Assalamualaikum…
Saya bukan ahli.
CMIIW
saya hanya sedih melihat pemberitaan yang tidak berimbang.
Tulisan ini saya kumpulkan dari berbagia sumber.
Siapa tahu bermanfaat…..
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Pada hari Selasa, 6 Mei 2008, Koran Tempo menurunkan berita berjudul Menurunkan Resiko Autisme (http://www.korantempo.com/korantempo/2008/05/06/Gaya_Hidup/krn,20080506,69.id.html)
Quote :
Dampak merkuri pada janin akan terkonsentrasi dalam plasenta selama masa
kehamilan. Konsentrasi dalam janin delapan kali lipat, terutama dalam hati,
ginjal, dan otak. Jika sang ibu terkontaminasi pada waktu menyusui, merkuri
dapat mengalir melalui air susu ibu dan diabsorpsi dengan baik oleh bayi.
Untuk itu, sangat penting seorang wanita mempersiapkan kehamilan. MARLINA
Langkah Persiapan Ibu Hamil
1.Keluarkan semua tambalan amalgam dari gigi.
2.Beri tenggang waktu tiga bulan sebelum hamil untuk mengeluarkan toksin
tubuh.
3.Bila kadar merkuri tinggi pada ibu, lakukan dulu detoksifikasi sebelum
hamil.
4.Jangan makan ikan laut selama hamil dan menyusui.
dst….
Pada Sabtu, 7 Juni 2008, Koran Kompas memuat berita berjudul “Boom” Autisme Terus Meningkat (http://cetak.kompas.com/read/xml/2008/06/07/01452123/boom.autisme.terus.meningkat)
Quote :
“Jika ibu menyatakan kalau setelah divaksinasi, kondisi si anak
kemudian makin mundur, kita cari apakah anak ini keracunan merkuri.
Darahnya harus diperiksa untuk mencari tahu berapa kadar logam berat,
logam merkuri, diperiksa rambutnya, apakah merkurinya sudah lama
menumpuk di tubuh dan tidak bisa keluar, misalnya, papar Melly Budhiman.”
….
“Faktor pemicu autisme itu banyak, tidak mungkin satu pemicu saja.
Selain keracunan logam berat, anak-anak penyandang autisme biasanya
juga mengalami alergi, kondisi pencernaannya juga jelek, kata Melly.
Ada kecurigaan, salah satu faktor pencetus autisme adalah logam berat
merkuri.”
….
“Repotnya, menurut Melly, banyak vaksin yang beredar di pasaran
mengandung merkuri. Satu suntikan vaksin dari luar negeri biasanya
merkuri yang dikandung 25 mikrogram. Bahkan, ada vaksin yang kandungan
merkurinya lebih dari itu. Keterkaitan vaksin sebagai pencetus
autisme masih jadi perdebatan di dunia internasional. Ini tentunya
perlu penelitian lebih lanjut,ujarnya”
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Masyarakat awam seperti saya semakin binggung…apalagi yang ngomong mempunyai sederet gelar.
Siapa yang mesti diikuti…???
Senjata saya hanya satu…tanya Paman Google….namun..sekali lagi namun…..saya ingatkan…hati-hati dalam mencari informasi….carilah sumber yang benar-benar reliable…biasanya situs-situs resmi pemerintah….karena pemberitaan seputar autis di internet lebih banyak yang pseudoscince.
Sebenarnya siapa dr. Melly Budiman ini….
Mohon maaf…tanpa bermaksud mendeskriditkan beliau….beliau ini aktif di DAN (Defeat Autism Now) yang dengan gencarnya melakukan publikasi di media-media baik lokal maupun internasional.
DAN!(Defeat Autism Now!) ini adalah organisasi yang terdiri dari peneliti dan juga ilmuwan yang terbentuk tahun 1995 dibawah lindungan ARI(Autism Research Institue) yaitu sekumpulan orang tua yang anaknya menderita autisme.
Didirikan tahun 1967 oleh Dr. Bernard Rimland di US, adalah seorang psikolog dimana anaknya yang bernama Mark Rimland menyandng autis berat.
Lembaga ini adalah lembaga yang berkecimpung dalam terapi alternative untuk autism dan neurodevelopmental disorder lainnya. Jelas bentuk terapi dan pemikirannya bukanlah ilmu kedokteran. Namun karena menggunakan berbagai istilah medik dan mengatakan berbagai ilmunya juga riset, maka masyarakat akhirnya terkelabuhi juga.
Bentuk ilmu ini adalah PSEUDOSCIENCE karena berbagai yang diaku sebagai risetnya itu tidak memenuhi standard procedure penelitian ilmiah kedokteran.
Siapa saja dokter Indonesia yang masuk dalam daftar DAN :
Melly Budhiman, M.D.
Jalan Beton No. 9 (77)
Jakarta 13210
Indonesia
ph: 62-21-4892332
fax: same
Rudy Sutadi, Dr. SpA, M.D.
JL Buncit Raya No. 15
Jakarta Selatan 12740
Indonesia
ph: 62-79-408-36/7
fax: 62-21-794-0838
Kurniati Ihromi Tanjung, M.D.
Ave. Alfredo Jahn con Tercera Transv. Qta. Emaus.
Urb Los Chorros
Caracas 1071
Indonesia
ph: (58) 212-2371051
fax: (58) 212-2387339
Sasanti Yuntar, M.D.
Ketintang Selatan 8/14
Surabaya
60232
Indonesia
ph: 62-31-8380114
Sumber : http://www.autismwebsite.com/ari-lists/danforeign.html
DAN! 2003 FALLCONFERENCE
Sunday October 5: General Session
JAQUELYN McCANDLESS, M.D.
INTERVENTIONS for
Digestive, Immune, and Neurological Problems in Autism Spectrum
Disorder
INTERVENTIONS
• AFTER HISTORY, EXAMINATION, AND LABORATORY TESTING:
• TREATMENT CATEGORIES:
•
• 1) DIET, NUTRITION, NUTRIENTS, FOOD ALLERGY
• 2) GUT HEALTH, TREATING INFLAMMATION,
PATHOGENS
• 3) TOXIC ACCUMULATION, VARIOUS
DETOXIFICATION - CHELATION METHODS
• 4) IMMUNE ISSUES, VIRAL OVERLOAD
• 5) PSYCHOTROPICS: SSRI’S, STIMULANTS,
ANTI-PSYCHOTICS, ANTI-CONVULSANTS
DIAGNOSTIC EVALUATION
LAB WORKUP
GENERAL
•
• Routine Laboratory Screening (Any good lab will do these –
insurance almost always pays)
•
• 1) CBC w Differential and Platelets
• 2) Chemistry Panel Including Liver Enzymes
• 3) Thyroid Panel
• 4) Urinalysis
• 5) Plasma zinc, serum copper, ceruloplasmin
SPECIALTY LABORATORY TESTS
•
• General Biochemical (Must order kits from Specialty Labs –
Insurance variably pays for these tests)
•
• 1) Amino Acids (Plasma)
• 2) Organic Acid (Urine)
• 3) Comprehensive Stool Analysis
• 4) IgG 90-Food Delayed Sensitivity (Plasma)
• 5) Fatty Acids (Plasma)
• 6) Vitamin levels (Plasma)
• 7) Hair Analysis, RBC Minerals
• 
Immune Tests Incl. Metallothionein
BIOCHEMICAL IMBALANCES IN ASD CHILDREN
• Multiple nutritional deficiencies
• Elevated IgG antibodies to milk and wheat
• Imbalance of gut bacterial flora
• Elevated urinary bacterial metabolites
• Evidence of myelin sheath injury in brain
• Evidence of immune impairment
NUTRIENT DEFICIENCIES
• B6 and Magnesium
• Zinc, Selenium and other minerals
• Calcium
• Vitamins A, C, & E
• Essential Fatty Acids
• Amino Acids
• B-Vitamins: B1, 2, 3, 5, 12, & Folate
GUT I - CLINICAL HISTORY: EARLY INDICATIONS OF GUT DYSFUNCTION
1) Familial digestive dysfunctions
2) Inability to breast feed
3) Persistent colic in infancy
4) Frequent infections (e.g. ear) leading to frequent
antibiotics
5) Reaction to certain immunizations
GUT II - GASTROINTESTINAL PATHOLOGY SYMPTOMS REPORTED BY PARENTS
•
• Persistent diarrhea and/or constipation, bloating, gas,
abdominal pain
• Self-restriction of diet
• Night waking
• Greater allergic susceptibilities
GUT III: G.I. HEALTH:
Treatments That Parents Can Do
• •Eliminate sugars and junk food for everyone in the family
Read labels on foods, get educated about toxins in both food and
water
• GF/CF/SF, SCD Diet
• Enzymes and Probiotics
• Basic Nutrient Supplementation
GUT IV: G.I. HEALING:
Treatments That Require a Doctor’s Prescription
•
Lab Testing Must be Practitioner-Ordered
• Anti-Fungal Prescription Treatment
• Anti-Bacterial (Clostridia and other) Prescription Treatment
• Secretin, Vit. B12 shots, IV Glutathione
• Immunoglobulin, IV or Oral
Summary: TREATMENT FOR GUT DISORDER AND NUTRIENT DEFICIENCIES
•
• GF/CF/SF or SCD, Other Special Diets
• Removal of other offending foods per tests
• Replace nutrient deficiencies
• Treat for pathogen overgrowth; probiotics, if seriously
infested, systemic anti-fungals. If mild, natural antidotes, e.g.
Lauricidin, Grapefruit Seed Extract, Aqua Flora
TOXINS DIAGNOSTIC EVALUATION
1) Heavy Metals Exposure, History
2) Hair Elements Evaluation DD
3) RBC Minerals
4) Metallothionein, plasma zinc, serum copper, ceruloplasmin
5) Gut readiness, OAT to r/o pathogens
6) Mineralization readiness, vits/mins especially zinc
seterusnya bisa baca di:
http://64.202.182.52/powerpoint/dan2003/JacquelineMcCandless_files/frame.htm
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Yuk kita coba telusuri sedikit demi sedikit…terkait dengan pemberitaan Koran Tempo dan Kompas terkait statment yang dibuat dr. Melly Budiman.
1.Keluarkan semua tambalan amalgam dari gigi.
berikut jawaban dari ADA (American Dental Association)
ADA Positions & Statements
ADA Statement on Dental Amalgam
Revised: April 2007
Dental amalgam (silver filling) is considered a safe, affordable and
durable material that has been used to restore the teeth of more than
100 million Americans. It contains a mixture of metals such as
silver, copper and tin, in addition to mercury, which binds these
components into a hard, stable and safe substance. Dental amalgam has
been studied and reviewed extensively, and has established a record
of safety and effectiveness.
Issued in late 1997, the FDI World Dental Federation and the World
Health Organization consensus statement on dental amalgami
stated, “No controlled studies have been published demonstrating
systemic adverse effects from amalgam restorations.” The document
also states that, aside from rare instances of local side effects of
allergic reactions, “the small amount of mercury released from
amalgam restorations, especially during placement and removal, has
not been shown to cause any . adverse health effects.”
The ADA’s Council on Scientific Affairs’ 1998ii report on its review
of the recent scientific literature on amalgam states: “The Council
concludes that, based on available scientific information, amalgam
continues to be a safe and effective restorative material.” The
Council’s report also states, “There currently appears to be no
justification for discontinuing the use of dental amalgam.”
In an articleiii published in the February 1999 issue of the Journal
of the American Dental Association, researchers report finding “no
significant association of Alzheimer’s Disease with the number,
surface area or history of having dental amalgam restorations”
and “no statistically significant differences in brain mercury levels
between subjects with Alzheimer’s Disease and control subjects.”
In 2002, the U.S.Food and Drug Administration (FDA) and other
organizations of the U.S. Public Health Service (USPHS) that continue
to investigate the safety of dental amalgams released a consumer
update stating that there is “no valid scientific evidence has shown
that amalgams cause harm to patients with dental restorations, except
in the rare case of allergy.”
A 2003 paper published in the New England Journal of Medicineiv
states, “Patients who have questions about the potential relation
between mercury and degenerative diseases can be assured that the
available evidence shows no connection.”
