brain, and the body. This focuses on brain development and includes the Autism Tissue Program discussed further below.
  • Diagnosis includes epidemiology, early diagnosis, and biomarkers.
  • Autism therapies include medication, behavioral, and psychological interventions. It includes treatments for co-occurring medical conditions in children which are unrelated to autism, such as sleep disorders and gastrointestinal conditions that may hinder behavioral interventions, along with treatments for older individuals, and complementary and alternative medicine.

Autism Speaks funds the Autism Genetic Resource Exchange (AGRE), a DNA repository and family registry of genotypic and phenotypic information that is available to autism researchers worldwide.[18] The AGRE was established in the 1990s by a predecessor organization, Cure Autism Now.[19]
Autism Speaks funds the Autism Tissue Program, a network of researchers that manages and distributes brain tissues donated for autism research. These donations are rare and are a vital component of research into the causes of autism.[20]
Autism Speaks supports the Clinical Trials Network, which focuses on new pharmacological treatments. It also supports the Toddler Treatment Network, which develops new interventions for infants and toddlers.[17]
Autism Speaks believes that vaccines have been shown to be safe for most children, and are important for preventing serious diseases such asmeasles and mumps. It recognizes that some individuals may have adverse reactions, or respond poorly, to vaccines, and advocates research into identifying any subgroups of such individuals and mechanisms behind any such reactions.[17] This has strained relations between the Wrights and their daughter Katie, the mother of an autistic boy. Katie believes her son's autism was caused by thiomersal, a preservative that was formerly common in children's vaccines in the United States; no major scientific studies have confirmed this hypothesis.[9]
Since June 2014, Autism Speaks partnered with Google on a project called Mssng (pronounced “missing"). Previously known as The Autism Speaks Ten Thousand Genomes Program (AUT10K), it is an open source research platform for autism that aims to collect and study the DNA of 10,000 families that have been affected by autism. The goal is to create the world’s largest database of sequenced genomic information of Autism run on Google’s cloud-based genome database, Google Genomics. In December 2014, the pair announced a launch that will allow worldwide access the research for further collaboration and genome analysis.[21]

On April 2, 2013, the Cloth Hall, Ypres, Belgium with Nieuwerck (nl) was lit up blue for the World Autism Day.
The Walk for Autism Research program conducts an annual autism walk on Long Island, New York; the walk attracted 20,000 participants in October 2006 and raised $2 million.[22]
Ad Council launched a campaign in conjunction with Autism Speaks to raise autism awareness and to highlight the importance of early detection.[23] In February 2005, //The Today Show// aired a week-long series of stories highlighting autism research and treatment.[24]
Autism Speaks sponsored and distributes the short film //Autism Every Day//, produced by Lauren Thierry and Eric Solomon.[25]
In December 2007, Autism Speaks' founder Suzanne Wright met with Sheikha Moza bint Nasser of Qatarto urge the country to sponsor a United Nations resolution recognizing World Autism Awareness Day.[26]Qatar introduced the resolution, and the resolution was passed and adopted without a vote by the United Nations General Assembly, primarily as a supplement to previous United Nations initiatives to improve human rights.[27]
Wright helped launch the Autism Speaks' Light It Up Blue campaign and the annual World Focus on Autism event.[28]


Autism Speaks, through a series of mergers, has combined organizations that funded peer reviewed research into genetic causes, championed alternative theories and therapies, and advocated for individuals with autism.[9]

National Alliance for Autism Research[edit]

In early 2006, a year after its founding, Autism Speaks merged with the National Alliance for Autism Research (NAAR).[3] NAAR, founded in 1994, was the first U.S. nonprofit organization dedicated to supporting research into causes, treatment, and cures for autism spectrum disorders.[29] The founders comprised a small group of parents, including two psychiatrists, a lawyer and a chemistry professor.[30]
NAAR raised money to provide research grants focusing on autism and had committed in excess of $20 million to over 200 autism research projects, fellowships and collaborative programs—more than any other non-governmental organization. NAAR focused intently on its role in establishing and funding the Autism Tissue Program, a post-mortem brain tissue donation program designed to further autism research studies at the cellular and molecular level. Other major programs included the "High-Risk Baby Sibling Autism Research Project", and the "NAAR Genome Project". NAAR also published the NAARRATIVE, a newsletter on autism biomedical research.

