CAUSES OF AUTISM
Autism and Autism Spectrum Disorders are complex
neurodevelopmental disorders. Many causes of autism have been proposed,
but its theory of causation is still incomplete. Heritability
contributes about 90% of the risk of a child developing autism,
but the genetics of autism are complex and typically it is unclear
which genes are responsible. In rare cases, autism is strongly
associated with agents that cause birth defects. Many other causes
have been proposed, such as exposure of children to vaccines; these
proposals are controversial and the vaccine hypotheses have no convincing
Autism is a condition involving abnormalities
of brain development and behavior which manifests itself before
a child is three years old and has a steady course with no remission.
It is characterized by impairments in social interaction and communication,
as well as restricted and repetitive
behaviors. It is part of a larger family called the Autism Spectrum Disorders (ASD) or pervasive developmental disorders (PDD), which
include closely related syndromes such as Asperger syndrome and
PDD-NOS. This article uses autism to denote the classic autistic
disorder and Autism Spectrum Disorder to denote the wider family.
Autism's theory of causation is still incomplete.
There is increasing suspicion among researchers that autism does
not have a single cause, but is instead a complex disorder with
a triad of core aspects (social impairment, communication difficulties,
and repetitive behaviors) that have distinct causes but often co-occur.
The number of people known to have autism has increased dramatically
since the 1980s, at least partly due to changes in diagnostic practice;
it is unknown whether prevalence has increased as well. An increase
in prevalence would suggest directing more attention and funding
toward changing environmental factors instead of continuing to focus
on genetics. The consensus among mainstream autism researchers is
that genetic factors predominate, but some are concerned, as one
anonymous researcher put it, that "geneticists are running
the show, and ignoring the environmental aspects."
In 2007 the National Institutes of Health announced
an Autism Centers of Excellence (ACE) research program to find the
causes of autism and identify new treatments for the disorder. Initial
recipients are focusing on genetic factors, brain imaging, brain
chemicals and functions including mirror neurons, effect on early
parent-child behavior on autism, and learning in autistic children.
Genetic factors are the most significant cause
for Autism Spectrum Disorders. Early studies of twins estimated
heritability to be over 90%, in other words, that genetics explains
over 90% of whether a child will develop autism. This may be
an overestimate; new twin data and models with structural genetic
variation are needed. Many of the non-autistic co-twins had
learning or social disabilities. For adult siblings the risk for
having one or more features of the broader autism phenotype might
be as high as 30%.
The genetics of autism is complex. Linkage
analysis has been inconclusive; many association analyses have had
inadequate power. More than one gene may be implicated, different
genes may be involved in different individuals, and the genes may
interact with each other or with environmental factors. Several
candidate genes have been located, but the mutations that increase
autism risk have not been identified for most candidate genes.
Though autism's genetic factors explain most of
autism risk, they do not explain all of it. A common hypothesis
is that autism is caused by the interaction of a genetic predisposition
and an early environmental insult. Several theories based on
environmental factors have been proposed to address the remaining
risk. Some of these theories focus on prenatal environmental factors,
such as agents that cause birth defects; others focus on the environment
after birth, such as children's diets.
A 2007 review of risk factors found associated
parental characteristics that included advanced maternal age, advanced
paternal age, and maternal place of birth outside Europe or North
America. It is not known whether these associations reflect genetic,
epigenetic, or environmental factors.
to read more about Genetics as a cause of autism.
The risk of autism is associated with several
prenatal risk factors. Autism has been linked to birth defect agents
acting during the first eight weeks from conception, though these
cases are rare. Other potential prenatal environmental factors do
not have convincing scientific evidence.
Teratogens are environmental agents that cause
birth defects. Some agents that are known to cause other birth defects
have also been found to be related to autism risk. These include
exposure of the embryo to thalidomide, valproic acid, or misoprostol,
or to rubella infection in the mother. These cases are rare.
