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The causes and etiology of autism are an area of debate and controversy. There is as yet no consensus, and researchers are studying a wide range of possible causes. Since people with autism are all somewhat different from one another there are probably multiple 'causes' that interact with each other in subtle and complex ways, and thus give slightly differing outcomes in each individual.

Further complications arise because there is no certainty that high-functioning Asperger's Syndrome actually has the same cause or causes as low-functioning autism. [How to reference and link to summary or text]

There is a further complication due to the possibility of mis-diagnosis (such as other pervasive developmental disorder instead of autism spectrum disorder). [How to reference and link to summary or text]

It should be noted that some of the theories given below apply more strongly to Asperger's Syndrome than Autism, and visa versa.

Physical disorder modelsEdit

  • Brain size

The majority of people with autism have slightly enlarged brain size, compared to the statistical average. Neurology Today (Volume 2,8: August 2002) stated that "Although it is accepted that individuals with autism have, on average, an enlarged brain size, the nature of this abnormality remains unknown.".[How to reference and link to summary or text] (See also the paper "Brain Volume in Autism" PDF link).

  • The extreme male brain theory

In his 2003 book The Essential Difference, professor Simon Baron-Cohen of the Autism Research Centre argued for the "extreme male brain" theory, which suggests that Asperger's Syndrome and autism represent an extreme form of the way in which men's brains differ from those of women [2][3]. He claims that people with Asperger Syndrome excel at systemizing and are less capable of empathizing [4][5]. The theory is linked with Baron-Cohen's "empathizing/systemizing (E-S)" theory which states that, in general, men are better at systemizing than women, and that women are better at empathizing than men due to physical differences between male and female brains. [How to reference and link to summary or text] Hans Asperger himself said that his patients had "an extreme version of the male form of intelligence." [How to reference and link to summary or text]

The concept of differing types of intelligence in males and females is controversial, and remains largely speculative. Baron-Cohen claims to have based his ideas on a study on a small group of infants he did in 2000, but according to Harvard researchers the study lacked critical controls, has never been replicated and the results were not published in a peer-reviewed journal. Dr. Elizabeth Spelke of Harvard's Mind, Brain and Behavior Interfaculty Initiative states that there is a large body of literature which contradicts Baron-Cohen's ideas.[1]

  • The preoperational-autism theory

The preoperational-autism theory states that people with autism are those who become neurologically impeded at the preoperational stage of cognitive development, where much of information processing is at a holistic-visual level and largely musical and nonverbal. This also addresses the issue of 'theory of mind', where children (with and without autism) at the preoperational stage of cognitive development have not attained decentralization from egocentrism. [How to reference and link to summary or text]

  • Underconnectivity theory

Underconnectivity theory theorizes that autism is a system-wide brain disorder that limits the coordination and integration among brain areas. With the aid of fMRI, it was seen that white matter, which connects various areas of the brain like cables, has abnormalities in people with autism. This theory may be related to the "lack of central coherence" theory proposed by Uta Frith, which suggests that children with autism are good at paying attention to detail, but have difficulty integrating information from a range of sources.[How to reference and link to summary or text]

  • Mind blindness theory

This theory says that the person with autism has "mind blindness", or the inability to create accurate models of other people's thoughts. The theory was proposed by Uta Frith and Simon Baron-Cohen. The typical example of this is the Sally-Anne test where the subjects have to try to determine what a third party's action will be (see theory of mind also). Some people with autism do not seem to fit this model, however. [How to reference and link to summary or text]

  • Faulty mirror neuron theory

The human brain is believed to contain mirror neurons which match actions performed by the self and those performed by other people. Scientists speculate that mirror neurons provide a neural basis for language, empathy and social interaction, though the evidence is still weak. A recent study (Dapretto et al, Nature Neuroscience, 2006) suggests that children with autism show less activity in the mirror neuron regions than typical children when they are imitating facial expressions. Based on this work, it has been suggested that children with autism might have a faulty mirror neuron system (see Scientific American, 2006), which could cause the social difficulties seen in these children. However, this is a very novel theory which has not been extensively tested. Research in this area is on-going.