Cure Autism Now[edit]

In 2007, Autism Speaks completed its merger with Cure Autism Now (CAN).[4] CAN was founded in 1995 by Jonathan Shestack and Portia Iversen, the parents of a child with autism whose story is told in the book //Strange Son//. It was an organization of parents, doctors and scientists devoted to research to prevent, treat and cure autism.[31] Iversen and Shestack were invited to join NAAR's board but declined, impatient with what they considered NAAR's excess of caution in staying with the scientific establishment.[32] In 1997, CAN established the Autism Genetic Resource Exchange; CAN was successful in establishing AGRE despite an initially negative reaction from scientists who were concerned whether CAN could carry out rigorous work, and despite what CAN considered to be scientists' reluctance to share their data.[32] During its existence, Cure Autism Now provided more than $39 million for research grants and other programs. Its flagship programs included the AGRE, Autism Treatment Network, Clinical Trials Network, and Innovative Technology for Autism. It also funded education and outreach efforts.[4]

Autism Coalition for Research and Education[edit]

Autism Speaks is also allied with Autism Coalition for Research and Education, an advocacy group.[9]


View of autism as a disease[edit]

See also: //Medical model of autism//
Autism Speaks's advocacy has been based on the mainstream medical view of autism as a disease: "This disease has taken our children away. It’s time to get them back." This is a view that "many but not all autism scientists would endorse."[33] In contrast, some autistic activists have promoted the idea of neurodiversity and the social model of disability, asserting that people with autism are "different but not diseased" and challenging "how we conceptualize such medical conditions".[33]
In January 2008, an autistic blogger, upset with the portrayal of autism at Autism Speaks's website, "Getting the Word Out",[34] created a criticalparody website titled "Getting the Truth Out".[35] It was later taken down in response to legal demands from Autism Speaks to stop using its name and logo without permission. Autism Speaks said the spoof could confuse people looking for information about autism. New parody sites were later launched by Gareth Nelson, founder of the autism rights group Aspies for Freedom.[36]
In September 2009, Autism Speaks screened the short video "I Am Autism" at its annual World Focus on Autism event; the video was created byAlfonso Cuarón and by Autism Speaks board member Billy Mann. With narration closely resembling the 1954 short Taming the Crippler, which personified poliomyelitis as a kind of grim reaper figure, I Am Autism has been criticized by autism advocates and researchers for its negative portrayal of autism.[37][38]
In response to an editorial by Steve Silberman in the Los Angeles Times criticizing Autism Speaks,[39] then-president Liz Feld stated that one-third of people with autism also have a seizure disorder, half suffer serious digestive complications, 49 percent wander, and more than 30 percent are nonverbal. Feld also discussed Autism Speaks' legal achievements in providing families of those affected with autism more financial assistance and funding, and the various services and awareness initiatives the organization provided.[40]

Position on vaccines[edit]

See also: //Causes of autism § Vaccines//
Autism Speaks formerly assigned a high priority to research into the now-discredited claim that immunization is associated with an increased risk of autism. This raised concerns among parents and scientific researchers, because "funding such research, in addition to being wasteful, unduly heightens parents' concerns about the safety of immunization".[41]
Alison Singer, a senior executive of Autism Speaks, resigned in January 2009 rather than vote to commit money to new studies of vaccination and autism. The U.S. Interagency Autism Coordinating Committee, of which Singer was a member, voted against committing the funds; this was contrary to the Autism Speaks policy on vaccine safety research. Singer said that "there isn't an unlimited pot of money, and every dollar spent looking where we know the answer isn't is one less dollar we have to spend where we might find new answers. The fact is that vaccines save lives; they don't cause autism."[42]
She said that numerous scientific studies have disproved the link first suggested more than a decade ago and that Autism Speaks needs to "move on".[42] Later that year, along with NAAR's co-founder Karen London, Singer launched the Autism Science Foundation (ASF), a nonprofit organization supporting autism research premised on the principles that autism has a strong genetic component, that vaccines do not cause autism, and that evidence-based early diagnosis and intervention are critical.[43]
Eric London resigned from Autism Speaks's Scientific Affairs Committee in June 2009, saying that arguments that "there might be rare cases of 'biologically-plausible' vaccine involvement … are misleading and disingenuous", and that Autism Speaks was "adversely impacting" autism research. London is a founding member of the ASF's Scientific Advisory Board.[44]
Autism Speaks now takes the position that studies into the matter "have not found a link between vaccines and autism", and that they "strongly encourage parents to have their children vaccinated for protection against serious disease".[45]