Questions have also been raised whether ethanol (grain alcohol)
increases autism risk, as part of fetal alcohol syndrome or alcohol-related
birth defects, but current evidence is insufficient to determine
whether autism risk is actually elevated with ethanol. All known
teratogens appear to act during the first eight weeks from conception,
and though this does not exclude the possibility that autism can
be initiated or affected later, it is strong evidence that autism
arises very early in development. Infection-associated immunological
events in early pregnancy may affect neural development more than
infections in late pregnancy, not only for autism, but also for
other psychiatric disorders of presumed neurodevelopmental origin,
A 2007 study by the California Department of Public
Health found that women in the first eight weeks of pregnancy who
live near farm fields sprayed with the organochlorine pesticides
dicofol and endosulfan are several times more likely to give birth
to children with autism. The association appeared to increase with
dose and decrease with distance from field site to residence. The
study's findings suggest that on the order of 7% of autism cases
in the California Central Valley might have been connected to exposure
to the insecticides drifting off fields into residential areas.
These results are highly preliminary due to the small number of
women and children involved and lack of evidence from other studies.
It is not known whether these pesticides are human teratogens, though
endosulfan has significant teratogenic effects in laboratory rats.
A 2005 study showed indirect evidence that prenatal
exposure to organophosphate pesticides such as diazinon and chlorpyrifos
may contribute to autism in genetically vulnerable children.
Several other studies demonstrate the neurodevelopmental toxicity
of these agents at relatively low exposure levels.
Folic acid taken during pregnancy might play an
important role in causing autism by modulating gene expression through
epigenetic mechanism. This hypothesis is untested.
The fetal testosterone theory hypothesizes that
higher levels of testosterone in the amniotic fluid of mothers pushes
brain development towards improved ability to see patterns and analyze
complex systems while diminishing communication and empathy, emphasizing
"male" traits over "female", or in EQ SQ Theory
terminology, emphasizing "systemizing" over "empathizing".
One project has published several reports suggesting that high levels
of fetal testosterone could produce behaviors relevant to those
seen in autism. The theory and findings are controversial and
many studies contradict the idea that baby boys and girls respond
differently to people and objects.
A 2006 study found that sustained exposure of
mouse embryos to ultrasound waves caused a small but statistically
significant number of neurons to fail to acquire their proper position
during neuronal migration. It is highly unlikely that this result
speaks directly to risks of fetal ultrasound as practiced in competent
and responsible medical centers. There is no scientific evidence
of an association between prenatal ultrasound exposure and autism,
but there are very little data on human fetal exposure during diagnostic
ultrasound, and the lack of recent epidemiological research and
human data in the field has been called "appalling".
Autism is associated with some perinatal and obstetric
conditions. A 2007 review of risk factors found associated obstetric
conditions that included low birth weight and gestation duration,
and hypoxia during childbirth. This association does not demonstrate
a causal relationship; an underlying cause could explain both autism
and these associated conditions. A 2007 study of premature infants
found that those who survived cerebellar hemorrhagic injury (bleeding
in the brain that injures the cerebellum) were significantly more
likely to show symptoms of autism than controls without the injury.
A wide variety of postnatal contributors to autism
have been proposed, including gastrointestinal or immune system
abnormalities, allergies, and exposure of children to drugs, vaccines,
infection, certain foods, or heavy metals. The evidence for these
risk factors is anecdotal and has not been confirmed by reliable
studies. The subject remains controversial and extensive further
searches for environmental factors are underway.
Leaky gut syndrome
Parents have reported gastrointestinal (GI) disturbances
in autistic children, and several studies have investigated possible
associations between autism and the gut. The controversial Wakefield
et al. vaccine paper discussed in "MMR vaccine" below
also suggested that some bowel disorders may allow antigens to pass
from food into the bloodstream and then to contribute to brain dysfunction.
This produced several lines of investigation.
For example, employing secretin's effects on digestion,
a 1998 study of three children with Autism Spectrum Disorder treated with secretin infusion
reported improved GI function and dramatic improvement in behavior,
which suggested an association between GI and brain function in
autistic children. After this study, many parents sought secretin
treatment and a black market for the hormone developed quickly.
However, later studies found secretin ineffective in treating autism.