In 2004, an expert panel reviewed the peer-reviewed, scientific
literature published from 1996 to December 2003 on potential adverse
human health effects caused by dental amalgam and published a report.
The review was conducted by the Life Sciences Research Office (LSRO)
and funded by the National Institutes of Dental and Craniofacial
Research, National Institutes of Health and the Centers for Devices
and Radiological Health, U.S.Food and Drug Administration (FDA). The
resulting report states that, “The current data are insufficient to
support an association between mercury release from dental amalgam
and the various complaints that have been attributed to this
restoration material. These complaints are broad and nonspecific
compared to the well-defined set of effects that have been documented
for occupational and accidental elemental mercury exposures.
Individuals with dental amalgam-attributed complaints had neither
elevated urinary mercury nor increased prevalence of hypersensitivity
to dental amalgam or mercury when compared with controls.” The full
report is available from LSRO (www.lsro.org). A summary of the review
is published in Toxicological Reviewsv.
In 2006, the Journal of the American Medical Association (JAMA) and
Environmental Health Perspectives published the results of two
independent clinical trials designed to examine the effects of
mercury release from amalgam on the central and peripheral nervous
systems and kidney function. The authors concluded that “there were
no statistically significant differences in adverse
neuropsychological or renal effects observed over the 5-year period
in children whose caries are restored using dental amalgam or
composite materials”;vi,vii and “children who received dental
restorative treatment with amalgam did not, on average, have
statistically significant differences in neurobehavioral assessments
or in nerve conduction velocity when compared with children who
received resin composite materials without amalgam. These finding,
combined with the trend of higher treatment need later among those
receiving composite, suggest that amalgam should remain a viable
dental restorative option for children.”viii
The ADA supports ongoing research in the development of new
materials. However, the ADA continues to believe that amalgam is a
valuable, viable and safe choice for dental patients.
Footnotes
i.FDI Policy Statement/WHO Consensus Statement on Dental Amalgam .
September 1997. (accessed March 8, 2007)
ii. ADA Council on Scientific Affairs. Dental Amalgam: Update on
Safety Concerns. J Am Dent Assoc. 1998;129:494-503.
iii. Saxe SR et al. Alzheimer’s disease, dental amalgam and mercury.
J Am Dent Assoc. 1999;130:191-9.
iv. Clarkson TW, Magos L, Myers GJ. The toxicology of mercury -
Current exposures and clinical manifestations. N Engl J Med.
2003;349:1731-7.
v. Brownawell AM et al. The Potential Adverse Health Effects of
Dental Amalgam. Toxicol Rev. 2005;24:1-10.
vi. Bellinger DC, Trachtenberg F, Barregard L, Tavares M, Cernichiari
E, Daniel D, McKinlay S. Neuropsychological and Renal Effects of
Dental Amalgam in Children: A Randomized Clinical Trial. JAMA
2006;295:1775-83.
vii. Bellinger DC, Daniel D, Trachtenberg F, Tavares M, KcKinlay.
Dental Amalgam Restorations and Children’s Neuropsychological
Function: The New England Children’s Amalgam Trial. Environ Health
Perspect (online 30 October 2006).
viii. DeRouen TA, Martin MD, Leroux BG, Townes BD, Woods JS, Leitao
J, Castro-Caldas A, Luis H, Bernardo M, Rosenbaum G, Martins IP.
Neurobehavioral Effects of Dental Amalgam in Children: A Randomized
Clinical Trial. JAMA 2006;295:1784-92.
Return to Top
Page Updated: April 06, 2007
http://www.ada.org/prof/resources/positions/statements/amalgam.asp
2. Faktor pemicu autisme itu banyak, tidak mungkin satu pemicu saja.
Selain keracunan logam berat, anak-anak penyandang autisme biasanya
juga mengalami alergi, kondisi pencernaannya juga jelek, kata Melly.
Ada kecurigaan, salah satu faktor pencetus autisme adalah logam berat
merkuri.
Berikut jawabannya :
Separating Fact from Fiction in the Etiology and Treatment of
Autism:A Scientific Review of the Evidence
James D. Herbert, Ph.D.Ian R. Sharp, Ph.D.Brandon A. Gaudiano, Ph.D.
Autistic-spectrum disorders are among the most enigmatic forms of
developmental disability. Although the cause of autism is largely
unknown, recent advances point to the importance of genetic factors
and early environmental insults, and several promising behavioral,
educational, and psychopharmacologic interventions have been
developed. Nevertheless, several factors render autism especially
vulnerable to pseudoscientific theories of etiology and to
intervention approaches with grossly exaggerated claims of
effectiveness. Despite scientific data to the contrary, popular
theories of etiology focus on maternal rejection, candida
infections, and childhood vaccinations. Likewise, a variety of
popular treatments are promoted as producing dramatic results,
despite scientific evidence suggesting that they are of little
benefit and in some cases may actually be harmful. Even the most
promising treatments for autism rest on an insufficient research
base, and are sometimes inappropriately and irresponsibly promoted
as “cures.” We argue for the importance of healthy skepticism in
considering etiological theories and treatments for autism.
Note: We use the term “autism” throughout this paper to refer not
only to classic autistic disorder (American Psychiatric Association,
1994), but in some cases to the full range of autistic-spectrum
disorders. The vast majority of the research reviewed in this paper
does not distinguish among the various subtypes of autistic-spectrum
disorders. It is therefore often impossible to judge the degree to
which research findings are unique to autistic disorder per se, or
are generalizable to other pervasive developmental disorders.
This article was first published in the Spring-Summer edition of The
Scientific Review of Mental Health Practice.
Autism is a pervasive developmental disorder marked by profound
deficits in social, language, and cognitive abilities. Prevalence
rates range from 7 to 13 cases per 10,000 (Bryson, 1997; Bryson,
Clark, & Smith, 1988; Steffenberg & Gillberg, 1986; Sugiyama & Abe,
1989). It is not clear if the actual prevalence of autism is
increasing, or if the increased frequency of diagnosis has resulted
from wider recognition of the disorder and especially recognition of
the full range of pervasive developmental disorders, often referred
to as “autistic-spectrum disorders.” Either way, autism is no longer
considered rare, occurring more commonly than Downs syndrome, cystic
fibrosis, and several childhood cancers (Fombonne, 1998; Gillberg,
1996).
The degree of impairment associated with autism varies widely, with
approximately 75% of autistic individuals also meeting criteria for
mental retardation (American Psychiatric Association [APA], 1994).
Autism occurs three to four times more frequently in males than
females (Bryson et al., 1988; Steffenberg & Gillberg, 1986; Volkmar,
Szatmari, & Sparrow, 1993). Although recent advances have been made
with respect to possible causal factors (Rodier, 2000), the exact
etiology of autism remains unknown. Moreover, although certain
behavioral, educational, and pharmacological interventions have been
demonstrated to be helpful for many individuals with autism, there
is currently no cure for the disorder.
WHY AUTISM IS FERTILE GROUND FOR PSEUDOSCIENCE
Several factors render autism especially vulnerable to etiological
ideas and intervention approaches that make bold claims, yet are
inconsistent with established scientific theories and unsupported by
research (Herbert & Sharp, 2001). Despite their absence of grounding
in science, such theories and techniques are often passionately
promoted by their advocates. The diagnosis of autism is typically
made during the preschool years and, quite understandably, is often
devastating news for parents and families. Unlike most other
physical or mental disabilities that affect a limited sphere of
functioning while leaving other areas intact, the effects of autism
are pervasive, generally affecting most domains of functioning.
Parents are typically highly motivated to attempt any promising
treatment, rendering them vulnerable to promising “cures.” The
unremarkable physical appearance of autistic children may contribute
to the proliferation of pseudoscientific treatments and theories of
etiology.
Autistic children typically appear entirely normal; in fact, many of
these children are strikingly attractive. This is in stark contrast
to most conditions associated with mental retardation (e.g., Downs
syndrome), which are typically accompanied by facially dysmorphic
features or other superficially evident abnormalities. The normal
appearance of autistic children may lead parents, caretakers, and
teachers to become convinced that there must be a
completely “normal” or “intact” child lurking inside the normal
exterior. In addition, as discussed above, autism comprises a
heterogeneous spectrum of disorders, and the course can vary
considerably among individuals. This fact makes it difficult to
identify potentially effective treatments for two reasons.
First, there is a great deal of variability in response to
treatments. A given psychotropic medication, for example, may
improve certain symptoms in one individual, while actually
exacerbating those same symptoms in another.
Second, as with all other developmental problems and
psychopathology, persons with autism sometimes show apparently
spontaneous developmental gains or symptom improvement in a
particular area for unidentified reasons. If any intervention has
recently been implemented, such improvement can be erroneously
attributed to the treatment, even when the treatment is actually
ineffective. In sum, autisms pervasive impact on development and
functioning, heterogeneity with respect to course and treatment
response, and current lack of curative treatments render the
disorder fertile ground for quackery.
A number of contemporary treatments for autism can be characterized
as pseudoscientific. Most scientists agree that there are no hard-
and-fast criteria that distinguish science from pseudoscience; the
differences are in degree, rather than kind (Bunge, 1994; Herbert et
al., 2000; Lilienfeld, 1998). Although a detailed treatment of
pseudoscience in mental health is beyond the scope of this paper, a
brief discussion of the features that distinguish it from legitimate
science is important in order to provide a context for considering
currently popular etiological theories and treatments for autism. In
general, pseudoscience is characterized by claims presented as being
scientifically verified even though in reality they lack empirical
support (Shermer, 1997).
Pseudoscientific treatments tend to be associated with exaggerated
claims of effectiveness that are well outside the range of
established procedures. They are often based on implausible theories
that cannot be proven false. They tend to rely on anecdotal evidence
and testimonials, rather than controlled studies, for support. When
quantitative data are considered, they are considered selectively.
That is, confirmatory results are highlighted, whereas unsupportive
results are either dismissed or ignored. They tend to be promoted
through proprietary publications or Internet Web sites rather than
refereed scientific journals. Finally, pseudoscientific treatments
are often associated with individuals or organizations with a direct
and substantial financial stake in the treatments. The more of these
features that characterize a given theory or technique, the more
scientifically suspect it becomes.
A number of popular etiological theories and treatment approaches to
autism are characterized by many of the features of pseudoscience
described above (Green, 1996a; Green, 2001; Herbert & Sharp, 2001;
Smith, 1996). Still other treatments, although grounded on a sound
theoretical basis and supported by some research, are nonetheless
subject to exaggerated claims of efficacy. What follows is a review
of the most popular dubious theories and questionable intervention
approaches for autism. We also review promising etiologic theories
and treatments. Some intervention programs are designed specifically
for young children, whereas others are applied across a wider age
range.
THE ETIOLOGY OF AUTISM: SEPARATING FACT FROM FICTION
Psychoanalytic Explanations
Although modern theories of autism posit the strong influence of
biological factors in the etiology of the disorder, psychoanalytic
theories have abounded traditionally. Kanner (1946) was the first to
describe the parents of children with autism as interpersonally
distant. For example, he concluded that the autistic children he
observed were “kept neatly in refrigerators which did not defrost”
(Kanner, 1973, p. 61). However, Kanner also stressed that the
disorder had a considerable biological component that produced
disturbances in the formation of normal emotional contact. It was
Bruno Bettelheim who was perhaps the most influential theorist
promoting psychoanalytic interpretations of autism. Bettelheim rose
to prominence as director of the University of Chicagos Orthogenic
School for disturbed children from 1944 to 1978. He rejected Kanners
conclusions positing a biological role in the etiology in autism and
was convinced that autism was caused by “refrigerator” mothers.
According to Bettelheim, autistic symptoms are viewed as defensive
reactions against cold and detached mothers. These unloving mothers
were sometimes assumed to be harboring “murderous impulses” toward
their children. For example, in his book The Empty Fortress,
Bettelheim (1967) wrote that one autistic girls obsession with the
weather could be explained by dissecting the word to
form “we/eat/her,” indicating that she was convinced that her
mother, and later others, would “devour her.” Based on his
conceptualization of autism, Bettelheim promoted a policy
of “parentectomy” that entailed separation of children from their
parents for extended periods of time (Gardner, 2000).