  • Blanket term

There is increasing suspicion among researchers that autism is not a condition with a single cause, but a number of yet unidentified conditions with different or variably co-mingling causes. See: Happe, Francesca, Angelica Ronald and Robert Plomin (2006). Time to give up on a single explanation for autism. Nat Neurosci 9 (10): 1218-20.

Etiology theories for physical disorder modelsEdit

While the etiology of autism is largely unknown, many theories have been advanced in this growing area of research. Better explanations for the condition are expected to help with the development of autism therapies and to resolve the question of whether or not an apparent autism epidemic has a factual basis. In part, the mystery of autism has been slow to resolve due to its relatively recent identification as a disorder, in 1943, and because government funding of autism research lags far behind that of less common diagnoses, [How to reference and link to summary or text] such as juvenile diabetes. Available funding has largely been directed toward genetic and epidemiological research, rather than clinical studies investigating possible environmental triggers. In addition, since the 1970s, the recorded frequency of autism has risen dramatically in the west.

  • Genetics theory
For more details on this topic, see Heritability of autism.

Autism is known to be highly heritable.[How to reference and link to summary or text] Autism research at some institutions seeks methods for earlier and more accurate detection of autism, similar to specific tests for Rett syndrome. Instead of searching for one particular gene as the cause for autism, many studies currently underway are investigating complex interactions between multiple genes.

A recent paper on the genetic basis of autism suggests that autism is not a single disorder (Happe F, Ronald A, Plomin R. Time to give up on a single explanation for autism. Nat Neurosci. 2006 Oct;9(10):1218-20. ). The social difficulties, communicative difficulties and repetitive behaviours seen in people with autism may be distinct symptoms each with different causes. This implies that a search for a general 'cure' for autism is unlikely to succeed.

A 2005 study, conducted by the Duke Center for Human Genetics at Duke University, found some evidence that complex interactions between GABA (gamma aminobutyric acid) receptor genes might contribute significantly to the onset of autism in many cases. One of the functions of the GABA system is to inhibit the transmission of other neurotransmitter signals. The theory is that somehow the GABA signaling system suffers or contributes to neurological damage of some kind, leading to an overwhelmed sensory system, which in turn causes the characteristics or symptoms of autism.[6],[7]

  • Brain testosterone theory

The brain testosterone theory proposes that high levels of testosterone in the amniotic fluid of mothers influences the development of the growing fetus. The high levels of testosterone is theorized to push brain development towards improved ability to see patterns and analyze complex systems while diminishing communication and empathy, emphasizing 'male' traits over 'female'.[8] The primary proponent of this theory is Simon Baron-Cohen, who bases it on his empathizing-systemizing (E-S) theory.[9] In one set of studies, infants with higher exposure to testosterone in the womb had smaller vocabularies and less eye contact at one year, while at four years they were less socially developed and males demonstrated more restricted interests than females.[10] The theory and findings are controversial and have been refuted by other research,[1] though other researchers are also pursuing testosterone-related research, notably Dr. Mark Geier.

Dr. Mark Geier, with his son David Geier, have published a study, "A Clinical and Laboratory Evaluation of Methionine Cycle-Transsulfuration and Androgen Pathway Markers in Children with Autistic Disorders" in Hormone Research. In the Geiers' study, pre-pubertal age children with autism spectrum disorders were assessed for metabolites in the methionine cycle-transsulfuration and androgen pathways, and for present physical development/behaviors indicative of hyperandrogenicity. Significantly increased levels of serum/plasma dehydroepiandrosterone (DHEA) and serum total testosterone relative to the age- and sex-specific normal laboratory reference ranges were observed. Conversely, serum follicle-stimulating hormone (FSH) levels were significantly decreased. Reduced glutathione, plasma cysteine, plasma methionine, serum cystathionine, and serum homocysteine were all significantly decreased. The Geiers' concluded that their results suggest a possible cyclical interaction between the methionine cycle-transsulfuration and androgen pathways in some children with autism spectrum disorders.