Leaky gut syndrome theories also inspired several
dietary treatments, including gluten-free diets, casein-free diets,
antifungal diets, low-sugar diets, as well as supplements that include
nystatin, B12, and probiotics. Parents are more likely to get advice
about these diets from other parents, the media, and the Internet
than from medical experts. There is no solid research evidence that
autistic children are more likely to have GI symptoms than typical
children. In particular, design flaws in studies of elimination
diets mean that the currently available data are inadequate to guide
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.
This theory hypothesizes that toxicity and oxidative
stress may cause autism in some cases by damaging Purkinje cells
in the cerebellum after birth. One possibility is that glutathione
This theory hypothesizes that an early developmental
failure involving the amygdala cascades on the development of cortical
areas that mediate social perception in the visual domain. The fusiform
face area of the ventral stream is implicated. The idea is that
it is involved in social knowledge and social cognition, and that
the deficits in this network are instrumental in causing autism.
This theory hypothesizes that autism is caused
by vitamin D deficiency, and that recent increases in diagnosed
cases of autism are due to medical advice to avoid the sun. The
theory has not been studied scientifically.
Lead poisoning has been suggested as a possible
risk factor for autism, as the lead blood levels of autistic children
has been reported to be significantly higher than typical. The atypical
eating behaviors of autistic children, along with habitual mouthing
and pica, make it hard to determine whether increased lead levels
are a cause or a consequence of autism.
This theory hypothesizes that autism is associated
with mercury poisoning, based on perceived similarity of symptoms.
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.
A 2003 study reported that mercury measurements
of hair samples from autistic children's first haircuts were significantly
lower than a matched group of normal children, declining as measures
of severity increased, but a later meta-analysis based on two
studies found that there was not enough evidence to conclude that
hair mercury level is lower in autistic children. A 2006 study
found an association between autism and environmental releases of
mercury, primarily from coal power plants; this study used Texas
county-wide data and did not distinguish between prenatal and postnatal
Perhaps the best-known theory involving mercury
and autism involves the use of the mercury-based compound thiomersal,
a preservative that has been phased out from most childhood vaccinations
in developed countries. Parents may first become aware of autistic
symptoms in their child around the time of a routine vaccination.
There is no convincing scientific evidence for a causal connection
between thiomersal and autism, but parental concern about the thiomersal
controversy has led to decreasing uptake of childhood immunizations
and increasing likelihood of disease outbreaks.
The MMR vaccine theory of autism is one of the
most extensively debated theories regarding the origins of autism.
A controversial 1998 paper by Andrew Wakefield et al. reported a
study of 12 children who had autism and bowel symptoms, in some
cases reportedly with onset after MMR. Though the paper concluded
"We did not prove an association between measles, mumps, and
rubella vaccine and the syndrome described," Wakefield
nevertheless suggested during a 1998 press conference that giving
children the vaccines in three separate doses would be safer than
a single jab. This suggestion was again not supported by the paper,
his co-authors or by any scientific evidence and has been heavily
criticized, both on scientific grounds and for triggering a decline
in vaccination rates. Using separate, single vaccines in place
of MMR is widely believed to put children at increased risk since
the combined vaccine reduces the risk of them catching the diseases
while they are waiting for full immunization cover. Numerous
peer-reviewed studies have also since failed to show any association
between MMR vaccine and autism.
In 2004, the interpretation of a causal link between
MMR vaccine and autism was formally retracted by ten of Wakefield's
twelve co-authors. The retraction followed an investigation
by The Sunday Times. The Centers for Disease Control and Prevention,
the Institute of Medicine of the National Academy of Sciences,
and the U.K. National Health Service have all concluded that
there is no evidence of a link between the MMR vaccine and autism.
In July 2007 Andrew Wakefield and coauthors John
Walker-Smith and Simon Murch faced charges of serious professional
misconduct at the General Medical Council. It is alleged that the
trio acted unethically in preparing the research into safety of
the MMR vaccine. Wakefield denies the charges.
Three economists hypothesized that early childhood
television viewing acts as an environmental trigger for an underlying
genetic predisposition. They found that precipitation was associated
with autism by examining county-level autism data for California,
Oregon, and Washington. Precipitation is also associated with television
watching, and their analysis concluded that just under 40% of autism
diagnoses in the three states result from television watching due
to precipitation. This study has not been published in a refereed
journal and its results have not been confirmed by others.