Other psychoanalytic therapists such as Mahler (1968) and Tustin
(1981) promoted similar theories positing problems in the mother-
child relationship as causing autism (see Rosner, 1996, for a review
of psychoanalytic theories of autism).
After his suicide in 1990, stories began to emerge that tarnished
Bettelheims reputation (Darnton, 1990). Several individuals claimed
abuse at the hands of the famous doctor when they were at the
Orthogenic School. Furthermore, information emerged that Bettelheim
often lied about his background and training. For example, although
he frequently claimed to have studied under Freud in Vienna,
Bettelheim possessed no formal training in psychoanalysis
whatsoever, and instead held a degree in philosophy. Also,
Bettelheim claimed that 85% of his patients at the Orthorgenic
School were cured after treatment; however, most of the children
were not autistic and the case reports he presented in his books
were often fabrications (Pollak, 1997). Despite the continued
acceptance of Bettelheims theories in some circles, no controlled
research has been produced to support the refrigerator mother theory
of autism. For example, Allen, DeMeyer, Norton, Pontus, and Yang
(1971) did not find differences between parents of autistic and
mentally retarded children and matched comparison children on
personality measures. Despite the complete absence of controlled
evidence, even today some psychoanalytic theorists continue in the
tradition of Bettelheim by highlighting the putative role of early
mother-child attachment dysfunctions in causing autism (Rosner,
1996).
Candida Infection
Candida albicans is a yeastlike fungus found naturally in humans
that aids in the destruction of dangerous bacteria. Candidiasis is
an infection caused by an overgrowth of candida in the body. Women
often contract yeast infections during their childbearing years. In
addition, antibiotic medication can disrupt the natural balance
among microorganisms in the body, resulting in an overgrowth of
candida (Adams & Conn, 1997). In the 1980s, anecdotal reports began
to emerge suggesting that some children with candidiasis later
developed symptoms of autism. Supporters of this theory point to
animal studies in which candida was shown to produce toxins that
disrupted the immune system, leading to the possibility of brain
damage (Rimland, 1988). Furthermore, Rimland speculated that perhaps
5 to 10% of autistic children could show improved functioning if
treated for candida infection. Proponents often recommend that
Nystatin, a medication used to treat women with yeast infections, be
given to children whose mothers had candidiasis during pregnancy,
whether or not the children show signs of infection. However, there
is no evidence that mothers of autistic children have a higher
incidence of candidiasis than mothers in the general population and
only uncontrolled case reports are presented as evidence for the
etiological role of candida infection in autism (Siegel, 1996).
Adams and Conn (1997) presented the case study of a 3-year-old
autistic boy who reportedly showed improved functioning following a
vitamin treatment for candida infection. However, the boy was never
medically diagnosed with candidiasis and was only reported to meet
criteria based on questionnaire data. In addition, reports of the
childs functioning were mostly based on parental report (especially
concerning functioning prior to the course of vitamin treatment) and
not on standardized assessment instruments. Although interesting,
such presentations provide no probative data on the possible role of
candidiasis in causing autism. Without reliable and valid evidence
to the contrary, case reports cannot rule out a host of confounding
variables, including any natural remission or change in symptoms due
to developmental maturation or even merely to the passage of time.
It is important to remember that many people, especially women,
contract candidia infections at different points in their lives,
sometimes without even knowing that they are infected because the
symptoms are so mild (Siegel, 1996). However, there is no evidence
that even severe candidiasis in humans can produce brain damage that
leads to the profound deficits in functioning found in autism.
MMR Vaccination
There has recently been much public concern that the mumps, measles,
and rubella (MMR) vaccine is causing an increased incidence of
autism. As evidence of the link between the MMR vaccine and autism,
proponents point to the fact that reported cases of autism have
increased dramatically over the past two decades, which appear to
coincide with the widespread use of the MMR vaccine starting in
1979. In fact, Dales, Hammer, and Smith (2001) found in their
analyses of California Department of Developmental Services records
that the number of autistic disorder caseloads increased
approximately 572% from 1980 to 1994. Indicating a similar trend in
Europe, Kaye, Melero-Montes, and Jick (2001) reported that the
yearly incidence of children diagnosed with autism increased
sevenfold from 1988 to 1999 in the United Kingdom. Fears that the
MMR vaccine may be responsible for this rise in the increasing
incidence of autism have been picked up in the media and some
parents have decided to decline vaccinations for their children in
an effort to protect them from developing autism (Manning, 1999).
Rimland (2000) saw “medical overexuberance” as producing a tradeoff
in which vaccinations protect children against acute diseases while
simultaneously increasing their susceptibility to more chronic
disorders, including autism, asthma, arthritis, allergies, learning
disabilities, Crohns disease, and attention deficit hyperactivity
disorder. Pointing out that the average number of vaccines school-
age children receive is now at 33, Rimland blamed the “vaccine
industry” for making products that have not been properly tested
before their widespread usage. He concluded by stating that research
on this problem should be of the “highest priority.”
In fact, it was preliminary research findings that initially raised
the possibility that the MMR vaccine might be related to the
apparent increase in the incidence of autism. The British researcher
Andrew Wakefield and colleagues (1998) reported 12 case studies of
children who were diagnosed with particular forms of intestinal
abnormalities (e.g., ileal-lymphoid-nodular hyperplasia). Eight out
of the 12 children demonstrated behavioral disorders diagnosed as
representing autism, which reportedly occurred after MMR
vaccination. The authors concluded that “the uniformity of the
intestinal pathological changes and the fact that previous studies
have found intestinal dysfunction in children with autistic-spectrum
disorders, suggests that the connection is real and reflects a
unique disease process” (p. 639). However, Wakefield et al. made it
clear in their report that they did not prove an actual causal
connection between the MMR vaccine and autism.
Although the Wakefield et al. (1998) case reports suggested that the
MMR vaccine may be associated with autism, recent epidemiological
research has provided strong evidence against any such connection.
Kaye et al. (2001) conducted a time trend analysis on data taken
from the UK general practice research database. As discussed
earlier, they found that the yearly incidence of diagnosed autism
increased dramatically over the last decade (0.3 per 10,000 persons
in 1988 to 2.1 per 10,000 persons in 1999). However, the prevalence
of MMR vaccination among children remained virtually constant during
the analyzed time period (97% of the sample). If the MMR vaccine
were the major cause of the increased reported incidence of autism,
then the risk of being diagnosed with autism would be expected to
stop rising shortly after the vaccine was instated at its current
usage. However, this was clearly not the case in the Kaye study, and
therefore no time correlation existed between MMR vaccination and
the incidence of autism in each birth order cohort from 1998 to 1993.
In an analogue study in the United States, Dales et al. (2001) found
the same results when using California Department of Developmental
Services autism caseload data from the period 1980 to 1994. Once
again, the time trend analysis did not show a significant
correlation between MMR vaccine usage and the number of autism
cases. Although MMR vaccine usage remained fairly constant over the
observed period, there was a steady increase of autism caseloads
over the time studied. It is important to note that the increased
incidence of autism found in these two studies most likely reflects
an increased awareness of autism-spectrum disorders by professionals
and the public in general, along with changes in diagnostic
criteria, rather than a true increase in the incidence of the
disorder (Kaye et al., 2001). Most recently, the U.S. governments
Institute of Medicine, in a comprehensive report cosponsored by the
National Institutes of Health and the Centers for Disease Control
and Prevention, recently concluded that there exists no good
evidence linking the MMR vaccine and autism (Stratton, Gable,
Shetty, & McCormick, 2001).
The MMR hypothesis reveals several important lessons for the student
of autism. First, parents and professionals alike can easily
misinterpret events that co-occur temporally as being causally
related. The fact that the MMR vaccine is routinely given at around
the same age that autism is first diagnosed reinforces the
appearance of a link between the two. Second, the MMR-autism link
reveals nicely the self-correcting nature of science. Like many
hypotheses in science, the MMR-autism hypothesis, although
reasonable when initially proposed, turned out to be incorrect or at
best incomplete. Third, the issue illustrates the persistence of
incorrect ideas concerning the etiology and treatment of autism even
in the face of convincing evidence to the contrary. For example,
Rimland (2000) purported to warn the public of the dangers of child
vaccinations because of their link to autism and begins his article
with the decree: “First, do no harm.” However, recent research
indicates that the MMR vaccine cannot be responsible for the sharp
increases in diagnosed autism, and the real harm is the public
health concern raised by encouraging parents to avoid vaccinating
their children from serious diseases that can easily be prevented.
Current Scientific Findings
Research has implicated genetic factors, in utero insults, brain
abnormalities, neurochemical imbalances, and immunological
dysfunctions as contributing to autism. Siblings of individuals with
autism have about a 3% chance of having the disorder, which is 50
times greater than the risk in the general population. In
monozygotic twins, if one twin has autism, the second has a 36%
chance of being diagnosed with the disorder and an 82% chance of
developing some autistic symptoms (Trottier, Srivastava, & Walker,
1999). Although not definitive, the higher concordance rates in
monozygotic twins relative to fraternal siblings suggests a genetic
contribution to the etiology of autism. Nevertheless, the lack of
100% concordance for monozygotic twins suggests that the disorder
probably develops as the result of combined effects of genetic and
environmental factors.
Genetic disorders that have been identified as producing an
increased risk of developing autism or pervasive developmental
disorders include tuberous sclerosis, phenylketonuria,
neurofibromatosis, fragile X syndrome, and Rett syndrome (Folstein,
1999; Trottier et al., 1999). Recent findings have also implicated a
variation of the gene labeled HOXA1 on chromosome 7 as doubling the
risk of autism, although this is only one of the many possible genes
linked to the disorder (Rodier, 2000). Nevertheless, although some
gene variants may increase the risk of developing autism, other
variants may act to decrease the risk, explaining the large
variability in the expression of autism.
Rubella infection of the mother during pregnancy and birth defects
resulting from ethanol, valproic acid, and thalidomide exposure are
also known in utero risk factors (Rodier, 2000). However, these
factors can only explain the development of autism in a small subset
of individuals. Regarding time for increased vulnerability, evidence
from individuals exposed to thalidomide now points to the conclusion
that the in utero insults that increase the risk of the autism
probably occur quite early, within the first trimester of gestation
(Stromland, Nordin, Miller, Akerstrom, & Gillberg, 1994). Other
research that has compared individuals with autism with those
without the disorder found differences in brain wave activity, brain
(e.g., cerebellar) structures, and neurotransmitter levels (Trottier
et al., 1999).
Scientific evidence supports the conclusion that autism is a
behavioral manifestation of various brain abnormalities that likely
develop as the result of a combination of genetic predispositions
and early environmental (probably in utero) insults. Although recent
scientific discoveries provide important clues to the development of
the disorder, the etiology of autism is complex and the specific
causes are still largely unknown.
Summary of Etiologic Theories and Research
There is currently no empirical support for theories that implicate
unloving mothers, yeast infections, or childhood vaccinations as the
cause of autism. The evidence invoked in support of these claims
involves uncontrolled case studies and anecdotal reports. The
confusion about the causes of autism appears to stem largely from
illusory temporal correlations between the diagnosis of the disorder
and normal events occurring in early childhood. No research has
demonstrated a differential risk for autism due to maternal
personality characteristics, the presence of candidiasis, or the use
of the MMR vaccine. Scientific evidence points to genetic
predispositions and various early environmental insults to the
developing fetus as responsible for the development of the disorder.
QUESTIONABLE TREATMENTS FOR AUTISM: BOLD CLAIMS, DUBIOUS THEORIES,
AND LITTLE DATA
A number of interventions have been promoted as providing
breakthroughs in the treatment of autism. These treatments share
many of the features of pseudoscience described earlier. Despite the
absence of supportive data and even in the face of contradictory
data, these treatments continue to be passionately promoted by their
supporters.
Sensory-Motor Therapies
Smith (1996) reported that over 1,800 variations of sensory-motor
therapy have been developed to treat individuals with autism. The
popularity of these approaches derives from the observation that
many individuals with autism exhibit sensory-processing
abnormalities, although these types of dysfunctions are neither
universal nor specific to the condition (Dawson & Watling, 2000).
