Separating Fact from Fiction in the Etiology and Treatment of Autism

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Separating Fact from Fiction in the Etiology and Treatment of Autism

A Scientific Review of the Evidence

Authors:

D. Herbert - Department of Clinical and Health Psychology, MCP

Hahnemann University

Ian R. Sharp - Department of Clinical and Health Psychology, MCP

Hahnemann University

A. Gaudiano - Department of Clinical and Health Psychology,

MCP Hahnemann University

Author Note:

Correspondence concerning this article should be addressed to

D. Herbert, Department of Clinical and Health Psychology, MCP

Hahnemann University, Mail Stop 988, 245 N. 15th Street,

Philadelphia, PA 19102-1192; E-mail: james.herbert@....

Abstract:

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.

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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,

, & , 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. " [1] Either way, autism is no

longer considered rare, occurring more commonly than Down's 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., Down's 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, autism's 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;

, 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 Chicago's Orthogenic

School for disturbed children from 1944 to 1978. He rejected Kanner's

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 girl's 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

Bettelheim's 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 Bettelheim's

theories in some circles, no controlled research has been produced to

support the refrigerator mother theory of autism. For example, ,

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

( & 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).

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

child's 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 (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, Crohn's 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

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. government's 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, & , 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, , 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

(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. [2] The

technique involves a trained " facilitator " holding the disabled

person's hand, arm, or shoulder while the latter apparently types

messages on the keyboard device. The basic rationale behind FC is

that persons with autism suffer from a neurological impairment called

apraxia, which interferes with purposeful motoric behavior. This

neurological abnormality in motor functioning is often hypothesized

to be unrelated to intellectual functioning. Thus, many if not all

people with autism are believed to possess a " hidden literacy " that

can be expressed by overcoming these motoric deficits (Green, 1994).

FC was originally conceived in the early 1970s in Australia by

Rosemary Crossley, a teacher at St. Hospital in Melbourne.

Crossley later cofounded and directed the Dignity Through Education

and Language Center, which promoted the use of FC in Australia.

Syracuse University education professor Biklen witnessed

Crossley's use of FC in Australia and brought the technique to the

United States. In 1992, Biklen formed the Facilitated Communication

Institute at Syracuse University and began to promote its use for

persons with autism. Biklen continues to maintain the Facilitated

Communication Institute at Syracuse University and to be a vocal

proponent of FC for autism (Gardner, 2001; son, Mulick, &

Schwartz, 1995).

FC initially inspired great hope in many family members (especially

parents) of people with autism. Their heretofore largely

uncommunicative son or daughter appeared to begin communicating via

typed messages such as " I love you, " presenting them with poems, or

carrying on highly intellectual conversations. It is not surprising

that FC went largely unquestioned by understandably desperate family

members and even many professionals, despite several obvious causes

for skepticism. For example, autistic individuals often did not even

look at the keyboard while apparently typing with a single digit, yet

expert typists were unable to type coherent sentences with one finger

without looking at the keyboard (Gardner, 2001). Such observations

did not dampen the enthusiasm for FC by its proponents.

Despite this enthusiasm, the dramatic claims for FC have not survived

scientific scrutiny. A number of scientifically rigorous studies have

investigated FC, and the results of these studies clearly point to

facilitators as the source of the typed information (son,

Mullick, & Schwartz, 1995). For example, Wheeler, son, Paglieri,

and Schwartz (1993) conducted a study in which autistic participants

were asked to type the names of everyday objects that were shown to

them on picture cards. The typing was done under three conditions:

(a) the facilitators were not shown the picture; ( the facilitators

did not assist the typing, and © both the participants and the

facilitators were shown pictures that were varied so that the

participants and facilitators sometimes saw the same picture and

sometimes saw different pictures. Not surprisingly, participants were

unable to type the correct response in any of the conditions except

when they were shown the same picture as the facilitators.

Furthermore, in the condition in which the participants and the

facilitators were shown different cards, the typed responses were of

the pictures that were shown only to the facilitators. This study

provided clear evidence that the facilitators were the source of the

typed information.