  • Nutritional deficiencies

Children exhibiting behavioral and learning disorders may do so in part because of diets deficient in vital nutrients needed for their brains to function and develop normally.

In 1998, a small study published in the medical journal Lancet found a consistent set of bowel disorders among a dozen children with autism. Although an emphasis was placed by the authors on a possible link to the MMR vaccine, the study also suggested nutritional deficits caused by bowel disorders may have contributed to the onset of neurological disorders. It should be noted that the sample was very small, and definitive replications of the results have not yet been published by other researchers.

  • Leaky Gut Syndrome and related deficiencies

Some children with autism are said to have responded well to dietary intervention, such as eliminating gluten, a protein found in most grains (see gluten-free diet), and casein, a protein found in milk. Elimination of phenyls and food coloring, also recommended by many experts for ADHD, is another approach (see Feingold diet). Most data regarding the validity of these interventions have been criticized as the subjective observations of parents and caretakers. Critics allege that no scientific study with proper subject elimination has taken place. The effectiveness of dietary interventions may be affected by co-morbid conditions, such as asthma, eczema, diarrhea and constipation, 'yeasty' diaper rash, and the difficulty of altering rigid eating habits (a common characteristic among people with autism).

Claims for the possible effectiveness of dietary interventions have been criticized for reliance on unproven theories involving evidence of damage to the stomach lining and/or intestines of children with autism (see autistic enterocolitis). Proponents of dietary interventions point out that damage to the digestive tract, compounded by dietary problems, may allow certain proteins to be improperly metabolized as glutomorphine and casomorphine, which are both opiates. The digestive tract damage is theorized to be caused by immune system abnormalities, and possibly by early oral-antibiotic use combined with a genetic predisposition. However, this is speculation and there is, as yet, no proof for these theories.

  • Folic acid

Increased intake of folic acid by pregnant women roughly coincides with the reported increase in the prevalence of autism. The explanation offered is that folic acid allows more brain cells to survive than should. This hypothesis is untested at this point.[2]

  • Vaccine theory

Controversial research, led by British gastroenterologist Andrew Wakefield and published in in the February 1998 issue of The Lancet, suggested a possible link between autism and the MMR vaccine. The original research has come under criticism, largely due to conflict of interest allegations.[11] In March 2004, most of the paper's co-authors retracted its 'interpretation' section, which claimed a potential link between pervasive developmental disorders and "possible environmental triggers," after a heated public debate about the propriety of Wakefield's statements about the possible link between autism and the MMR.

Critics have claimed that Wakefield's study contains many flaws, including lack of recognition of sample bias. In October, 2005, a study by the respected Cochrane Library said, on the basis of 31 pieces of research into the possible side effects of MMR, that it found no association between MMR and autism. Several scientific groups, including the National Academy of Sciences, have also conducted investigations and concluded that the evidence does not support a link.

One study by Gillberg and Heijbel, in 1998, which examined the prevalence of autism in children born in Sweden from 1975 to 1984,[12] found no difference in the prevalence of autistic children born before the introduction of the MMR vaccine in Sweden and those born after the vaccine was introduced. Another study, conducted by Madsen and other researchers in 2002, studied all children born in Denmark from January 1991 through December 1998[13]. There were a total of 537,303 children in the study; 440,655 of the children were vaccinated with MMR and 96,648 were not. The researchers did not find a higher risk of autism in the vaccinated than in the unvaccinated group of children. These studies also have detractors, who note that important criteria changed during the course of research, such as the diagnostic definition of autism that was used.

Research in the US has suggested a similar link between autism and the DPT vaccine, although this is not referenced. Earlier DPT vaccines have been replaced by the DPaT vaccine due to serious adverse reactions. However, contrary to early claims from Wakefield, it is doubtful that a large majority of autism cases could have resulted from administration of DPT vaccines. Controversy surrounding autism and vaccines continues to this day.