Furthermore, many individuals with autism exhibit a relatively high
prevalence of fine and gross motor impairments. Nevertheless, little
controlled research has examined the effectiveness of sensory-motor
treatments for autism. We next briefly review the most commonly
promoted treatments for autism that emphasize the importance of
ameliorating the sensory-motor deficits often associated with the
disorder.
Facilitated Communication
Facilitated communication (FC) is a method designed to assist
individuals with autism and related disabilities to communicate
through the use of a typewriter, keyboard, or similar
device.<>PROMISING TREATMENTS FOR AUTISM: REVIEWING THE EVIDENCE AND
REINING IN CLAIMS
The interventions reviewed thus far give little reason for hope in
the treatment of autism. Fortunately, the situation is not so bleak.
Several promising programs have been developed. Although some
research has been conducted on these programs, none has been
sufficiently evaluated using experimental research designs. In
effect, no treatment currently meets the criteria established by the
American Psychological Associations Committee on Science and
Practice as an empirically supported treatment for autism (Gresham,
Beebe-Frankenberger, & MacMillan, 1999; Rogers, 1998). Nevertheless,
the intervention programs reviewed in the following section are
based on sound theories, are supported by at least some controlled
research, and clearly warrant further investigation.
Applied Behavior Analysis
Among the currently most popular interventions for autism are
programs based on applied behavior analysis (ABA), an approach to
behavior modification rooted in the experimental analysis of
behavior, in which operant conditioning and other learning
principles are used to change problematic behavior (Cooper, Heron &
Heward, 1989). Several intervention programs for autism based on ABA
methods have been developed. Rogers (1998) noted that many studies
of behavioral interventions for autism have focused on a single
discrete symptom, and that such interventions have often been shown
to be quite effective for such limited targets. In contrast to the
single-symptom approach, some programs have been designed to target
the core deficits of autism and thereby improve the overall
functioning of autistic individuals. By far the most popular of
these programs are modeled after the Young Autism Project (YAP)
developed at the University of California at Los Angeles by O. Ivar
Lovaas and colleagues. Initiated in 1970, the YAP aims to improve
the functioning of young children with autism through the use of an
intensive, highly structured behavioral program delivered one-on-one
by specially trained personnel. The program is designed to be
implemented full-time during most of the childs waking hours, and
family involvement is deemed to be critical. Treatment is initially
delivered in the clients home, with eventual progression to
community and school settings. The program is often referred to
as “discrete trial training,” reflecting the fact that each specific
intervention utilizes a discrete stimulus-response-consequence
sequence. For example, a child might be presented with three blocks
of different colors, and given the verbal stimulus “touch red.” If
the child touches the red block, a reward is provided (e.g., a small
snack, verbal praise). Lovaas (1981) described the program in a
treatment manual designed for parents and professionals.
The YAP was evaluated in a widely cited study by Lovaas (1987), with
long-term follow-up data reported by McEachlin, Smith, and Lovaas
(1993). Lovaas (1987) treated 19 young children with the ABA program
described above for 40 or more hours per week for at least 2 years.
Two control conditions were employed, one in which 19 children
received 10 hours or less per week of the ABA program (minimal
treatment condition), and another in which 21 children received
unspecified community interventions but no ABA. Outcome measures
were IQ and educational placement.
Lovaas (1987) reported dramatic results: After at least 2 years of
intervention, almost half (47%) of the experimental group was found
to have IQ scores in the normal range, and were reported to be
functioning in typical first grade classrooms without special
support services. Lovaas described these children as
having “recovered” from autism. Only one child from either of the
two control groups demonstrated similar gains. In addition, there
were large differences in IQ scores between the experimental group
and the two control groups. McEachlin et al. (1993) followed up
participants from the experimental and minimal ABA treatment
conditions several years later. The difference in IQ scores between
the two groups was maintained. Of the 9 children with the best
outcomes from the original report, 8 continued to function in
regular education classrooms.
Not surprisingly, a great deal of enthusiasm was generated by these
reports, and demand for ABA programs modeled after the YAP has grown
rapidly since their publication. Unlike other treatment or
educational programs, the YAP offered not only the possibility of
significant improvement in functioning, but also suggested that a
substantial number of autistic youngsters could achieve completely
normal functioning. Several commentators, however, raised serious
concerns about the conclusions reached by Lovaas (1987) and
McEachlin et al. (1993). Schopler, Short, and Mesibov (1989) noted
that the outcome measures employed, IQ and school placement, might
not reflect true overall functional changes. Increases in IQ scores,
for example, could reflect increased compliance with testing rather
than true changes in intellectual abilities, and school
mainstreaming may be more a function of parental and therapist
advocacy and changing school policies than increased educational
functioning per se. In addition, Schopler et al. argued that the
participants in the YAP study appeared to be relatively high-
functioning individuals with good prognosis, and were
unrepresentative of the larger population of autistic children. Most
importantly, they pointed out that the study design was not a true
experiment, as subjects were not randomly assigned to the
experimental and control groups. They suggested that the procedures
for assigning subjects to groups likely resulted in important
differences between the experimental and control conditions that may
have contributed to the observed outcome differences. Schopler et
al. (1989) concluded that that “it is not possible to determine the
effects of this intervention” from this study (p. 164).
Others subsequently raised similar criticisms. Gresham and MacMillan
(1997, 1998) expanded on the threats to both internal and external
validity raised by Schopler et al. (1989) and called for “healthy
skepticism” in evaluating the claims of the YAP studies. Mesibov
(1993) expressed concerns about pretreatment differences between the
experimental and control groups, and about the many domains of
functioning in which deficits commonly associated with autism (e.g.,
social interactions and conceptual abilities) that were not
assessed. Mundy (1993) raised similar concerns, noting that many
high-functioning autistic individuals achieve IQ levels in the
normal range, thereby raising questions about the use of IQ scores
to measure “recovery” from autism.
Although they uniformly take exception with the claims of “recovery”
from autism proffered by Lovaas and colleagues, even these critics
concede that the YAP study yielded promising results that merit
further investigation. Although several studies of similar ABA
interventions have now been published, two points about these
studies are noteworthy. First, each is methodologically even weaker
than the original YAP study. Second, the results of these studies,
although generally promising, fall significantly short of those
obtained by Lovaas (1987) and McEachlin et al. (1993). Birnbrauer
and Leach (1993) reported on 9 children who received 19 hours per
week of a one-on-one ABA program for 2 years, and 5 control children
who received no ABA. Four of the 9 children in the experimental
group made significant gains in IQ, relative to 1 of the 5 control
children, although none of the participants achieved completely
normal functioning. Sheinkopf and Siegel (1998) conducted a
retrospective study of 11 children who received between 12 and 43
hours per week of home-based ABA programs for between 7 and 24
months, relative to a matched control group of children who received
unspecified school-based treatment. Data were obtained through
record reviews of an existing database. Relative to the control
group, children in the experimental group achieved higher gains in
IQ, although few differences emerged between the groups in autistic
symptoms. Finally, in an uncontrolled, pre-post design study,
Anderson, Avery, DiPietro, Edwards, and Christian (1987) reported on
14 children who received between 15 and 25 hours per week of home-
based ABA for 1 year. Modest gains were reported in mental age
scores and communication skills for most children, although those
with the lowest baseline functioning made essentially no progress.
In addition, no children were able to be integrated into regular
educational settings.
All of these studies involved ABA programs modeled on Lovaass YAP,
in which services were delivered one-on-one in the childs home,
although each study differed from the original YAP study in several
respects (e.g., the number of hours per week of intervention, the
duration of the program, the nature and training of the therapists).
Two additional studies evaluated similar ABA interventions, in which
services were delivered in school- or center-based programs. Fenske,
Zalenski, Krantz, and McClannahan (1985) compared 9 children who
began receiving an ABA program through the Princeton Child
Development Institute prior to the age of 60 months, relative to 9
who enrolled after the age of 60 months. After at least 2 years of
treatment, 4 of the 9 children in the younger group were enrolled in
regular school classes, relative to 1 of the 9 children from the
older group. No data were provided on autistic symptoms or
functioning level. Harris and colleagues reported pre-post data on
children treated with an ABA program through the Douglas
Developmental Center of Rutgers University. Harris, Handleman,
Gordon, Kristoff, and Fuentes (1991) reported average IQ gains of
approximately 19 points after 10 to 11 months of intervention. It
should be noted that this sample of children was relatively high
functioning, with an average pretreatment IQ of 67.5 and with
symptoms rated as “mild to moderate.” Nevertheless, despite the
observed gains in IQ, all children were described as having
significant impairments after treatment.
Taken together, the literature on ABA programs for autism clearly
suggest that such interventions are promising. Methodological
weaknesses of the existing studies, however, severely limit the
conclusions that can be drawn about their efficacy. Of particular
note is the fact that no study to date has utilized a true
experimental design, in which subjects were randomly assigned to
treatment conditions. This fact limits the inferences that can be
drawn about the effects of the programs studied. Moreover, these
concerns are compounded by pretreatment differences between
experimental and control conditions in each of the studies reviewed.
Other methodological concerns include questions about the
representativeness of the samples of autistic children, unknown
fidelity to treatment procedures, limited outcome data for most
studies, and problems inherent in relying on IQ scores and school
placement as primary measures of autistic symptoms and functioning.
S
o what are we to make of the claims that ABA programs, and those
modeled after the YAP in particular, can result in “recovery” from
autism? After more than 30 years since its initiation and 14 years
since the first published outcome report, no study has replicated
the results of the original YAP study and several critics have
challenged its conclusions. Subsequent research has yielded more
modest gains in functioning, casting further doubt on the claims
that autistic youngsters can be “cured” through ABA programs.
Nevertheless, these caveats have not tempered the enthusiasm of some
proponents of ABA programs. Consider, for example, the following
quotes from leading advocates of ABA intervention programs for
autism:
Several studies have now shown that one treatment approachtearly,
intensive instruction using the methods of Applied Behavior
Analysistcan result in dramatic improvements for children with
autism: successful integration in regular schools for many,
completely normal functioning for some. . . . No other treatment for
autism offers comparable evidence of effectiveness. (Green, 1996b,
p. 29; emphasis in original)
There is little doubt that early intervention based on the
principles and practices of Applied Behavior Analysis can produce
large, comprehensive, lasting, and meaningful improvements in many
important domains for a large proportion of children with autism.
For some, those improvements can amount to achievement of completely
normal intellectual, social, academic, communicative, and adaptive
functioning. (Green, 1996b, p. 38)
Furthermore, we also now know that applying effective interventions
when children are very young (e.g., under the age of 3c4 years) has
the potential for achieving substantial and widespread gains and
even normal functioning in a certain number of these youngsters.
(Schreibman, 2000, p. 374)
During the past 15 years research has begun to demonstrate that
significant proportions of children with autism or PDD who
participate in early intensive intervention based on the principles
of applied behavior analysis (ABA) achieve normal or near-normal
functioning. . . . (Jacobson, Mulick, & Green, 1998, p. 204)
It is difficult to justify such assertions in light of the extant
scientific literature on ABA programs for autism. Ironically, many
of these same authors have been highly critical of the exaggerated
claims made for nonbehavioral interventions. Clearly, ABA programs
do not possess most of the features of pseudoscience that typify
many of the highly dubious treatments for autism. ABA programs are
based on well-established theories of learning and emphasize the
value of scientific methods in evaluating treatment effects.
Nevertheless, given the current state of the science, claims
of “cure” and “recovery” from autism produced by ABA are misleading
and irresponsible.
Other Comprehensive Behavioral Programs
Although ABA programstthe YAP in particulartare the best-known
behavioral interventions for autism, other programs have been
developed that draw to varying degrees on behavioral learning
principles. One of the most significant ways in which these programs
differ from the ABA programs described earlier is that they make no
claims of “curing” autism. Rather, they strive to ameliorate the
functioning of autistic individuals by utilizing a variety of
educational and therapeutic strategies. Few studies have been
conducted on these programs, and those that have utilize only pre-
post research designs, thereby limiting the conclusions that can be
drawn.