Much of the controversy surrounding FC has stemmed from many

facilitators' vehement denials of responsibility for the typed

information. In one study, for example, Burgess et al. (1998)

demonstrated that FC involves a form of " automatic writing " (i.e.,

writing without awareness that one is doing so), technically called

an ideomotor response, on the part of the facilitator. Forty college

students were trained to facilitate communication with a confederate

in the role of a person with a developmental disability. Each

participant was given different information about the confederate,

who was then asked questions related to this information. Eighty-nine

percent of the responses corresponded to the information provided to

the facilitators, yet all but two reported that the information came

from the confederate. In discussing the results of the Burgess et al.

(1998) study, Kirsch and Lynn (1999) concluded that:

The attribution of the response to the confederate was clearly an

error. Just as clearly, participants were not aware of generating

responses. Instead, their responses were automatic behaviors prepared

by the intention to facilitate and their knowledge of the answers to

the questions. (p. 510)

These are merely two of dozens of studies that have demonstrated

conclusively that the source of messages in FC is the facilitator

rather than the disabled individual, despite the absence of conscious

intent or awareness on the part of facilitators. It is therefore not

surprising that so many facilitators became ardent believers in FC.

The dangers of FC extend well beyond the disappointment of family

members and the disillusionment of former facilitators who have

acknowledged the actual origins of passages produced through the

technique. Beginning the in late 1990s, facilitated messages

describing vivid instances of sexual abuse at the hands of parents

began to emerge. Such reports resulted in several cases of autistic

individuals being removed from their homes, and parents being

arrested and jailed on charges of sexual abuse. Although such charges

were eventually dismissed, some accused parents were forced to spend

their family savings on legal defense fees (Gardner, 2001; son

et al., 1995).

Auditory Integration Training

Auditory Integration Training (AIT) involves listening to filtered,

modulated music that presents sounds of varying volumes and pitches.

AIT was initially developed by French physician Guy Berard as a

treatment for auditory disorders. In the late 1970s, Berard began

promoting the use of AIT for autism. The technique gained larger

recognition with the publication of the book The Sound of a Miracle

(Stehli, 1991), written by the mother of a child who was

allegedly " cured " of autism through the use of AIT.

AIT is typically administered in two daily half-hour sessions for

approximately 10 days. Proponents theorize that a major factor in the

problem behaviors of people with autism is hypersensitive hearing.

The premise is that upon listening to the random variations in sounds

the individual's " auditory system " adjusts to the sounds and thus

becomes more normal. Proponents of AIT claim that benefits include

improvement in memory, comprehension, eye contact, articulation,

independent living skills, appropriate social behavior, willingness

to interact with others, and responsibility in school (Berard, 1993;

Stehli, 1991).

Once again, scientific research casts serious doubt on the claims

made for this innovative treatment for autism. One pilot study

(Rimland & Edelson, 1995), one uncontrolled study (Rimland & Edelson,

1994), and one small controlled study (Edelson et al., 1999)

suggested possible limited benefits of AIT. In the recent controlled

study, Edelson et al. (1999) claimed to demonstrate that AIT produced

significant improvements in aberrant behavior in a group of autistic

children and adults relative to a placebo condition in which

participants listened to unmodulated music. In addition to behavioral

improvements, the authors further purported to demonstrate that AIT

resulted in improved information processing as reflected in brain

wave changes. In describing the results of this study, Edelson (2001)

recently went so far as to claim that AIT produced " normalization of

brain wave activity " in treated subjects.