Dr. Mark Geier and his son David Geier have published eleven peer-reviewed studies on the possible link between autism spectrum disorders and childhood vaccines (TCVs). In their first study, they compared the number of complaints associated with TCVs, administered between 1992 and 2000, to the number of complaints resulting from a thimerosal-free vaccine administered between 1997 and 2000. The children who received greater amounts of ethylmercury from TCVs were more likely to have a complaint filed with the Vaccine Adverse Event Reporting System (VAERS). Further studies by the Geiers yielded similar results. In 2006, the Geiers published an article , "Early Downward Trends in Neurodevelopmental Disorders Following Removal of Thimerosal-Containing Vaccines", which contends that recent data confirms a reduction in autism diagnoses corresponds directly with the removal of TCVs from childhood vaccination schedules.

US health agencies have uniformly rejected the conclusions of the Geiers' studies. One of the Geiers' articles was the subject of heavy criticism by the American Academy of Pediatrics.

One of the problems with Geier's research is that the drop (if any) in autism in children who received no thimerosal brings the rate down to the level that is still higher than that in children who received over 50% of the maximum thimerosal burden before removal of mercury from all children's vaccines. In other words, the 1995 birth cohort, having received at least 5 to 10 doses of mercury-containing vaccine, had fewer cases of autism than the 2000 birth cohort having none. This is evident from Dr Geier's own graphs in the below referenced article.

On the other hand, a report prepared by the staff of the Subcommittee on Human Rights and Wellness, House Committee on Government Reform, chaired by Dan Burton, was published in the Congressional Record in May, 2003, stating:

"However, the Committee upon a thorough review of the scientific literature and internal documents from government and industry did find evidence that thimerosal did pose a risk. Thimerosal used as a preservative in vaccines is likely related to the autism epidemic. This epidemic in all probability may have been prevented or curtailed had the FDA not been asleep at the switch regarding the lack of safety data regarding injected thimerosal and the sharp rise of infant exposure to this known neurotoxin. Our public health agencies’failure to act is indicative of institutional malfeasance for self-protection and misplaced protectionism of the pharmaceutical industry."

In a controversial article in June 2005, Robert F. Kennedy, Jr. described research suggesting that it is not the vaccines themselves, but a mercury-based preservative called thimerosal, used in some vaccine preparations (although not MMR), that may be a cause of autism[14]. Kennedy argues that autism was first observed in children who were born around the time of introduction of thiomersal into mass-produced vaccines, and that the incidence of autism in the United States is well correlated with the amounts of thiomersal children receive during their first two years of life. Kennedy also noted that the there is a low reported incidence of autism in the Amish, who do not immunize their children. However, the CDC has described a link between thiomersal and autism as 'unlikely'.[15]

In 1999 the Public Health Service (including the CDC, FDA, and NIH) recommended that thiomersal no longer be used in vaccine preparations. The CDC and some medical organizations continue to assert that no available evidence supports a causal link between thiomersal and autism. Critics have in turn claimed that the CDC analysis demonstrates deliberate bias in the CDC research[16].

For example, an analysis by Madsen et al. in Demark noted that the incidence of autism remained fairly constant while thiomersal was being phased out and started to rise beginning in 1991, even after thimerosal was discontinued in 1992.[17] Critics of this analysis point out that the methodology was biased[18], [19]. Dissenters to the Denmark data point out a significant increase in autism rates[20] among children whose childhood vaccines contained thiomersal. However, in Madsen et al.'s study, the amount in the vaccinations actually decreased while autism rates increased (specifically, during the period 1961–1970, infants had received a total of 400 µg of thiomersal by the age of 15 months, and during the period 1970–1992, infants had received a total of 250 µg at 10 months of age).

The California Department of Developmental Services (DDS), considered to have the best reporting system for autism in the US[21], has reported a levelling-off in caseload increase, indicating a deceleration in the number of new reports of autism (i.e. the caseload is still increasing, but at a slower rate). The caseload increase went from 734 during the second quarter of 2005 to 678 during the third quarter of 2005, a 7.5% decline in one quarter.