LEAP
Hoyson, Jamieson, and Strain (1984) described the effects of a
program known as Learning Experiences: An Alternative Program for
Preschoolers and Parents (LEAP). The LEAP program is composed of an
integrated preschool and a behavior-management skills training
program for parents. The preschool program, which was one of the
first to integrate normally developing children with those with
autism, blends normal preschool curricula with activities designed
specifically for children with autism. Peer modeling is encouraged
in an effort to develop play and social skills. The parental skills-
training component aims to teach parents effective behavior-
management and educational skills in natural contexts (i.e., home
and community). In a pre-post study, Hoyson et al. (1984) reported
accelerated developmental rates in 6 “autistic-like” children over
the course of their participation in the LEAP program. Strain,
Kohler, and Goldstein (1996) reported that 24 out of 51 children
were attending regular education classes, although no information
was provided regarding functioning level or special school supports.
Although certain aspects of the LEAP program appear promising, the
paucity of the available research, and especially the absence of
controlled research, preclude judgments about its usefulness.
Denver Health Sciences Program
Developed by Sally Rogers and colleagues at the University of
Colorado School of Medicine, the Denver Health Sciences Program is a
developmentally oriented preschool program designed not only for
children with autism-spectrum disorders, but varied other behavioral
problems. Several pre-post studies have reported that autistic
children participating in the program demonstrated accelerated
developmental rates in several domains, including language, play
skills, and social interactions with parents (Rogers & DiLalla,
1991; Rogers, Herbison, Lewis, Pantone, & Reis, 1986; Rogers &
Lewis, 1989; Rogers, Lewis, & Reis, 1987). Once again, the lack of
controlled research makes it impossible to draw firm conclusions
about the effectiveness of this program.
Project TEACCH
The program for the Treatment and Education of Autistic and Related
Communication Handicapped Children (TEACCH) is a university-based
project founded by Eric Schopler at the University of North Carolina
at Chapel Hill (Schopler & Reichler, 1971). TEACCH programs have
become among the more widely used intervention programs for autism.
Project TEACCH incorporates behavioral principles in treating
children with autism, but differs from ABA in several fundamental
ways. Most significantly, TEACCH focuses on maximizing the skills of
children with autism while drawing on their relative strengths,
rather than attempting “recovery” from the disorder. The program is
designed around providing structured settings in which children with
autism can develop their skills. Teachers establish individual
workstations where each child can practice various tasks, for
example, such visual-motor activities as sorting objects by color.
Visual cues are often provided in an effort to compensate for the
deficits in auditory processing often characteristic of autism. Like
the YAP, LEAP, and Denver programs, TEACCH emphasizes a
collaborative effort between treatment staff and parents. For
example, parents are encouraged to establish routines and cues in
the home similar to those provided in the classroom environment
(Gresham, Beebe-Frankenberger, & MacMillan, 1999).
Only two treatment outcome studies to date have investigated the
effectiveness of project TEACCH. Schopler, Mesibov, and Baker (1982)
collected questionnaire data from 348 families whose children were
currently or previously enrolled in the program. Individuals with
autism who participated ranged in age from 2 to 26, and ranged
cognitively from severe mental retardation to normal intellectual
functioning. The majority of respondents indicated that the program
was helpful. Also, the institutionalization rate of participants was
7%, as compared with the rates of 39% to 75% reported for
individuals with autism in the general population based on data from
the 1960s. Nevertheless, this study is marked by many serious
methodological weaknesses. These include a highly heterogeneous
sample (not all participants had autism), the absence of a
meaningful control condition, and the lack of standardized and
independent assessment measures. In addition, Schopler and
colleagues comparison of the institutionalization rate in their
study with 1960s data is probably misleading. Changes in government
policy during the 1960s and 1970s led to decreased
institutionalization rates in general (Smith, 1996).
More recently, Ozonoff and Cathcart (1998) tested the effectiveness
of TEACCH home-based instruction for children with autism. Parents
were taught interventions for preschool children with autism
focusing on the areas of cognitive, academic, and prevocational
skills related to school success. The treatment group was composed
of 11 preschool children with autism who received 4 months of home
programming. The treatment group was assessed before and after
treatment with the Psychoeducational ProfilecRevised (Schopler,
Reichler, Bashford, Lansing, & Marcus, 1990), and results were
compared with those from a matched comparison group of children not
in the TEACCH program who were similarly assessed. Results showed
that the preschool children receiving TEACCH-based parent
instruction improved significantly more in the areas of imitation,
fine-motor, gross-motor, and nonverbal conceptual skills.
Furthermore, the treatment group showed an average developmental
gain of 9.6 months after the 4-month intervention. Although this
study provides some support for the TEACCH program, the conclusions
are tempered by methodological limitations, including the lack of a
randomized control condition and the absence of treatment fidelity
ratings.
Summary of Behavioral Intervention Programs
Several programs utilizing various behavioral and developmental
intervention strategies have been shown to yield promising results
in the treatment of children with autism. Among the most promising
are programs based on the intensive, one-on-one application of
applied behavior analysis (ABA). Some proponents of ABA have made
sweeping claims about the ability of such programs to “cure” autism
that are not supported by the available literature. Other
behaviorally based programs (e.g., LEAP, Denver Health Sciences
Program, TEACCH) have been less prone to exaggerated claims.
However, the available research on these programs is more akin to
program evaluations than to traditional studies of treatment
efficacy or effectiveness. For example, no studies have employed
experimental designs, and none has used objective measures of the
full range of symptoms and functional impairments associated with
autism. Component analysis studies have not evaluated the specific
mechanisms responsible for the programs effects, and no research has
compared the relative effectiveness of various behavioral programs.
Dawson and Osterling (1997) identified six features that are common
to most comprehensive early-intervention programs for autism. They
suggested that these “tried-and-true” features, rather than the
specific methods emphasized by each program, may be responsible for
the observed effects of early-intervention programs. These common
features include (a) curriculum content emphasizing selective
attention, imitation, language, toy play, and social skills; (b)
highly supportive teaching environments with explicit attention to
generalization of gains; (c) an emphasis on predictability and
routine; (d) a functional approach to problem behaviors; (e) a focus
on transition from the preschool classroom to kindergarten, first
grade, or other appropriate placements; and (f) parental involvement
in treatment. Several of these features were incorporated into the
treatment recommendations for autism made by the American Academy of
Child and Adolescent Psychiatry (AACAP, 1999). Further research is
clearly indicated to assess the effects of each of these components,
and to evaluate potential additive effects of the specific elements
of various early intervention programs.
Pharmacotherapy
A detailed review of the psychopharmacologic treatment of autism is
beyond the scope of this paper, and several excellent recent reviews
are available (AACAP, 1999; Aman & Langworthy, 2000; Campbell,
Schopler, Cueva, & Hallin, 1996; Gillberg, 1996; King, 2000).
Although not curative, in open-label case reports several
medications appeared to improve various symptoms associated with
autism, thereby increasing individuals ability to benefit from
educational and behavioral interventions. With a few noteworthy
exceptions, few studies have utilized double-blind, placebo-
controlled designs, especially with autistic children.
The most extensively studied agents are the dopamine antagonists,
especially haloperidol (Haldol). Several well-controlled studies
have shown haloperidol to be superior to placebo for a number of
symptoms, including withdrawal, stereotypies, and hyperactivity
(Anderson et al., 1984; Campbell et al., 1996; Locascio et al.,
1991), although drug-related dyskinesias appear to be relatively
common following long-term administration (Campbell et al., 1997).
There is growing interest in the atypical neuroleptics, risperidone
(Risperdal) in particular. In a double-blind, placebo-controlled
trial with autistic adults, McDougle et al. (1998) found risperidone
to be superior to placebo on several measures, and to be well
tolerated.
Several studies suggest the usefulness of various selective
serotonin reuptake inhibitors (SSRIs), including fluvoxamine (Luvox;
McDougle et al., 1996), fluoxetine (Prozac; Cook et al., 1992;
DeLong, Teague, & Kamran, 1998; Fatemi, Realmuto, Khan, & Thuras,
1998), and clomipramine (Anafranil; Gordon et al., 1992; 1993).
However, SSRIs are often associated with intolerable adverse events.
For example, recent open-label studies reveal significant rates of
adverse side effects of clomipramine, including seizures, weight
gain, constipation, and sedation (e.g., Brodkin et al, 1997).
Moreover, there is a growing consensus that children appear to
respond less well to SSRIs than do adolescents and adults (Brasic et
al., 1994; McDougle, Kresch, & Posey, 2000; Sanchez et al., 1996).
Tricyclic antidepressants are less frequently used relative to
SSRIs, given the possibility of cardiovascular side effects and
lowering of seizure threshold.
Although little research has examined anxiolytic agents in autism,
what little research has been conducted suggests that they are of
little benefit. In fact, Marrosu et al. (1987) found increases in
hyperactivity and aggression following treatment with the
benzodiazepine diazepam (Valium). More promising results have been
obtained in open-label studies of buspirone (Buspar; McCormick,
1997; Realmuto, August, & Garfinkel, 1989; Ratey, Mikkelsen, &
Chmielinski, 1989).
THE HARM IN PROMOTING UNPROVEN TREATMENTS
As the previous review illustrates, even the most promising
treatments for autism are typically far from ideally effective,
leaving the autistic individual with substantial impairments. It is
therefore natural for parents, educators, and even mental health
professionals to ask what the harm is in trying an unproven
treatment. This is a difficult question for which there is no easy
answer. On the one hand, we are not suggesting that parents and
professionals not be allowed to explore a range of treatment
options. What we are suggesting is that they do so with as much
information as possible, and armed with an attitude of healthy
skepticism. For several reasons, such skepticism is particularly
important in considering treatments for autism.
First, proponents of many treatments, both novel and established,
often make impressive claims that are simply not supported by
controlled research. Moreover, many mental health and educational
professionals who work with autistic individuals have been reluctant
to speak out against pseudoscientific theories and practices. This
silence places the burden directly on consumers to become educated
about the empirical status of various treatment options. Unless they
make efforts to become informed about the research literature
themselves, consumers can be easily misled and given false hope.
Second, no treatment is without cost. Aside from the obvious
financial burden, there are always other costs to consider when
contemplating a new treatment. In particular, time and resources
spent on an unproven therapy are time and resources that could have
been spent on an intervention with a greater likelihood of success
(what economists term “opportunity cost”). This point is especially
critical with respect to early-intervention programs, as a growing
literature suggests the importance of early intervention with
specialized behavioral and educational programs (Fenske, Zalenski,
Krantz, & McClannahan, 1985). The issue of cost is complicated by
the tendency, in the absence of appropriate control conditions, to
misattribute any positive changes that may be observed to an
intervention and then expend even more resources on that
intervention when the improvement may not be due to the treatment.
Alternatively, repeated experience with treatments that are promoted
with much fanfare but turn out to be ineffective might cause family
members of autistic individuals to become unnecessarily cynical
about even legitimate interventions.
Finally and perhaps most importantly, one must always be aware of
the potential for harm. There are numerous examples in the history
of pharmacotherapy of substances that were initially believed to be
therapeutically useful and devoid of harmful side effects that
turned out to be quite harmful (e.g., combined fenfluramine and
dexfenfluramine, thalidomide). The effects of long-term use of
substances like secretin and DMG have not been investigated and are
therefore unknown. The risk of harm is not limited to pharmacologic
interventions, however. Consider, for example, the case of FC. The
cases of family members being convicted of abuse and sent to prison
based on alleged communications provides a sobering example of the
harm that can arise from unvalidated interventions. Despite the
wealth of scientific data demonstrating that the “facilitator” is
the source of such messages, some courts still permit communications
derived via FC to be used as evidence (Gorman, 1999).
CAVEAT EMPTOR
Autistic-spectrum disorders are associated with serious psychiatric
symptoms, often profound developmental delays, and impairments in
many areas of functioning. Although the etiology of autism remains
largely unknown and there is currently no cure for the disorder,
some promising interventions appear to be useful in helping persons
with autism lead more productive lives. The nature of autism renders
family members and other stakeholders vulnerable to highly dubious
etiological theories and intervention strategies, many of which can
be characterized as pseudoscientific. We believe that parents and
professionals alike would do well to adopt the position of caveat
emptor, or “let the buyer beware,” when considering novel treatments
for autism. If something sounds too good to be true, it often is.