Nevertheless, this study is plagued by methodological problems, and

the actual results are in fact inconsistent with the authors'

conclusions and interpretations. For example, Edelson et al. (1999)

found a difference between the experimental and placebo groups on

only 1 of 3 primary outcome measures and only at 1 of the 4

assessment periods. Given the number of analyses conducted and the

absence of a statistical correction for multiple tests, this single

finding may well be the result of chance rather than representing a

legitimate effect of AIT. At other assessment periods the AIT-treated

participants' scores on this measure actually returned to baseline,

which the authors acknowledge reflects that one third of the subjects

in the experimental group actually became worse. The " normalization

of brain wave activity " consisted of a putative increase in P300

event-related potential (ERP) amplitude in a tonal discrimination

task. However, only 5 subjects (3 from the experimental group and 2

from the placebo group) completed this task. No information is

provided on how representative these 5 subjects were of the larger

subject pool, much less the general population of autistic

individuals. This small sample precluded statistical analyses of the

data. Furthermore, inspection of the raw ERP data reported by the

authors reveals apparently large baseline differences between the two

groups, casting further doubt on their conclusions.

Four other well-controlled studies (Bettison, 1996; Gillberg et al.,

1997; Mudford et al., 2000; Zollweg et al., 1997) failed to find any

specific benefit for AIT. In the most recent study, Mudford et al.

(2000) compared AIT with a control condition in which children

listened to ambient room music through nonfunctional headphones. No

benefit of AIT over the control condition was found on measures of

IQ, comprehension, or social adaptive behavior. Teacher-rated

measures showed no differences between the groups and parent-rated

measures of hyperactivity and direct observational measures of ear-

occlusion actually nonsignificantly favored the control group. The

authors concluded that " no individual child was identified as

benefiting clinically or educationally from the treatment " (p. 118).

The American Academy of Pediatrics' Committee on Children with

Disabilities published a statement in 1998 in the journal Pediatrics

on the use of both AIT and FC for autism. The statement suggested

that " currently available information does not support the claims of

proponents that these treatments are efficacious, " and further

that " their use does not appear warranted at this time, except within

research protocols " (American Academy of Pediatrics [AAP], 1998).

Sensory Integration Therapy

A. Ayres (1979), an occupational therapist, developed Sensory

Integration Therapy (SIT) in the 1950s. The treatment is a form of

sensory-motor therapy recommended for children with autism, learning

disabilities, mental retardation, cerebral palsy, and similar

developmental disabilities. Ayres posited that the child with autism

possesses deficits in registering and modulating sensory input, and a

deficit in the part of the brain that initiates purposeful behavior,

which she calls the " I want to do it " system. SIT, typically

delivered in individual sessions, purportedly ameliorates these

underlying deficits through sensory integration. In an attempt to

facilitate this integration, the treatment involves engaging the

child in full body movements that are designed to provide vestibular,

proprioceptive, and tactile stimulation. Sensory integration

activities include swinging in a hammock, spinning in circles on a

chair, applying brushes to various parts of the body, and engaging in

balance activities (, 1996). These activities are hypothesized

to correct the underlying neurological deficits producing the

perceptual-motor problems witnessed in many individuals with autism.

In other words, SIT is not designed to teach the child new

physical/motor activities, but to correct fundamental sensory-motor

dysfunctions underlying the disorder in order to increase the

individual's capacity for learning new activities (Hoehn &

Baumesiter, 1994).

Controlled studies have found little support for the efficacy of SIT

for treating children with various developmental disabilities. Mason

and Iwata (1990) found SIT ineffective for treating self-injurious

behaviors in three patients with mental retardation, although the

problematic behaviors were later reduced through behavioral

interventions. Furthermore, self-injurious behaviors paradoxically

increased in one 3-year-old patient when treated with SIT. Iwasaki

and Holm (1989) found no difference between the SIT and control

condition (described as informal talk and touch) in decreasing

stereotypic behaviors in young children and adults with mental

retardation. , Fewell, and (1983) found no differences

between young children with mild-to-moderate motor delays who

received either SIT or small group therapy for 17 weeks. Finally,

Densem, Nuthall, Bushnell, and Horn (1989) found no differences

between SIT and no-treatment control conditions for children with

learning disabilities. In fact, in their review of the literature

Hoehn and Baumeister (1994) concluded that controlled studies of SIT

demonstrate no unique benefits for the treatment on any outcome areas

in children with learning disabilities.