For example, from the 2nd to the 3rd quarter of 2004, the caseload went from 25,020 to 25,769 (a increase of 749 clients). Between the 1st and 2nd quarter of 2004, the caseload increased from 24,297 to 25,020 (a increase of 723 clients). These variations have led to speculation that removal of thiomersal from vaccines in California is starting to pay off. Others point out they are unremarkable and may simply be an indication that the awareness curve is starting to level off, and that the rate of caseload increase should be expected to decrease to population growth levels (1.6% annual) eventually. Caseload increase between 2004 and 2005 was about 10%.

A study published in the March 2006 issue of the Journal of American Physicians and Surgeons (JPANDS) by Dr. Mark Geier claimed to show that "new cases" of autism in California dropped as much as 35% following removal of thimerosal from vaccines. However, the study did not document incidence drops, and its definition of "new cases" is known to be flawed.

A study published in 2006 by Geier et al. indicates that the trends of newly diagnosed neurodevelopmental disorders (NDs) such as autism reported to VAERS "correspond directly to the expansion and subsequent contraction of the cumulative mercury dose to which children were exposed from TCVs through the U.S. immunization schedule."[3]

A study published in July 2006 claims that the MMR vaccinations are definitely not the cause of autism and Asperger Syndrome.[4]

Members of the autistic community and especially the autism rights movement heavily criticize the Geiers' work, alleging that the Geiers engage in profiteering from the fear and desperation of parents. The writer of a blog called Autism Diva goes into scientific detail as to exactly what is wrong with the Geiers' ideas and practices, and warns against the "chemical castration" of children with autism by injections of Lupron supposedly to reduce the amount of testosterone in their systems.

The Geiers have continued their research into the relationship between mercury exposure and autistic disorders by clinically helping to identify a unique urinary porphyrin pattern in patients with autism spectrum disorders that is indicative of heavy metal toxicity. Excess urinary porphyrin excretion or porphyrinuria results from inhibition of key enzymatic steps in conditions including genetic deficiencies in heme production enzymes, hepatitis, renal, and erythroid disease, and also by toxic inhibition of heme synthesis enzymes. In both experimental animals and humans exposed to heavy metals, porphyrins are exported at elevated levels into urine. The Geiers' research was conducted following a study by Nataf et al. (Nataf R, Skorupka C, Amet L, Lam A, Springbett A, Lathe R. Porphyrinuria in childhood autistic disorder: implications for environmental toxicity. Toxicol Appl Pharmacol 2006;214:99-108) on a large cohort of French children with autistic disorders that showed a urinary pattern indicative of mercury toxicity. The Geiers research resulted in the first US publication, "A Prospective Assessment of Porphyrins in Autistic Disorders: A Potential Marker for Heavy Metal Exposure" in Neurotoxicity Research that confirmed the observations made in France. The Geiers observed an apparent dose-response effect between autism severity and increased urinary porphyrins. Patients with non-chelated autism (2.25-fold, 83% had levels > 2 standard deviations above the control mean) and non-chelated autism spectrum disorders (2-fold, 58% had levels > 2 standard deviations above the control mean), but not patients with non-chelated pervasive developmental delay not otherwise specified or Asperger's disorder (1.4-fold, 46% had levels > 2 standard deviations above the control mean), had significantly increased median coproporphyrin levels versus controls. A significant increase (1.7-fold) in median coproporphyrin levels was observed among non-chelated autism spectrum disorder patients versus chelated autism spectrum disorder patients. The Geiers' concluded that porphyrins should be routinely clinically measured in autism spectrum disorders, and potential autism spectrum disorder treatments should consider monitoring porphyrin levels.

  • Brain trauma

Susan Bryson has claimed that some individuals with autism have evidence of trauma to the brain stem in early development, and that a small portion of the thalidomide victims have become autistic. The victims' limbs were normal unless thalidomide use continued later in the pregnancy. The brain stem anomaly's most striking feature is inability to focus attention away from a stimulus in a short time like neurotypicals, as demonstrated in a psychological test.