Bruno Bettelheim believed that autism was linked
to early childhood trauma, and his work was highly influential for
decades both in the medical and popular spheres. Parents, especially
mothers, of individuals with autism were blamed for having caused
their child's condition through the withholding of affection.
Leo Kanner, who first described autism, suggested that parental
coldness might contribute to autism. Although Kanner eventually
renounced the theory, Bettelheim put an almost exclusive emphasis
on it in both his medical and his popular books. Treatments based
on these theories failed to help children with autism, and after
Bettelheim's death it came out that his reported rates of cure (around
85%) were found to be fraudulent.
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"
features without the neuroanatomical differences. Other
case reports have suggested that children predisposed genetically
to autism can develop "autistic devices" in response to
traumatic events such as the birth of a sibling.
Like ADHD, which has a similar social construct
theory, a spectral disorder such as autism may be understood
as a cultural or social construct. The theory says that the
boundary between normal and abnormal is subjective and arbitrary,
so autism does not exist as an objective entity, but only as a social
construct. It further argues that autistic individuals themselves
have a way of being that is partly socially constructed. This
theory does not say that there are no neurological or quality-of-life
differences between groups deemed "autistic" and "non-autistic".
To falsify this theory it would need to be shown that an objective
characteristic can clearly separate both groups. For example, a
genetic test that can fully substitute for a psychiatric diagnosis
would undermine this theory.Asperger syndrome and high-functioning
autism are particular targets of the theory that social factors
determine what it means to be autistic. The theory hypothesizes
that individuals with these diagnoses inhabit the identities that
have been ascribed to them, and promote their sense of well-being
by resisting or appropriating autistic ascriptions.
the mechanism of autism
Despite extensive investigation, how autism occurs
is not well understood. Its mechanism can be divided into two areas:
the pathophysiology of brain structures and processes associated
with autism, and the neuropsychological linkages between brain structures
and behaviors. The behaviors appear to have multiple pathophysiologies.
Autism appears to result from developmental factors
that affect many or all functional brain systems. Neuroanatomical
studies and the associations with teratogens strongly suggest that
autism's mechanism includes alteration of brain development soon
after conception. This localized anomaly appears to start a cascade
of pathological events in the brain that are significantly influenced
by environmental factors. Many major structures of the human
brain have been implicated. Consistent abnormalities have been found
in the development of the cerebral cortex; and in the cerebellum
and related inferior olive, which have a significant decrease in
the number of Purkinje cells. Brain weight and volume and head circumference
tend to be greater in autistic children. The cellular and molecular
bases of pathological early overgrowth are not known, nor is it
known whether the overgrown neural systems cause autism's characteristic
signs. Current hypotheses include:
* An excess of neurons that causes local overconnectivity
in key brain regions.
* Disturbed neuronal migration during early gestation.
* Unbalanced excitatory-inhibitory networks.
* Abnormal formation of synapses and dendritic spines.
Interactions between the immune system and the
nervous system begin early during embryogenesis, and successful
neurodevelopment depends on a balanced immune response. Several
symptoms consistent with a poorly regulated immune response have
been reported in autistic children. It is possible that aberrant
immune activity during critical periods of neurodevelopment is part
of the mechanism of some forms of Autism Spectrum Disorder. As autoantibodies have
not been associated with pathology, are found in diseases other
than Autism Spectrum Disorder, and are not always present in ASD, the relationship
between immune disturbances and autism remains unclear and controversial.
Several neurotransmitter abnormalities have been
detected in autism, notably increased blood levels of serotonin.
Whether these lead to structural or behavioral abnormalities is
The mirror neuron system (MNS) theory of autism
hypothesizes that distortion in the development of the MNS interferes
with imitation and leads to autism's core features of social impairment
and communication difficulties. The MNS operates when an animal
performs an action or observes another animal of the same species
perform the same action. The MNS may contribute to an individual's
understanding of other people by enabling the modeling of their
behavior via embodied simulation of their actions, intentions, and
emotions. Several studies have tested this hypothesis by demonstrating
structural abnormalities in MNS regions of individuals with Autism Spectrum Disorder,
delay in the activation in the core circuit for imitation in individuals
with Asperger's, and a correlation between reduced MNS activity
and severity of the syndrome in children with Autism Spectrum Disorder. A variant
theory, EP-M, segments the MNS into an indirect route for goal emulation
and planning (EP) and a direct route for mimicry (M), and hypothesizes
that only the M route is impaired in autism.