REFERENCES
Adams, L., & Conn, S. (1997). Nutrition and its relationship to
autism. Focus on Autism & Other Developmental Disabilities, 12,
53c58.
Allen, J., DeMeyer, M. K., Norton, J. A., Pontus, W., & Yang, E.
(1971). Intellectuality in parents of psychotic, subnormal, and
normal children. Journal of Autism & Childhood Schizophrenia, 3,
311c326.
Aman, M. G., & Langworthy, K. S. (2000). Pharmacotherapy for
hyperactivity in children with autism and other pervasive
developmental disorders. Journal of Autism and Developmental
Disorders, 30, 451c459.
American Academy of Child and Adolescent Psychiatry (1999). Practice
parameters for the assessment and treatment of children,
adolescents, and adults with autism and other pervasive
developmental disorders. Journal of the American Academy of Child
and Adolescent Psychiatry, 38, 32c54.
American Academy of Pediatrics (1998). Auditory integration training
and facilitated communication for autism. American Academy of
Pediatrics. Committee on children with disabilities. Pediatrics,
102, 431c433.
American Psychiatric Association (1994). Diagnostic and statistical
manual of mental disorders (4th ed.). Washington, DC: Author.
Anderson, L. T., Campbell, M., Grega, D. M., Perry, R., Small, A.
M., & Green, W. H. (1984). Haloperidol in the treatment of infantile
autism: Effects on learning and behavioral symptoms. American
Journal of Psychiatry, 141, 1195c1202.
Anderson, S. R., Avery, D. L., DiPietro, E. K., Edwards, G. L., &
Christian, W. P. (1987). Intensive home-based early intervention
with autistic children. Education and Treatment of Children, 10,
352c366.
Ayres, A. J. (1979). Sensory integration and the child. Los Angeles,
CA: Western Psychological Services.
Berand, G. (1993). Hearing equals behavior. New Canaan, CT: Keats.
Beratis, S. (1994). A psychodynamic model for understanding
pervasive developmental disorders. European Journal of Psychiatry,
8, 209c214.
Bettelheim, B. (1967). The empty fortress. New York: Free Press.
Bettison, S. (1996). The long-term effects of auditory training on
children with autism. Journal of Autism & Developmental Disorders,
26, 361c374.
Birnbrauer, J., & Leach, D. (1993). The Murdoch early intervention
program after 2 years. Behavior Change, 10, 63c74.
Bolman, W. M., & Richmond, J. A. (1999). A double-blind, placebo-
controlled, crossover pilot trial of low dose dimethylglycine in
patients with autistic disorder. Journal of Autism and Developmental
Disorders, 29, 191c194.
Brasic, J. R., Barnett, J. Y., Kaplan, D., Sheitman, B. B.,
Aisemberg, P., Lafargue, R. T., Kowalik, S., Clark, A., Tsaltas, M.
O., & Young, J. G. (1994). Clomipramine ameliorates adventitious
movements and compulsions in prepubertal boys with autistic disorder
and severe mental retardation. Neurology, 44, 1309c1312.
Brodkin, E. S., McDouble, C. J., Naylor, S. T., Cohen, D. J., &
Price, L. H. (1997). Clomipramine in adults with pervasive
developmental disorders: A prospective open-label investigation.
Journal of Child and Adolescent Psychopharmacology, 7, 109c121.
Bromfield, R. (2000). Its the tortoises race: Long-term
psychodynamic psychotherapy with a high-functioning autistic
adolescent. Psychoanalytic Inquiry, 20, 732c745.
Bryson, S. (1997). Epidemiology of autism: Overview and issues
outstanding. In D. J. Cohen & F. R. Volkmar (Eds.), Handbook of
autism and pervasive developmental disorders (2nd ed., pp. 41c46).
New York: Wiley.
Bryson, S. E., Clark, B. S., & Smith, I. M. (1988). First report of
a Canadian epidemiological study of autistic syndromes. Journal of
Child Psychology and Psychiatry, 29, 433c445.
Bunge, M. (1984). What is pseudoscience? Skeptical Inquirer, 9,
36c46.
Burgess, C. A., Kirsch, I., Shane, H., Niederauer, K. L., Graham, S.
M., & Bacon, A. (1998). Facilitated communication as an ideomotor
response. Psychological Science, 9, 71c74.
Campbell, M., Armenteros, J. L., Malone, R. P., Adams, P. B.,
Eisenberg, Z. W., & Overall, J. E. (1997). Neuroleptic-related
dyskinesias in autistic children: A prospective, longitudinal study.
Journal of the American Academy of Child and Adolescent Psychiatry,
36, 835c843.
Campbell, M., Schopler, E., Cueva, J. E., & Hallin, A. (1996).
Treatment of autistic disorder. Journal of the American Academy of
Child and Adolescent Psychiatry, 35, 134c143.
Case-Smith, J., & Bryan, T. (1999). The effects of occupational
therapy with sensory integration emphasis on preschool-age children
with autism. American Journal of Occupational Therapy, 53, 489c497.
Chez, M. G., & Buchanan, C. P. (2000). Reply to B.
Rimlands “Comments on `Secretin and autism: A two-part clinical
investigation. ” Journal of Autism & Developmental Disorders, 30,
97c98.
Chez, M. G., Buchanan, C. P., Bagan, B. T., Hammer, M. S., McCarthy,
K. S., Ovrutskaya, I., Nowinski, C. V., & Cohen, Z. S. (2000).
Secretin and autism: A two-part clinical investigation. Journal of
Autism & Developmental Disorders, 30, 87c94.
Cook, E. H., Rowlett, R., Jaselskis, C., & Leventhal, B. L. (1992).
Fluoxetine treatment of children and adults with autistic disorder
and mental retardation. Journal of the American Academy of Child and
Adolescent Psychiatry, 31, 739c745.
Cooper, J. O., Heron, T., & Heward, W. (1989). Applied behavior
analysis. Columbus, OH: Merrill.
Dales, L., Hammer, S. J., & Smith, N. J. (2001). Time trends in
autism and in MMR immunization coverage in California. Journal of
the American Medical Association, 285, 1183c1185.
Darnton, N. (1990, September 10). Beno Brutalheim? Newsweek, 111
(11), 59c60.
Dawson, G., & Osterling, J. (1997). Early intervention in autism:
Effectiveness and common elements of current approaches. In M.
Guralnick (Ed.), The effectiveness of early intervention (pp.
307c326). Baltimore: Brookes.
Dawson, G., & Watling, R. (2000). Interventions to facilitate
auditory, visual, and motor integration in autism: A review of the
evidence. Journal of Autism & Developmental Disorders, 30, 415c421.
DeLong, G. R., Teague, L. A., & Kamran, M. M. (1998). Effects of
fluoxetine treatment in young children with idiopathic autism.
Developmental Medicine and Child Neurology, 40, 551c562.
Denson, J. F., Nuthall, G. A., Bushnell, J., & Horn, J. (1989).
Effectiveness of a sensory integrative therapy program for children
with perceptual-motor deficits. Journal of Learning Disabilities,
22, 221c229.
Deutsch, R. M., & Morrill, J. S. (1993). Realities of nutrition.
Palo Alto, CA: Bull Publishing.
Dunn-Geier, J., Ho H. H., Auersperg, E., Doyle, D., Eaves, L.,
Matsuba, C., Orrbine, E., Pham, B., & Whiting, S. (2000). Effect of
secretin on children with autism: A randomized controlled trial.
Developmental Medicine & Child Neurology, 42, 796c802.
Edelson, S. M. (2001). Disappointed [Letter to the editor].
Priorities for Health, 13(1), 4c6.
Edelson, S. M., Arin, D., Bauman, M., Lukas, S. E., Rudy, J. H.,
Sholar, M., Rimland, B. (1999). Auditory integration training: A
double-blind study of behavioral and electrophysiological effects in
people with autism. Focus on Autism and Other Developmental
Disabilities, 14, 73c81.
Fatemi, S. H., Realmuto, G. M., Khan, L., & Thuras, P. (1998).
Fluoxetine in treatment of adolescent patients with autism: A
longitudinal open trial. Journal of Autism & Developmental
Disorders, 28, 303c307.
Fenske, E. C., Zalenski, S., Krantz, P. J., & McClannahan, L. E.
(1985). Age at intervention and treatment outcome for autistic
children in a comprehensive intervention program. Analysis and
Intervention in Developmental Disabilities, 5, 49c58.
Findling, R. L., Maxwell, K., Scotese-Wojtila, L., & Huang, J.
(1997). High-dose pyridoxine and magnesium administration in
children with autistic disorder: An absence of salutary effects in a
double-blind, placebo-controlled study. Journal of Autism &
Developmental Disorders, 27, 467c478.
Folstein, S. E. (1999). Autism. International Review of Psychiatry,
11, 269c278.
Fombonne, E. (1998). Epidemiology of autism and related conditions.
In F. R. Volkmar (Ed.), Autism and pervasive developmental disorders
(pp. 32c63). New York: Cambridge University Press.
Gardner, M. (2000). The brutality of Dr. Bettelheim. Skeptical
Inquirer, 24(6), 12c14.
Gardner, M. (2001). Facilitated communication: A cruel farce.
Skeptical Inquirer, 25, 17c19.
Gillberg, C. (1996). The psychopharmacology of autism and related
disorders. Journal of Psychopharmacology, 10, 54c63.
Gillberg, C., Johansson, M., Steffenburg, S., & Berlin, O. (1997).
Auditory integration training in children with autism: Brief report
of an open pilot study. Autism, 1, 97c100.
Gordon, C. T., Rapoport, J. L., Hamburger, S. D., State, R. C., &
Mannheim, G. B. (1992). Differential response of seven subjects with
autistic disorder to clomipramine and desipramine. American Journal
of Psychiatry, 149, 363c366.
Gordon, C. T., State, R. C., Nelson, J. E., Hamburger, S. D., &
Rapoport, J. L. (1993). A double-blind comparison of clomipramine,
desipramine, and placebo in the treatment of autistic disorder.
Archives of General Psychiatry, 50, 441c447.
Gorman, B. J. (1999). Facilitated communication: Rejected in
science, accepted in courtta case study and analysis of the use of
FC evidence under Frye and Daubert. Behavioral Sciences and the Law,
17, 517c541.
Green, D. (2001). Autism and “voodoo science” treatments. Priorities
for Health, 13(1), 27c32, 69.
Green, G. (1994). Facilitated communication: Mental miracle or
sleight of hand? Skeptic, 2, 68c76.
Green, G. (1996a). Evaluating claims about treatments for autism. In
C. Maurice, G. Green, & S. C. Luce (Eds.), Behavioral intervention
for young children with autism: A manual for parents and
professionals (pp. 15c28). Austin, TX: PRO-ED.
Green, G. (1996b). Early behavioral intervention for autism: What
does research tell us? In C. Maurice, G. Green, & S. C. Luce (Eds.),
Behavioral intervention for young children with autism: A manual for
parents and professionals (pp. 29c44). Austin, TX: PRO-ED.
Gresham, F. M., Beebe-Frankenberger, M. E., & MacMillan, D. L.
(1999). A selective review of treatments for children with autism:
Description and methodological considerations. School Psychology
Review, 28, 559c576.
Gresham, F. M., & MacMillan, D. L. (1998). Early intervention
project: Can its claims be substantiated and its effects replicated?
Journal of Autism & Developmental Disorders, 28, 5c13.
Harris, S. L., Handleman, J. S., Gordon, R., Kristoff, B., &
Fuentes, F. (1991). Changes in cognitive and language functioning of
preschool children with autism. Journal of Autism and Developmental
Disorders, 21, 281c290.
Herbert, J. D. Lilienfeld, S. O., Lohr, J. M., Montgomery, R. W.,
ODonohue, W. T., Rosen, R. M., & Tolin, D. F. (2000). Science and
pseudoscience in the development of eye movement desensitization and
reprocessing: Implications for clinical psychology. Clinical
Psychology Review, 20, 945c971.