Some people claim the inability to shift attention quickly interferes with the ability to read nonverbal language where fast attention shifts are needed (such as eye language), suggesting that being nonverbal is not a primary feature of autism. Strong and shiftless focus is, however, a benefit in some areas like science, programming, and advanced mathematics. This is supported by the monotropism hypothesis.

Dr. Bernard Rimland's influential research and his book Infantile Autism (1967) argued that autism was not caused by childhood trauma or abuse, but by damage to certain areas of the brain, particularly the reticular formation which associates present sensory input with memories of past experiences. Dr. Rimland is a foremost advocate of the theory that autism may be precipitated by mercury and heavy metal toxicity [22]. He is also prominent in claims of successful treatment of autism in children — particularly regarding improvements in ability to comprehend the spoken word— with megavitamin therapy, a gluten-free, casein-free diet and mercury chelation therapy.

Others suggest Dr. Bernard Rimland's methods alleviate the symptoms of heavy metal poisoning, but not autism. Curing heavy metal poisoning when it is present is a worthy goal (it helps with comprehension and learning difficulties as well as general health), but claiming a benefit for autism is a misrepresentation. Heavy metal poisoning may be more common among individuals with autism due to a severe metallothionein deficiency, but more evidence is needed to substantiate the idea that heavy metals cause autism. It is still being studied.

A large-scale study in Sweden[5] found that ultrasound scanning during pregnancy significantly increased the number of male babies born who would become left-handed children. This suggests that the male brain may be especially vulnerable to small amounts of ultrasound heating while in the womb. Research is ongoing, with theoretical causal links possible, but as yet no proven link between ultrasound scans and autism spectrum disorders.

  • Viral or bacterial infection

A growing body of peer-reviewed studies published in mainstream journals has shown that many common diseases of previously unknown origin are caused by the presence of slowly acting viruses. For example, cervical cancer is caused by the human papilloma virus, some cases of liver cancer are caused by hepatitis C or B and there is a suggested link between schizophrenia and the Borna virus. Paul W. Ewald, among others, argues that the available data on the origin of autism is consistent with the possibility that it is being caused by a virus or infection. Alternatively, it was hypothesized that use of certain antibiotics may be associated with autism; that is, depending on certain conditions they could be either harmful or helpful.[23]

  • Immune disorders and immune system insults

An increasing number of studies in national journals are linking the regulation of the immune system with nervous system diseases such as multiple sclerosis and even Alzheimer's disease. Cognitive function, memory, and fatigue may all be influenced by small molecule immune modulators, and there may be a link between immune function and autism, but there is no evidence.

  • Blood type theory

D'Adamo and Whitney report that although there is not a published study , an informal accounting shows a marked prevalence of blood type A among children with Asperger's syndrome. The other blood types have low incidence, risk or severity of Asperger's Syndrome and Autism. Since the type A limits several dietary lectins that are thought to interfere with secretin, it is possible that improvement in these children may have actually resulted from enhancement of their own secretin metabolism [24].

A study by Horvath et. al (1998) on secretin and Asperger's reported that children with Asperger's Syndrome or Autism and gastrointestinal problems had improved gastrointestinal function after secretin infusion and that the children become more sociable and communicative. They also benefited with a low lectin and wheat diet. This suggest that there might be a gastrointestinal and diet cause of Asperger's or Autism [25]. However, there was no control group of normal children who had the same treatment. (See also: QuackWatch: Secretin)

  • Amygdala neurons and fear theory

Two preliminary studies have linked lower neuron density in the amygdala with autism. It is unclear whether this could be a cause or an effect of the condition. It is postulated that this physical difference may directly lead to symptoms of increased anxiety and nervousness, and indirectly to poor social skills (possibly by downregulation of the typical emotional responsiveness to faces, resulting in reduced accumulation of facial processing experience). [6]

Psychological disorder modelsEdit

  • Refrigerator mother
For more details on this topic, see Refrigerator mother.