The underconnectivity theory of autism hypothesizes
that autism is marked by underfunctioning high-level neural connections
and synchronization, along with an excess of low-level processes.
Evidence for this theory has been found in functional neuroimaging
studies on autistic individuals and by a brain wave study that
suggested that adults with Autism Spectrum Disorder have local overconnectivity in the
cortex and weak functional connections between the frontal lobe
and the rest of the cortex. Other evidence suggests the underconnectivity
is mainly within each hemisphere of the cortex and that autism is
a disorder of the association cortex.
Two major categories of cognitive theories have
been proposed about the links between autistic brains and behavior.
The first category focuses on deficits in social
cognition. Hyper-systemizing hypothesizes that autistic individuals
can systematize—that is, they can develop internal rules of operation
to handle internal events—but are less effective at empathizing
by handling events generated by other agents. It extends the
extreme male brain theory, which hypothesizes that autism is an
extreme case of the male brain, defined psychometrically as individuals
in whom systemizing is better than empathizing. This in turn is
related to the earlier theory of mind, which hypothesizes that autistic
behavior arises from an inability to ascribe mental states to oneself
and others. The theory of mind is supported by autistic children's
atypical responses to the Sally-Anne test for reasoning about others'
motivations, and is mapped well from the mirror neuron system theory
The second category focuses on nonsocial or general
processing. Executive dysfunction hypothesizes that autistic behavior
results in part from deficits in flexibility, planning, and other
forms of executive function. A strength of the theory is predicting
stereotyped behavior and narrow interests; a weakness is that executive
function deficits are not found in young autistic children.
Weak central coherence theory hypothesizes that a limited ability
to see the big picture underlies the central disturbance in autism.
One strength of this theory is predicting special talents and peaks
in performance in autistic people. A related theory—enhanced perceptual
functioning—focuses more on the superiority of locally oriented
and perceptual operations in autistic individuals. These theories
map well from the underconnectivity theory of autism.
Neither category is satisfactory on its own; social
cognition theories poorly address autism's rigid and repetitive
behaviors, while the nonsocial theories have difficulty explaining
social impairment and communication difficulties. A combined
theory based on multiple deficits may prove to be more useful.
1. ^ a b c Trottier G, Srivastava L, Walker CD
(1999). "Etiology of infantile autism: a review of recent advances
in genetic and neurobiological research". J Psychiatry Neurosci
24 (2): 103–115. PMID 10212552. Retrieved on 2007-07-16.
2. ^ a b c Freitag CM (2007). "The genetics of autistic disorders
and its clinical relevance: a review of the literature". Mol
Psychiatry 12 (1): 2–22. doi:10.1038/sj.mp.4001896. PMID 17033636.
3. ^ a b Arndt TL, Stodgell CJ, Rodier PM (2005). "The teratology
of autism". Int J Dev Neurosci 23 (2–3): 189–99. doi:10.1016/j.ijdevneu.2004.11.001.
4. ^ a b Rutter M (2005). "Incidence of Autism Spectrum Disorders:
changes over time and their meaning". Acta Paediatr 94 (1):
2–15. PMID 15858952.
5. ^ American Psychiatric Association (2000). "Diagnostic criteria
for 299.00 Autistic Disorder", Diagnostic and Statistical Manual
of Mental Disorders, 4th ed., text revision (DSM-IV-TR). ISBN 0890420254.
6. ^ World Health Organization (2006). "F84. Pervasive developmental
disorders", International Statistical Classification of Diseases
and Related Health Problems, 10th ed. (ICD-10).
7. ^ Happé F, Ronald A, Plomin R (2006). "Time to give up on
a single explanation for autism". Nat Neurosci 9 (10): 1218–20.
doi:10.1038/nn1770. PMID 17001340.