Herbert, J. D., & Sharp, I. R. (2001). Pseudoscientific treatments
for autism. Priorities for Health, 13(1), 23c26, 59.
Hoehn, T. P., & Baumesiter, A. A. (1994). A critique of the
application of sensory integration therapy to children with learning
disabilities. Journal of Learning Disabilities, 27, 338c351.
Horvath, K., Stefanatos, G., Sokolski, K. N., Wachtel, R., Nabors,
L., & Tildon, J. T. (1998). Improved social and language skills
after secretin administration in patients with autistic spectrum
disorders. Journal of the Association for Academic Minority
Physicians, 9, 9c15.
Hoyson, M., Jamieson, B., & Strain, P. S. (1984). Individualized
group instruction of normally developing and autistic-like children:
The LEAP curriculum model. Journal of the Division of Early
Childhood, 8, 157c172.
Iwasaki, K., & Holm, M. B. (1989). Sensory treatment for the
reduction of stereotypic behaviors in persons with severe multiple
disabilities. Occupational Therapy Journal of Research, 9, 170c183.
Jacobson, J. W., Mulick, J. A., & Green, G. (1998). Cost-benefit
estimates for early intensive behavioral intervention for young
children with autismtGeneral model and single state case. Behavioral
Interventions, 13, 201c226.
Jacobson, J. W., Mulick, J. A., & Schwartz, A. A. (1995). A history
of facilitated communication: Science, pseudoscience, and
antiscience: Science working group on facilitated communication.
American Psychologist, 50, 750c765.
Jenkins, J. R., Fewell, R. R., & Harris, S. R. (1984). Comparison of
sensory integrative therapy and motor programming. American Journal
of Mental Deficiency, 88, 221c224.
Kanner, L. (1946). Autistic disturbances of affective contact.
American Journal of Psychiatry, 103, 242c246.
Kanner, L. (1973). Childhood psychosis: Initial studies and new
insights. Washington, DC: V. H. Winston & Sons.
Kaufman, B. N. (1976). Son rise. New York: Harper & Row.
Kaye, J. A., Melero-Montes, M., & Jick, H. (2001). Mumps, measles,
and rubella vaccine and the incidence of autism recorded by general
practitioners: A time trend analysis. British Medical Journal, 322,
460c463.
King, B. H. (2000). Pharmacological treatment of mood disturbances,
aggression, and self-injury in persons with pervasive developmental
disorders. Journal of Autism & Developmental Disorders, 30, 439c445.
Kirsch, I., & Lynn, S. J. (1999). Automaticity in clinical
psychology. American Psychologist, 54, 504c515.
Kvinsberg, A. M., Reichelt, K. L., Nodland, M., Hoien, T. (1996).
Autistic syndromes and diet: A follow-up study. Scandinavian Journal
of Educational Research, 39, 223c236.
Lilienfeld, S. O. (1998). Pseudoscience in contemporary clinical
psychology: What it is and what we can do about it. The Clinical
Psychologist, 51, 3c9.
Linderman, T. M., & Stewart, K. B. (1999). Sensory integrative-based
occupational therapy and functional outcomes in young children with
pervasive developmental disorders: A single-subject study. American
Journal of Occupational Therapy, 53, 207c213.
Locascio, J. J., Malone, R. P., Small, A. M., Kafantaris, V., Ernst,
M., Lynch, N. S., Overall, J. E., & Campbell, M. (1991). Factors
related to haloperidol response and dyskinesias in autistic
children. Psychopharmacology Bulletin, 27, 119c126.
Lovaas, O. I. (1981). Teaching developmentally disabled children:
The me book. Austin, TX: PRO-ED.
Lovaas, O. I. (1987). Behavioral treatment and normal educational
and intellectual functioning in young autistic children. Journal of
Consulting and Clinical Psychology, 55, 3c9.
Mahler, M. (1968). On human symbiosis and the vicissitudes of
individuation. New York: International Universities Press.
Manning, A. (1999, August 16). Vaccine-autism link feared. USA Today.
Marrosu, F., Marrosu, G., Rachel, M. G., & Biggio, G. (1987).
Paradoxical reactions elicited by diazepam in children with classic
autism. Functional Neurology, 3, 355c361.
Mason, S. M., & Iwata, B. A. (1991). Artifactual effects of sensory-
integrative therapy on self-injurious behavior. Journal of Applied
Behavior Analysis, 23, 361c370.
McCormick, L. H. (1997). Treatment with buspirone in a patient with
autism. Archives of Family Medicine, 6, 368c370.
McDougle, C. J., Holmes, J. P., Carlson, D. C., Pelton, G., Cohen,
D. J., & Price, L. H. (1998). A double-blind, placebo-controlled
study of risperidone in adults with autistic disorder and other
pervasive developmental disorders. Archives of General Psychiatry,
55, 633c641.
McDougle, C. J., Kresch, L. E., & Posey, D. J. (2000). Repetitive
thoughts and behavior in pervasive developmental disorders:
Treatment with serotonin reuptake inhibitors. Journal of Autism &
Developmental Disorders, 30, 427c435.
McDougle, C. J., Naylor, S. T., Cohen, D. J., Volkmar, F. R.,
Heninger, G. R., & Price, L. H. (1996). A double-blind, placebo-
controlled study of fluvoxamine in adults with autistic disorder.
Archives of General Psychiatry, 53, 1001c1008.
McEachlin, J., Smith, T., & Lovaas, O. I. (1993). Long-term outcome
for children with autism who received early intensive behavioral
treatment. American Journal on Mental Retardation, 97, 359c372.
Mesibov, G. B. (1993). Treatment outcome is encouraging. American
Journal on Mental Retardation, 97, 379c380.
Mudford, O. C. (1995). Review of the gentle teaching data. American
Journal on Mental Retardation, 99, 345c355.
Mudford, O. C., Cross, B. A., Breen, S., Cullen, C., Reeves, D.,
Gould, J., Douglas, J. (2000). Auditory integration training for
children with autism: No behavioral benefits detected. American
Journal on Mental Retardation, 105, 118c129.
Mundy, P. (1993). Normal versus high-functioning status in children
with autism. American Journal on Mental Retardation, 97, 381c384.
New update. (1999, August). Psychopharmacology Update, 10, 2.
Owley, T., Steele, E., Corsello, C., Risi, S., McKaig, K., Lord, C.,
Leventhal, B. L., & Cook, E. H. (1999). A double-blind placebo-
controlled trial of secretin for the treatment of autistic disorder.
Medscape General Medicine, 1. Retrieved December 6, 2001, from
http://www.medscape.
com/medscape/GeneralMedicine/journal/1999/v01.n10/
mgm1006.owle/mgm1006.owle-01.html.
Ozonoff, S., & Cathcart, K. (1998). Effectiveness of a home program
intervention for young children with autism. Journal of Autism &
Developmental Disorders, 28, 25c32.
Pollak, R. (1997). Creation of Dr. Bettelheim: A biography of Bruno
Bettelheim. New York: Simon & Schuster.
Ratey, J. J., Mikkelsen, E., Chmielinski, H. E. (1989). Buspirone
therapy for maladaptive behaviors and anxiety in developmentally
disabled persons. Journal of Clinical Psychiatry, 50, 382c384.
Realmuto, G. M., August, G. J., & Garfinkel, B. D. (1989). Clinical
effect of buspirone in autistic children. Journal of Clinical
Psychopharmacology, 9, 122c125.
Reilly, C., Nelson, D. L., & Bundy, A. C. (1984). Sensorimotor
versus fine motor activities in eliciting vocalizations in autistic
children. Occupational Therapy Journal of Research, 3, 199c212.
Rimland, B. (1988). Candida-caused autism? Autism Research Review
International Newsletter. Retrieved December 6, 2001, from
http://www.autism.com/ari/editorials/candida. html.
Rimland, B. (1996). Dimethylglycine (DMG), a nontoxic metabolite,
and autism. Autism Research Review International. Retrieved December
6, 2001, from http://www. autism.com/ari/editorials/dmg1.html.
Rimland, B. (1999). The use of secretin in autism: Some preliminary
answers. Autism Research Review International Newsletter. Retrieved
December 6, 2001, from http://
www.autism.com/ari/editorials/findings.html.
Rimland, B. (2000, April 26). Do childrens shots invite autism? Los
Angeles Times. Retrieved from http://www. latimes.com/archives.
Rimland, B., & Edelson, S. M. (1994). The effects of auditory
integration training on autism. American Journal of Speech-Language
Pathology, 5, 16c24.
Rimland, B., & Edelson, S. M. (1995). Auditory integration training
in autism: A pilot study. Journal of Autism & Developmental
Disorders, 25, 61c70.
Rodier, P. M. (2000). The early origins of autism. Scientific
American, 282, 56c63.
Rogers, S. J. (1998). Empirically supported comprehensive treatments
for young children with autism. Journal of Clinical Child
Psychology, 27, 168c179.
Rogers, S. J., & DiLalla, D. (1991). A comparative study of a
developmentally based preschool curriculum on young children with
autism and young children with other disorders of behavior and
development. Topics in Early Childhood Special Education, 11, 29c48.
Rogers, S. J., Herbison, J., Lewis, H., Pantone, J., & Reis, K.
(1986). An approach for enhancing the symbolic, communicative, and
interpersonal functioning of young children with autism and severe
emotional handicaps. Journal of the Division of Early Childhood, 10,
135c148.
Rogers, S. J., & Lewis, H. (1989). An effective day treatment model
for young children with pervasive developmental disorders. Journal
of the American Academy of Child and Adolescent Psychiatry, 28,
207c214.
Rogers, S. J., Lewis, H. C., & Reis, K. (1987). An effective
procedure for training early special education teams to implement a
model program. Journal of the Division of Early Childhood, 11,
180c188.
Roser, K. (1996). A review of psychoanalytic theory and treatment of
childhood autism. Psychoanalytic Review, 83, 325c341.
Sanchez, L. E., Campbell, M., Small, A. M., Cueva, J. E.,
Armenteros, J. L., & Adams, P. B. (1996). A pilot study of
clomipramine in young autistic children. Journal of the American
Academy of Child and Adolescent Psychiatry, 35, 537c544.
Sandler, A. D., Sutton, K. A., DeWeese, J., Girardi, M. A.,
Sheppard, V., & Bodfish, J. W. (1999). Lack of benefit of a single
dose of synthetic human secretin in the treatment of autism and
pervasive developmental disorder. New England Journal of Medicine,
341, 1801c1806.
Schopler, E., Mesibov, G. B., & Baker, A. (1982). Evaluation of
treatment for autistic children and their parents. Journal of the
American Academy of Child Psychiatry, 21, 262c267.
Schopler, E., & Reichler, R. J. (1971). Parents as cotherapists in
the treatment of psychotic children. Journal of Autism and Childhood
Schizophrenia, 1, 87c102.
Schopler, E., Reichler, R. J., Bashford, A., Lansing, M. D., Marcus,
L. M. (1990). Individualized assessment and treatment for autistic
and developmentally disables children (Vol. 1): Psychoeducational
profile revised. Austin, TX: PRO-ED.
Schopler, E., Short, A., & Mesibov, G. (1989). Relation of
behavioral treatment to “normal functioning”: Comments on Lovaas.
Journal of Consulting and Clinical Psychology, 57, 162c164.
Sheinkopf, S., & Siegel, B. (1998). Home-based behavioral treatment
of young children with autism. Journal of Autism & Developmental
Disorders, 28, 15c23.
Siegel, B. (1996). The world of the autistic child: Understanding
and treating autistic spectrum disorders. New York: Oxford
University Press.
Schreibman, L. (2000). Intensive behavioral/psychoeducational
treatments for autism: Research needs and future directions. Journal
of Autism & Developmental Disorders, 30, 373c378.
Shermer, M. (1997). Why people believe weird things: Pseudoscience,
superstition, and other confusions of our time. New York: W. H.
Freeman.
Smith, T. (1996). Are other treatments effective? In C. Maurice, G.
Green, & S. C. Luce (Eds.), Behavioral intervention for young
children with autism: A manual for parents and professionals (pp.
45c59). Austin, TX: PRO-ED.