Dr. Bruno Bettelheim believed that autism was linked to early childhood trauma, and his work was highly influential for decades both in the medical and popular spheres. Parents, especially mothers, of individuals with autism were blamed for having caused their child's condition through the withholding of affection. Leo Kanner, who first described autism (Autistic disturbances of affective contact, 1943) originated the "refrigerator mother" hypothesis, which held that autism was at least partly caused by a lack of affection from the mother. Although Kanner eventually renounced the theory and apologized publicly, 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.

  • Other psychogenic theories

Psychogenic theories in general have become increasingly unpopular, particularly since twin studies have shown that autism is highly heritable. Nevertheless, some case reports have found that deep institutional privation can result in "quasi-autistic" symptoms without the neuroanatomical differences [26][27]. Other case reports have suggested that children predisposed genetically to autism can develop "autistic devices" in response to traumatic events such as the birth of a sibling [28].

Natural variation modelsEdit

  • Neurodiversity

Many people diagnosed with autism and Asperger's syndrome don't think a disease model is appropriate to explain autistic behavior. They argue in favor of the neurodiversity model. Currently, no theories based on the neurodiversity model have been proposed by scientists, but there's no shortage of theories and insight from individuals with autism themselves. Unlike the 'social construct' theory (below), the neurodiversity view is consistent with the eventual existence of an objective test to diagnose autism.

  • Monotropism

In this model of mind, mental events compete for and consume attention. In a polytropic mind, many interests have a moderate amount of attention put into them, while in a monotropic mind, the person's attention is put into a few more specialized interests. The theory argues that when many interests are aroused, multiple complex behaviors emerge, but if only a few interests are aroused, fewer—but more intense—behaviors emerge. A May 2005 article in The Autism Journal [29] and information available from the group Autism and Computing[30] delves further into this subject.

  • Social construct theory

A spectrum disorder such as autism may be understood as a cultural or social construct.[7] The theory says that the boundary between normal and abnormal is subjective and arbitrary, so autism does not exist as an objective entity, but only as a 'construct'. Note that this theory does not say that there are no neurological or quality-of-life differences between groups deemed 'autistic' and 'non-autistic'. To falsify this theory it would need to be shown that an objective characteristic can clearly separate both groups. For example, a genetic test that can fully substitute for a psychiatric diagnosis would undermine this theory. The kind of phenomena this theory explains well are: (1) Differences in the prevalence of autism through time and geography, (2) The emergence of Asperger's syndrome as a form of autism, (3) The apparent difficulty in finding a single broad model to explain autistic behavior. There is some overlap between this theory and the view that autism is just a 'way of being' or a form of 'neurodiversity'. There are also some similarities between this theory and the view that autism is a 'blanket term'.

Some people, including some people diagnosed with Asperger syndrome, argue that Asperger syndrome is a social construct and that, as a category claimed to have a clearly defined neurobiological basis, Asperger syndrome may be analogous to a host of other psychiatric labels such as ADHD, criticized by psychiatrists such as Peter Breggin and Sami Timimi; obsessive compulsive disorder; and clinical depression, much promoted by the mental health and pharmaceutical industries.

All the behavioral traits associated with autism and Asperger syndrome occur to varying degrees in the general population. People diagnosed with either condition vary widely in terms of intellectual, professional, and social performance, range of interests, loquacity, conformity, and hypersensitivity. Those who support the social construct theory state that no scientific proof exists of a link between severe Kanner's type autism and the "geeky" and slightly quirky attributes of so many in our society, and suggest that many of the typically "Aspergian" characteristics are merely on the introverted or socially less-capable end of the normality spectrum.

Dr. Tony Attwood notes a strong association between certain types of interests and Asperger syndrome (AS). In a talk for partners of people with AS in 2000 he illustrated what he describes as the "courtship" phase of AS by reference to Star Trek conventions, calling them "reunions for people with Asperger's" -- a classification he also extended to train spotters in the UK similarly characterised.[8]


Proposed causesEdit

  • Genetics theory
For more details on this topic, see Heritability of autism.

Current genetic findings are consistent with a neurodiversity model, particularly since alleles involved are not rare mutations.

  • Extreme male brain

This theory proposed by Simon Baron-Cohen is also consistent with a neurodiversity or social construct model.