8. ^ Newschaffer CJ, Croen LA, Daniels J et al. (2007). "The
epidemiology of Autism Spectrum Disorders". Annu Rev Public
Health 28: 235–58. doi:10.1146/annurev.publhealth.28.021406.144007.
9. ^ a b c Szpir M (2006). "Tracing the origins of autism:
a spectrum of new studies". Environ Health Perspect 114 (7):
A412–8. PMID 16835042.
10. ^ National Institutes of Health (2007-08-02). NIH funds new
program to investigate causes and treatment of autism. Press release.
Retrieved on 2007-08-03.
11. ^ a b Sykes NH, Lamb JA (2007). "Autism: the quest for
the genes". Expert Rev Mol Med 9 (24): 1–15. doi:10.1017/S1462399407000452.
12. ^ Folstein SE, Rosen-Sheidley B (2001). "Genetics of autism:
complex aetiology for a heterogeneous disorder". Nat Rev Genet
2 (12): 943–55. doi:10.1038/35103559. PMID 11733747.
13. ^ Persico AM, Bourgeron T (2006). "Searching for ways out
of the autism maze: genetic, epigenetic and environmental clues".
Trends Neurosci 29 (7): 349–58. doi:10.1016/j.tins.2006.05.010.
14. ^ a b Kolevzon A, Gross R, Reichenberg A (2007). "Prenatal
and perinatal risk factors for autism". Arch Pediatr Adolesc
Med 161 (4): 326–33. PMID 17404128.
15. ^ Fombonne E (2002). "Is exposure to alcohol during pregnancy
a risk factor for autism?". J Autism Dev Disord 32 (3): 243.
doi:10.1023/A:1015466100838. PMID 12108626.
16. ^ Meyer U, Yee BK, Feldon J (2007). "The neurodevelopmental
impact of prenatal infections at different times of pregnancy: the
earlier the worse?". Neuroscientist 13 (3): 241–56.. doi:10.1177/1073858406296401.
17. ^ Roberts EM, English PB, Grether JK, Windham GC, Somberg L,
Wolff C (2007). "Maternal residence near agricultural pesticide
applications and Autism Spectrum Disorders among children in the
California Central Valley". Environ Health Perspect 115 (10):
1482–9. doi:10.1289/ehp.10168. PMID 17938740. Lay summary – EHP
18. ^ Singh ND, Sharma AK, Dwivedi P, Patil RD, Kumar M (2007).
"Citrinin and endosulfan induced teratogenic effects in Wistar
rats". J Appl Toxicol 27 (2): 143–51. doi:10.1002/jat.1185.
19. ^ D'Amelio M, Ricci I, Sacco R et al. (2005). "Paraoxonase
gene variants are associated with autism in North America, but not
in Italy: possible regional specificity in gene-environment interactions".
Mol Psychiatry 10 (11): 1006–16. doi:10.1038/sj.mp.4001714. PMID
20. ^ Karr CJ, Solomon GM, Brock-Utne AC (2007). "Health effects
of common home, lawn, and garden pesticides". Pediatr Clin
North Am 54 (1): 63–80. doi:10.1016/j.pcl.2006.11.005. PMID 17306684.
21. ^ Muskiet FA, Kemperman RF (2006). "Folate and long-chain
polyunsaturated fatty acids in psychiatric disease". J Nutr
Biochem 17 (11): 717–27. doi:10.1016/j.jnutbio.2006.02.001. PMID
22. ^ Baron-Cohen S (2004). The Essential Difference: Male and Female
Brains and the Truth About Autism. Basic Books. ISBN 046500556X.
23. ^ Fetal testosterone studies:
* Knickmeyer RC, Baron-Cohen S (2006). "Fetal testosterone
and sex differences". Early Hum Dev 82 (12): 755–60. doi:10.1016/j.earlhumdev.2006.09.014.
* Morelle R. "Hormone linked to autistic traits", BBC,
2007-09-11. Retrieved on 2007-09-11.
24. ^ Rivers C (2006-09-28). Discrimination against the female brain.