Dawson and Watling (2000) recently reviewed studies that used

objective behavioral measures in investigating the efficacy of SIT

for autism. Only one of the four studies had more than 5 participants

and no study included a comparison group. In the study with the

largest sample size, Reilly, , and Bundy (1984) used a

randomized, ABAB counterbalanced design to compare SIT with tabletop

activities (e.g., puzzles and coloring). Eighteen children with

autism received an hour of SIT and tabletop activities each. The

authors reported that verbal behavior was superior in the tabletop as

compared with the SIT condition because children spoke more during

the fine motor activities. Nevertheless, the brevity of treatment,

lack of specific training in SIT for the therapists, and failure of

the researchers to assess verbal behavior outside the experimental

condition limit the conclusions that can be drawn.

Other single-case studies comparing SIT with no-treatment baseline

among autistic children have reported beneficial results (Case-

& , 1999; Linderman & , 1999). However, these designs

cannot demonstrate that the benefits were produced specifically by

SIT. As Reilly et al. (1984) demonstrated, simple tabletop activities

actually appeared to result in benefits superior to SIT in their

study. Green (1996a) pointed out that although children may find SIT

activities enjoyable, this does not provide evidence of any

significant, long-lasting benefits in the child's behavior or in any

underlying neurological deficits. Furthermore, applying brushes of

increasing firmness to the arms of autistic children, a common SIT

activity, may help to desensitize them to certain tactile stimuli,

but such benefits are most parsimoniously explained by well-known

behavioral principles (e.g., habituation) rather than anything

specific to SIT (Seigel, 1996). In conclusion, the general null

effects for SIT relative to control conditions in treating other

developmental disabilities, combined with the results of the Reilly

et al. (1984) study with autistic children, suggest little benefit of

SIT for autism.

Psychotherapies

Various forms of psychotherapy have been applied to autism, although

there is a dearth of research on their effects. The American Academy

of Child and Adolescent Psychiatry (AACAP) recently issued a

statement of practice parameters for the assessment and treatment of

autism and related developmental disorders. The AACAP work group

concluded that " it now appears that the usefulness of psychotherapy

in autism is very limited " (AACAP, 1999). Nevertheless, various forms

of psychotherapy continue to be used with autism. We briefly discuss

three of the currently most popular psychotherapies: psychoanalytic

psychotherapy, holding therapy, and options therapy.

Psychoanalysis

As discussed earlier, psychoanalytic theories have long been applied

to the etiology of autism despite considerable evidence that many of

the basic tenets of these theories are inaccurate; nonetheless,

psychoanalytic conceptualization and treatment of autism continues

(Beratis, 1994; Bromfield, 2000). Far from being innocuous,

psychoanalytic treatments for autism can be quite harmful. The focus

on parental (and especially maternal) rejection in the etiology and

treatment of autism can lead to a misplaced blame and a deep sense of

guilt in parents. The highly unstructured nature of many

psychoanalytic treatments, including granting autistic individuals

wide latitude to pursue preferred activities in treatment and the

lack of focus on contingencies between behaviors and their

consequences, can lead to a worsening of problems (, 1996).

Holding Therapy

Holding therapy has been promoted for numerous childhood problems,

including autism (Welch, 1988). Proponents of holding therapy

theorize that autism results from a lack of appropriate attachment of

child to mother. This deficit in mother-child bonding presumably

causes the child to withdraw inward, thereby resulting in social and

communicative deficits. It therefore follows that if the mother

provides intense physical contact with the child, the previously

deficient bond can be reestablished and the " normal " child can

emerge. As is evident from this discussion, holding therapy is

largely based on psychoanalytic theories of autism, and no

researchers have examined its efficacy.

Options Therapy

Options therapy grew out of the book Son Rise (Kaufman, 1976),

written by parents of an autistic child. The parents reported that

they spent many hours every day mirroring the actions of their

autistic child without placing demands on him. They theorized that

they could enter the world of their son and in turn gradually draw

him out. Following the reported success of this treatment with their

son, the couple began charging fees to teach this method in

workshops. Questions have been raised as to whether the boy was

actually autistic (Siegal, 1996). We could locate no published

studies investigating the use of options therapy for autism.