Rhetoric used[edit]

Autism Speaks sponsored and distributes the short film //Autism Every Day//, produced by Lauren Thierry and Eric Solomon.[25] Autism Speaks staff member Alison Singer was reportedly criticized for a scene in which she said, in the presence of her autistic daughter, that when faced with having to place the girl in a school that she deemed inadequate, she contemplated driving her car off a bridge with her child in the car.[46] Thierry said that these feelings were not unusual among non-autistic mothers of autistic children.[47] According to the book Battleground: The Media, Thierry reportedly asked the parents featured in the film not to clean house, and the film crew showed up unexpectedly.[46][47]
In November 2013, Autism Speaks published an op-ed by co-founder Suzanne Wright.[48] Autistic people and their families criticized the piece for using inaccurate statistics and giving an unrepresentative and exaggerated depiction of the lives of autistic people and their families.[49][50][51]Autistic author John Elder Robison said that Wright's op-ed "articulates a view of the 'autism situation' that is very different from my own. She says things I would never say to people with autism and cannot in good conscience stand by. Given her role as leader of the organization, I am afraid it is my signal to exit the Autism Speaks stage."[52] Robison resigned from Autism Speaks saying he could no longer support an organization that "fail(ed) to connect to the community it purports to represent.".[52]

Financial spending[edit]

In 2009, Disability Scoop questioned Autism Speaks about its chief science officer, Geri Dawson, who received $669,751 in compensation in 2008, including $269,721 to relocate her family from Washington to North Carolina.[53] Autism Speaks responded that Dawson's compensation was mid-range for executives with similar positions in the nonprofit health sector,[53] and that Dawson's move benefited Autism Speaks because she would be more accessible to its offices, science divisions, government health agencies in Washington, D.C., and her new position at theUniversity of North Carolina at Chapel Hill.[53]
Compared to other autism-focused nonprofit organizations, Autism Speaks spends a smaller percentage of its revenue on furthering its mission. According to a report by The Daily Beast, 70.9% of Autism Speaks's revenue is devoted to directly furthering its mission, compared to 79.8% of Autistics Self-Advocacy Network's revenue and 91.5% of Autism Science Foundation's revenue.[54]
In 2012, Autism Speaks spent $2,252,334 on salaries for current officers, directors, trustees, and key employees, which //The Daily Beast//portrayed as controversial. Autism Speaks's former president Mark Roithmayr had a salary of $436,314 in 2012, and Chief Science OfficerGeraldine Dawson earned $465,671.[55]
Charity Navigator gave Autism Speaks a financial rating of two out of four stars.[54]

See also[edit]

|| [show]

**Autism** resources

The Autistic Self Advocacy Network (ASAN) is a 501(c)(3) nonprofit advocacy organization run by and for individuals on the autism spectrum. ASAN holds that the goal of autism advocacy should be a world in which Autistic people enjoy the same access, rights, and opportunities as all other people, and that Autistic voices should be included in any public discourse on autism, whether in public policy, mass media, or other venues. ASAN is based in Washington, D.C.[1]


The Autistic Self Advocacy Network provides community organizing, self-advocacy support, andpublic policy advocacy & education for autistic youth and adults, as well as working to improve the general public's understanding of autism and related conditions. The organization is "run by and for autistic adults."[2] ASAN's mission statement says that autistic people are equal to everyone else, and important and necessary members of society.[3] ASAN also maintains a network of 25 local chapters based in different states, with three chapter affiliates in Canada and Australia.[4][5]


The Autistic Self Advocacy Network was co founded in November 2006 by its current President, Ari Ne'eman,[6] and former Board of Trustees member and Vice Chair of Development, Scott Michael Robertson. By 2009, ASAN had 15 chapters.[7]
ASAN's early work mostly focused on fighting the use of aversives, restraint, and seclusion in special education;[8][9][10] in December 2007, they spoke out publicly against Autism Speaks,[11] and against the NYU Child Study Center's Ransom Notes ad campaign, which compared autism,ADHD, OCD, and eating disorders to kidnappers holding children hostage.[12][13] This counter-campaign[14] put ASAN on the public's radar and has been referred to as the neurodiversity movement's coming of age.[15] ASAN continues to protest Autism Speaks.[16]
On July 18, 2016, Ari Ne'eman announced that he would resign as president of the Autistic Self-Advocacy Network, to be replaced by Julia Bascom.[17]

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