AlterNet. Retrieved on 2006-12-10.
25. ^ Ang ES Jr, Gluncic V, Duque A, Schafer ME, Rakic P (2006).
"Prenatal exposure to ultrasound waves impacts neuronal migration
in mice". Proc Natl Acad Sci U S A 103 (34): 12903–10. doi:10.1073/pnas.0605294103.
26. ^ Caviness VS, Grant PE (2006). "Our unborn children at
risk?". Proc Natl Acad Sci U S A 103 (34): 12661–2. doi:10.1073/pnas.0605505103.
27. ^ Abramowicz JS (2007). "Prenatal exposure to ultrasound
waves: is there a risk?". Ultrasound Obstet Gynecol 29 (4):
363–7. doi:10.1002/uog.3983. PMID 17352453.
28. ^ Limperopoulos C, Bassan H, Gauvreau K et al. (2007). "Does
cerebellar injury in premature infants contribute to the high prevalence
of long-term cognitive, learning, and behavioral disability in survivors?".
Pediatrics 120 (3): 584–93. doi:10.1542/peds.2007-1041. PMID 17766532.
29. ^ a b c Johnson TW (2006). "Dietary considerations in autism:
identifying a reasonable approach". Top Clin Nutr 21 (3): 212–25.
30. ^ a b Wakefield A, Murch S, Anthony A et al. (1998). "Ileal-lymphoid-nodular
hyperplasia, non-specific colitis, and pervasive developmental disorder
in children". Lancet 351 (9103): 637–41. doi:10.1016/S0140-6736(97)11096-0.
PMID 9500320. Retrieved on 2007-09-05.
31. ^ Horvath K, Stefanatos G, Sokolski KN, Wachtel R, Nabors L,
Tildon JT (1998). "Improved social and language skills after
secretin administration in patients with autism spectrum disorders".
J Assoc Acad Minor Phys 9 (1): 9–15. PMID 9585670.
32. ^ Sturmey P (2005). "Secretin is an ineffective treatment
for pervasive developmental disabilities: a review of 15 double-blind
randomized controlled trials". Res Dev Disabil 26 (1): 87–97.
33. ^ Christison GW, Ivany K (2006). "Elimination diets in
Autism Spectrum Disorders: any wheat amidst the chaff?". J
Dev Behav Pediatr 27 (2 Suppl 2): S162–71. PMID 16685183.
34. ^ Libbey JE, Sweeten TL, McMahon WM, Fujinami RS (2005). "Autistic
disorder and viral infections". J Neurovirol 11 (1): 1–10.
doi:10.1080/13550280590900553. PMID 15804954.
35. ^ Kern JK, Jones AM (2006). "Evidence of toxicity, oxidative
stress, and neuronal insult in autism". J Toxicol Environ Health
B Crit Rev 9 (6): 485–99.. doi:10.1080/10937400600882079. PMID 17090484.
36. ^ Schultz RT (2005). "Developmental deficits in social
perception in autism: the role of the amygdala and fusiform face
area". Int J Dev Neurosci 23 (2–3): 125–41. doi:10.1016/j.ijdevneu.2004.12.012.
37. ^ Cannell JJ (2007). "Autsim and vitamin D". Med Hypotheses.
38. ^ Zafeiriou DI, Ververi A, Vargiami E (2007). "Childhood
autism and associated comorbidities". Brain Dev 29 (5): 257–72.
doi:10.1016/j.braindev.2006.09.003. PMID 17084999.
39. ^ Bernard S, Enayati A, Redwood L, Roger H, Binstock T (2001).
"Autism: a novel form of mercury poisoning". Med Hypotheses
56 (4): 462–71. doi:10.1054/mehy.2000.1281. PMID 11339848.
40. ^ Davidson PW, Myers GJ, Weiss B (2004). "Mercury exposure
and child development outcomes". Pediatrics 113 (4 Suppl):
1023–9. PMID 15060195.
41. ^ Holmes AS, Blaxill MF, Haley BE (2003). "Reduced levels
of mercury in first baby haircuts of autistic children". Int
J Toxicol 22 (4): 277–85. PMID 12933322.