Biological Treatments

Several factors have resulted in the increased popularity of

biologically oriented treatments for autism. These include the

increased consensus that autism is fundamentally a neurological

condition, the increased popularity of psychotropic medications in

psychiatry, and the increased popularity of homeopathic, herbal,

vitamin, and other " alternative medicine " interventions. Several such

treatments have been widely promoted as producing extraordinary

benefits for autistic individuals, despite the absence of supportive

data, or in some cases even in the face of disconfirming data.

Secretin

Secretin is a hormone involved in the control of digestion that

stimulates the secretion of pancreatic juices. It is used in a single

dose to help diagnose such gastrointestinal problems as pancreatic

disease or ulcers, and it is not approved by the Food and Drug

Administration for other uses. Nevertheless, the use of secretin in

the treatment of autism gained significant attention following a

report in 1998 of a child who appeared to show significant

improvement following a single dose (Horvath et al., 1998). Parents

of thousands of autistic children began requesting and receiving

injections of secretin for their children based solely on this single

case.

In 1999, a study published in the New England Journal of Medicine

reported the effects of a single dose of secretin on 56 children with

autistic-spectrum disorders. The researchers found that a single dose

of secretin had no effect on standard behavioral measures when

compared with placebo (Sandler et al., 1999). Several other studies

have since found similar results. For example, a study recently

completed by researchers at the University of California, San

Francisco found no effects of secretin on standard measures of

expressive or receptive language skills in 20 autistic children (see

www.ucsf.edu/pressrel/2000/05/051401.html for a description of the

study). Similarly, Chez et al. (2000) recently published a two-part

study that found no clinically significant differences between

secretin and placebo. Some parents reported improvements in their

childrens' functioning following the initial open-label trial phase

of the study after receiving an injection of secretin. However, in

the second part of the study that was a double-blind trial, children

given secretin did not show clinically meaningful improvements

compared with those given placebo injections. Chez and Buchanan

(2000) concluded that they " cannot rationalize the use of secretin at

this point as a `treatment' modality " (p. 97). Two additional studies

likewise found no differences between secretin and placebo in autism

(Dunn-Geier et al., 2000; Owley et al., 1999).

Despite these results, interest in secretin in the treatment of

autism continues. In fact, in the face of disconfirming research, an

influential psychologist and autism advocate, writing on the Internet

site of the Autism Research Institute, described secretin as " the

most promising treatment yet discovered for the treatment of autism "

(Rimland, 1999). Furthermore, likely due to the large consumer demand

for secretin for autism, the biopharmaceutical company Repligen

secured exclusive rights to a series of patent applications that

cover the use of secretin for autism (New update, 1999).

Gluten- and Casein-Free diets

Gluten is a mixture of proteins found in grain products such as wheat

bread. Casein is a protein found in milk. Anecdotal reports have

abounded that some persons with autism demonstrate increased negative

behaviors following the consumption of milk, wheat bread, or similar

products. There is some evidence that eliminating these proteins from

the diet of some autistic individuals can lead to improvements in

behavior (Kvinsberg, Reichelt, Nodland, & Hoien, 1996; Whitely,

Rodgers, Savery, & Shattock, 1999). Due to methodological weaknesses,

however, these studies cannot rule out alternative explanations for

any observed improvements following gluten- and casein-free diets.

The vast majority of the evidence for the benefits of these diets

derives from anecdotal reports or case studies (e.g., & Conn,

1997). More rigorous research is needed before the inclusion of these

diets as part of a comprehensive treatment plan can be recommended.