FootnotesEdit

  1. ^ Baron-Cohen S (2002). The extreme male brain theory of autism. Trends in cognitive sciences 6 (6): 248–254. PMID 12039606
  2. ^  Empathising-systemising (E-S) theory (Guardian). URL accessed on July 30, 2005.
  3. ^  empathising-systemising (E-S) theory. URL accessed on July 30, 2005.
  4. ^ Lawson J, Baron-Cohen S, Wheelwright S (2004). Empathising and systemising in adults with and without Asperger Syndrome. Journal of autism and developmental disorders 34 (3): 301–10. PMID 15264498
  5. ^ Baron-Cohen S, Knickmeyer RC, Belmonte MK (2005). Sex differences in the brain: implications for explaining autism. Science 310 (5749): 819–23. PMID 16272115
  6. ^  Autistic poetry example. URL accessed on July 30, 2005.
  7. ^  Murray D, Lesser M, Lawson W. (May 2005). Attention, monotropism and the diagnostic criteria for autism. Autism 9 (2): 139-56. Online PDF version from autismandcomputing.org.uk
  8. ^  Autism and Computing. URL accessed on July 30, 2005.
  9. ^  Clues to autism's neural basis. URL accessed on December 11, 2005.
  10. ^  Complex Gene Interactions Account for Autism Risk. URL accessed on August 10, 2005.
  11. ^  D. Q. Ma, P. L. Whitehead, M. M. Menold, E. R. Martin, A. E. Ashley-Koch, H. Mei, M. D. Ritchie, G. R. DeLong, R. K. Abramson, H. H. Wright, M. L. Cuccaro, J. P. Hussman, J. R. Gilbert, and M. A. Pericak-Vance (September 2005). Identification of Significant Association and Gene-Gene Interaction of GABA Receptor Subunit Genes in Autism. The American Journal of Human Genetics 77 (3): 477-88. (abstract)
  12. ^  Knickmeyer, R, Baron-Cohen, S, Hines, M, & Raggatt, P (2004). Foetal testosterone, social relationships, and restricted interests in children. Journal of Child Psychology & Psychiatry 45: 1-13.
  13. ^  Baron-Cohen, Simon (24 May 2003). The Essential Difference. The New Scientist 178 (2396): 54.
  14. ^  Challenges to Brain Testosterone Theory. URL accessed on July 30, 2005.
  15. ^  Wakefield conflict. URL accessed on July 30, 2005.
  16. ^  Gillberg C, Heijbel H. (1998). MMR and autism. Autism 2: 423-4.
  17. ^  Madsen KM, Hviid A, Vestergaard M, Schendel D, Wohlfahrt J, Thorsen P, Olsen J, Melbye M.A (7 November 2002). Population-based study of measles, mumps, and rubella vaccination and autism. N Engl J Med. 347 (19): 1477-82.
  18. ^  Autism Coach Immunization Poll. URL accessed on July 30, 2005.
  19. ^  Deadly Immunity. URL accessed on July 25, 2005.
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ReferencesEdit

  1. 1.0 1.1 Alternet article on male-female brain differences
  2. Article on autism and folic acid
  3. Geier DA, Geier MR. Early Downward Trends in Neurodevelopmental Disorders Following Removal of Thimerosal-Containing Vaccines. Med Sci Monit. 2006 May 29;12(6):CR231-239. PMID 16733480 full text (pdf)
  4. Fombonne, E., Zakarian, R., Bennett, A., Meng, L. & McLean-Heywood, D. (2006). Pervasive Developmental Disorders in Montreal, Quebec, Canada: Prevalence and Links With Immunizations. Pediatrics, 118(1), 139-150. (doi:10.1542/peds.2005-2993)[1]
  5. Ultrasound and autism in Sweden
  6. "New Autism Study Shows Discrepancy in Brains" by Jon Hamilton / National Public Radio. All Things Considered. July 19, 2006.
  7. (2004). Diagnosis of autism: Current epidemic has social context. BMJ.
  8. Tony Attwood and the interest of people with AS

See alsoEdit


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