Steffenburg, S., & Gillberg, C. (1986). Autism and autistic-like
conditions in Swedish rural and urban areas: A population study.
British Journal of Psychiatry, 149, 81c87.
Stehli, A. (1991). The sound of a miracle: A childs triumph over
autism. New York: Doubleday.
Stratton, K., Gable, A., Shetty, P., & McCormick, M. (Eds.) (2001).
Immunization safety review: Measles-mumps-rubella vaccine and
autism. Washington, DC: National Academy Press.
Stromland, K., Nordin, V., Miller, M., Akerstrom, B., & Gillberg, C.
(1994). Autism in thalidomide embryopathy: A population study.
Developmental Medicine and Child Neurology, 36, 351c356.
Sugiyama, T., & Abe, T. (1989). The prevalence of autism in Nagoya,
Japan: A total population study. Journal of Autism & Developmental
Disorders, 19, 87c96.
Tolbert, L. C., Haigler, T., Waits, M. M., & Dennis, T. (1993).
Brief report: Lack of response in an autistic population to a low
dose clinical trial of pyridoxine plus magnesium. Journal of Autism
& Developmental Disorders, 23, 193c199.
Trottier, G., Srivastava, L., & Walker, C. D. (1999). Etiology of
infantile autism: A review of recent advancements in genetic and
neurobiological research. Journal of Psychiatry & Neuroscience, 24,
103c115.
Tustin, F. (1981). Autistic states in children. Boston: Routledge.
Volkmar, F. R., Szatmari, P., & Sparrow, S. S. (1993). Sex
differences in pervasive developmental disorders. Journal of Autism
& Developmental Disorders, 23, 579c591.
Wakefield, A. J., Murch, S. H., Anthony, A., Linnell, J., Casson, D.
M., Malik, M., Berelowitz, M., Dhillon, A. P., Thomson, M. A.,
Harvey, P., Valentine, A., Davies, S. E., & Walker-Smith, J. A.
(1998). Ileal-lymphoid-nodular hyperplasia, non-specific colitis,
and pervasive developmental disorder in children. Lancet, 351,
637c641.
Welch, M. G. (1988). Holding time: How to eliminate conflict, temper
tantrums, and sibling rivalry and raise happy, loving, successful
children. New York: Simon & Schuster.
Wheeler, D. L., Jacobson, J. W., Paglieri, R. A., & Schwartz, A. A.
(1993). An experimental assessment of facilitated communication.
Mental Retardation, 31, 49c59.
Whiteley, P., Rodgers, J., Savery, D., & Shattock, P. (1999). A
gluten-free diet as an intervention for autism and associated
spectrum disorders: Preliminary findings. Autism, 3, 45c65.
Zollweg, W., Palm, D., & Vance, V. (1997). The efficacy of auditory
integration training: A double blind study. American Journal of
Audiology, 6, 39c47.
Quackwatch Home Page
This article was posted on June 13, 2003.
http://www.quackwatch.org/01QuackeryRelatedTopics/autism.html
#wwww.medscape.com/viewarticle/463573_print - 6k
Evidence does not support thimerosal-autism link - Literature Monitor
Clinician Reviews, Oct, 2003
The health care community has been uncertain about whether thimerosal, a
mercury based preservative found in some vaccines, is a contributing factor
for the seeming increased prevalence of autistic disorder (see Hudson GT,
Dixon D. Autism: challenges in diagnosis and treatment [Board Review].
Clinician Reviews. 2003;1317]:45-52). However, the results of a Danish
population-based study published in Pediatrics did not show such a
correlation.
For their analysis, Madsen et al obtained information from a Danish national
database regarding 956 children who were diagnosed with autism from age 2 up
to (but not including) their 10th birthday between 1971 and 2000. Children
who followed a full vaccination schedule between 1961 and 1970 received a
total of 400 mg of thimerosal by age 15 months; from 1970 to 1992, children
received a total of 250 ug by age 10 months. Thimerosal-containing vaccines
were discontinued in Denmark in March 1992.
Data showed that autism incidence remained stable until 1990. In 1991, the
incidence began to rise, but the greatest increases occurred after the
discontinuation of thimerosal. The rate of incidence peaked in 1999;
children between the ages of 2 and 6 who were diagnosed with autism that
year had been born after the introduction of thimerosal-free vaccines.
The spike in the incidence of autism after 1990 may be attributable to
increased attention to the disorder, as well as to a change in the
diagnostic criteria that occurred in 1994, the authors suggest. Furthermore,
they caution that their data “cannot, of course, exclude the possibility
that thimerosal at doses larger than [those] used in Denmark may lead to
neuro developmental damage.”
Madsen KM, Lauritsen MB, Pedersen CB, et al. Thimerosal and the occurance of
autism: negative ecological evidence from Danish population-based data.
Pediatrics. 2003;12:604-606.
COPYRIGHT 2003 Clinicians Publishing Group
COPYRIGHT 2003 Gale Group
Original article :
http://www.mmrthefacts.nhs.uk/news/newsitem.php?id=77
MMR news
10-Sep-04: New research finds no link between MMR and autism
Study published in the Lancet show that children who received MMR vaccine
were no more likely to develop autism than those who did not.
The results of a major new study were published in the Lancet today. The
study examined the medical records of nearly 1300 children in the UK
diagnosed with autism or similar conditions, and compared them to a control
group of over 4,500 children.
The results showed that children who received the combined MMR vaccine were
no more likely to develop autism than those children who did not receive the
jab.
The lead research Dr Liam Smeeth said “We hope the results of this study,
the most robust and comprehensive undertaken to date, will reassure parents
that MMR is not associated with increased risk of developing autism.”
The article can be accessed via the Lancet website
http://www.thelancet.com/journal
Original article :
http://www.mmrthefacts.nhs.uk/news/newsitem.php?id=76
MMR news
15-May-04: No evidence for links between autism, MMR and measles virus
Paper concludes no increased risk of autism following exposure to wild
measles and vaccinations
W. CHEN, S. LANDAU, P. SHAM and E. FOMBONNE Psychological Medicine (April
2004), Cambridge University Press 34:543-553
Paper examines whether, in the UK, there is an increased risk of autism (AD)
following exposures, in early life, to wild measles, live attenuated
measles, alone or in combination as MMR, and the alteration of the mumps
strain within MMR.
The paper concludes no increased risk of autism (AD) following exposures to
wild measles and vaccinations with monovalent measles, and Urabe or
Jeryl-Lynn variants of MMR, were detected.
To view an abstract of this paper please go to:
http://journals.cambridge.org/bin/bladerunner?REQUNIQ=1087906601&REQSESS=341067&117000REQEVENT=&REQINT1=211198&REQAUTH=0
Original article :
http://www.mmrthefacts.nhs.uk/news/newsitem.php?id=65
MMR news
12-Dec-03: No increase in autism prevalence associated with the use of the
MMR vaccine
Study shows no proof that the overall risk of autism is higher in children
who were vaccinated with MMR
Miller E (July 2003) Measles-mumps-rubella vaccine and the development of
autism, Seminars in Pediatric Infectious Diseases 14:No.3: 199-206
The measles-mumps-rubella (MMR) vaccine has been postulated to cause a form
of autism characterized by regression and bowel symptoms, and onset
occurring shortly after vaccination. It is also claimed that, as a result,
there has been a dramatic increase in autism prevalence. These hypotheses
have now been tested in a number of epidemiologic studies that are reviewed
in this article. None has found any evidence of the existence of a
phenotypically distinct form of autism in children who received the MMR
vaccine or of a clustering of onset symptoms in children who are autistic
after receiving the MMR vaccine. There is no proof that the overall risk of
autism is higher in children who were vaccinated with MMR or of an increase
in autism prevalence associated with the use of the MMR vaccine. No
epidemiologic evidence suggests an association between MMR vaccination and
autism. Moreover, epidemiologic evidence against such an association is
compelling.
http://www2.us.elsevierhealth.com/script… (Long link)
(Registration required for full text)
Original article :
http://www.mmrthefacts.nhs.uk/news/newsitem.php?id=68
MMR news
10-Feb-04: MMR Vaccine and Autism: An Update of the Scientific Evidence
Evidence favours the rejection of a causal relationship between MMR and
autistic spectrum disorder
Frank DeStefano and William W Thompson (Feb 2004) MMR Vaccine and Autism: An
Update of the Scientific Evidence Expert Review of Vaccines 3(1):19-22(2004)
Update of scientific evidence in published studies have continued not to
find an increased risk of autistic spectrum disorder associated with MMR.
MMR vaccine also has not been found to be associated with a unique syndrome
of developmental regression and gastrointestinal disorders. There is
convincing evidence that MMR does not cause autism or any particular
subtypes of autistic spectrum disorder.
To read a summary of this report:
http://www.future-drugs.com/summery.asp?… (Long link)
For full report or pdf subscription is required.
Original article :
http://aapnews.aappublications.org/cgi/content/full/e2004128v1
NEWS AND FEATURES
IOM report: Thimerosal, MMR vaccine not linked to autism
Neither thimerosal nor the measles-mumps-rubella (MMR) vaccine is associated
with autism, according to a new report from the Institute of Medicine (IOM)
of the National Academies Immunization Safety Review Committee.
Further, the hypotheses regarding how the MMR vaccine and thimerosal could
trigger autism lack supporting evidence and are theoretical only.
The report, Vaccines and Autism, is based on a thorough review of clinical
and epidemiological studies and updates two earlier IOM reports, published
in 2001. At that time, it was determined that the evidence did not show an
association between the MMR vaccine and autism, but there was not enough
evidence to determine whether thimerosal was associated with
neurodevelopmental disorders such as autism.
The committee also reviewed evidence related to possible biological
mechanisms by which immunizations might trigger autism, but said no evidence
has yet been found that the immune system or its activation play a role in
causing autism.
It reaffirms a previous recommendation to conduct studies to identify risk
factors and biological markers of autism spectrum disorders (ASD) in order
to better understand genetic and environmental causes of ASD.
Today, with the exception of some flu vaccines, vaccines routinely given to
young children either don’t contain thimerosal or have trace amounts.
Vaccine manufacturers are working to remove thimerosal from those flu
vaccines that still contain the preservative.
The study is the eighth and final in a series on vaccine safety conducted by
the IOM, a private, nonprofit institution that provides health policy advice
under a congressional charter granted to the National Academy of Sciences.
The report is available on the National Academies Press Web site.
Daftar vaksin yang mengandung thiomersal dapat dilihat di:
http://www.vaccinesafety.edu/thi-table.htm
Menurut ahlinya DR. drg Julia Maria (Pakar Antropologi asal Indonesia yang bermukim di Beelanda)
Jadi kalau kita ikuti terus, di dunia ini timbul 3 aliran besar:
1) yang menggunakan pendekatan multidisplin dalam penegakan diagnosa dengan pendekatan psikologi & pedagogi dalam penangannya, serta menggunakan pendekatan individual. Kelompok ini adalah kelompok mainstream ilmiah.
2) yang melihat bahwa berbagai gangguan bisa ditreat dengan beberapa model terapi perilaku dan sensori (nonbiomedical treatment), pendekatan non multidisiplin dalam penegakan diagnosa.
3) yang melihat bahwa berbagai gangguan itu bisa ditreat dengan biomedical (penggunaan probiotik, hormon, food supplement, garam nineral, anti oksidan, dlsb).
2) & 3) lebih kepada alternative medicine, tapi yang ngerjakan juga dokter & psikolog (profesional).
Masing-masing kelompok melansir teori-teorinya, yang ujungnya yang
klenger masyarakat luas, karena tidak tahu lagi mana yang benar.
Jadi sampai saat ini para ahli lebih menekankan bahwa gangguan autism berada di dalam gene.
Sekalipun kromosom mana yang mempengaruhi terjadinya gangguan autism masih belum diketahui secara pasti
(karena menyangkut setidaknya ada 12 kromosom - dan penelitiannya belum selesai)
tetapi dari berbagai penelitian kembar identik menunjukkan kemungkinan terjadinya autism jauh lebih besar secara siknifikan bila dibandingkan dengan nonidentik twins.
http://www.nichd.nih.gov/publications/pubs/upload/autism_genes_2005.pdf
Wassalam