42. ^ Ng DK, Chan CH, Soo MT, Lee RS (2007). "Low-level chronic
mercury exposure in children and adolescents: meta-analysis".
Pediatr Int 49 (1): 80–7. doi:10.1111/j.1442-200X.2007.02303.x.
43. ^ Palmer RF, Blanchard S, Stein Z, Mandell D, Miller C (2006).
"Environmental mercury release, special education rates, and
autism disorder: an ecological study of Texas". Health Place
12 (2): 203–9. doi:10.1016/j.healthplace.2004.11.005. PMID 16338635.
44. ^ a b c Doja A, Roberts W (2006). "Immunizations and autism:
a review of the literature". Can J Neurol Sci 33 (4): 341–6.
45. ^ MMR – the controversy. UK Prime Minister's Office (2005).
Retrieved on 2007-07-29.
46. ^ MMR the facts. NHS. Retrieved on 2007-07-29.
47. ^ Murch SH, Anthony A, Casson DH et al. (2004). "Retraction
of an interpretation". Lancet 363 (9411): 750. doi:10.1016/S0140-6736(04)15715-2.
48. ^ Deer B (2007). The MMR-autism scare – our story so far. Retrieved
49. ^ Autism and vaccines theory. Centers for Disease Control and
Prevention (2007-07-05). Retrieved on 2007-07-29.
50. ^ Immunization safety review: vaccines and autism. Institute
of Medicine, National Academy of Sciences (2004). Retrieved on 2007-06-13.
51. ^ MMR the facts. National Health Service. Retrieved on 2007-06-13.
52. ^ "MMR scare doctor 'paid children'", BBC News, 2007-07-16.
Retrieved on 2007-07-29.
53. ^ Waldman M, Nicholson S, Adliov N (2006). "Does television
cause autism?". Johnson School Research Paper Series No. 01-07.
Retrieved on 2007-07-27.
54. ^ Wallis C. "Does watching TV cause autism?", TIME,
2006-10-20. Retrieved on 2007-07-28.
55. ^ Bettelheim B (1967). The Empty Fortress: Infantile Autism
and the Birth of the Self. Free Press. ISBN 0029031400.
56. ^ Kanner L (1943). "Autistic disturbances of affective
contact". Nerv Child 2: 217–50.
57. ^ Kanner L (1949). "Problems of nosology and psychodynamics
in early childhood autism". Am J Orthopsychiatry 19: 416–26.
58. ^ Gardner M (2000). "The brutality of Dr. Bettelheim".
Skeptical Inquirer 24 (6): 12–4.
59. ^ Rutter ML, Kreppner JM, O'Connor TG, English and Romanian
Adoptees (ERA) study team (2001). "Specificity and heterogeneity
in children's responses to profound institutional privation".
Br J Psychiatry 179 (2): 97–103. PMID 11483469.
60. ^ Hoksbergen R, ter Laak J, Rijk K, van Dijkum C, Stoutjesdijk
F (2005). "Post-Institutional Autistic Syndrome in Romanian
adoptees". J Autism Dev Disord 35 (5): 615–23. doi:10.1007/s10803-005-0005-x.
61. ^ Gomberoff M, De Gomberoff LP (2000). "Autistic devices
in small children in mourning". Int J Psychoanal 81 (5): 907–20.
62. ^ Timimi S, Taylor E (2004). "ADHD is best understood as
a cultural construct". Br J Psychiatry 184: 8–9. PMID 14702221.
63. ^ Timimi S (2004). "Diagnosis of autism: current epidemic
has social context". BMJ 328 (7433): 226. doi:10.1136/bmj.328.7433.226-a.
64. ^ Hacking I (1999). The Social Construction of What?. Harvard
University Press, 114–23. ISBN 0674004124.
65. ^ Does autism exist?. Natural Variation – Autism Blog (2006-02-24).
Retrieved on 2007-07-29.
66. ^ Nadesan MH (2005). "The dialectics of autism: theorizing
autism, performing autism, remediating autism, and resisting autism",
Constructing Autism: Unravelling the 'Truth' and Understanding the
Social. Routledge, 179. ISBN 0415321816.
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