Vitamin B6 and Magnesium

(1996) reported that there have been at least 15 studies

demonstrating that vitamin B6 with magnesium can be somewhat helpful

for children with autism. However, the reports are mixed, with some

studies showing no positive effects of high doses of pyroxidine and

magnesium (HDPM) (Tolbert, Haigler, Waits, & Dennis, 1993) or no

difference between HDPM and placebo (Findling et al., 1997). Critics

have argued that a major methodological weakness in most of the

studies is that they rely on parent and staff reports instead of

assessments from independent observers (, 1996). Also, there are

some questions regarding the safety of megadoses of these substances.

One potential risk is that high doses of B6 can cause nerve damage

and high doses of magnesium can cause reduced heart rate and weakened

reflexes (Deutsch & Morrill, 1993). More research is needed to

evaluate the safety and effectiveness of long-term use of B6 and

magnesium before it can be considered as an efficacious treatment for

autism.

Dimethylglycine

Dimethylglycine (DMG) is an antioxidant that can be purchased over

the counter as a dietary supplement. In addition to its purported

usefulness in increasing energy and enhancing the immune system, DMG

is often marketed as a treatment for autism. Some professionals claim

that DMG increases eye contact and speech and decreases frustration

levels among individuals with autism (Rimland, 1996). In response to

the proliferation of anecdotal reports for the effectiveness of DMG,

Bolman and Richmond (1999) conducted a double-blind, placebo-

controlled, crossover pilot study of DMG in 8 males with autism.

Similar to the results of the secretin studies, this study found no

significant differences between DMG and placebo. DMG's proponents are

undeterred, however, claiming that controlled studies are not needed

to demonstrate DMG's effectiveness for autism (Rimland, 1996).

Summary of Questionable Treatments

A wide variety of treatments for autism abound, and families are

often persuaded to try methods that are highly unorthodox and

scientifically suspect. The observation that individuals with autism

sometimes exhibit sensory and motor abnormalities has resulted in the

promotion of treatments that claim either to unlock the hidden

communicator trapped by the disorder (e.g., FC) or to correct the

underlying neurological deficits that are thought responsible for the

impairments (e.g., sensory and auditory integration therapies).

Others, relying on scientifically untenable theories of the etiology

of autism such as the causal role of dysfunctional infant attachment,

seek to repair these relationships through intensive psychotherapies

(e.g., holding therapy and psychoanalysis). Among the currently most

popular treatments are biologically based interventions including

various diets, vitamins, or supplements (e.g., secretin). Even though

these intervention approaches are extremely heterogeneous in theory

and approach, they all share the characteristic of possessing little

or no scientific evidence of effectiveness. What is even more

distressing is that some of these treatments continue to be promoted

even after controlled studies have clearly demonstrated that they are

ineffective.

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 Association's Committee on Science and

Practice as an empirically supported treatment for autism (Gresham,

Beebe-enberger, & MacMillan, 1999; , 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 (, Heron & Heward,

1989). Several intervention programs for autism based on ABA methods

have been developed. (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 child's waking hours, and

family involvement is deemed to be critical. Treatment is initially

delivered in the client's 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, , 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, , Avery, DiPietro,

, 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 Lovaas's YAP,

in which services were delivered one-on-one in the child's 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. and colleagues reported pre-post data on

children treated with an ABA program through the

Developmental Center of Rutgers University. , 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.

So 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 approach—early,

intensive instruction using the methods of Applied Behavior Analysis—

can 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 3–4 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. . . . (son, 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 programs—the YAP in particular—are 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, son, 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 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 ( & DiLalla, 1991;

, Herbison, , Pantone, & Reis, 1986; & , 1989;

, , & 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 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-

enberger, & 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 (, 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 Profile–Revised (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; (

highly supportive teaching environments with explicit attention to

generalization of gains; © 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; ,

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 ( et

al., 1984; et al., 1996; Locascio et al., 1991), although

drug-related dyskinesias appear to be relatively common following

long-term administration ( 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; 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.

Notes

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.

It is important to distinguish facilitated communication from methods

of augmentative and alternative communication (AAC), in which

disabled persons independently utilize various keyboard devices to

communicate. In legitimate AAC, the individual uses the keyboard

independently, and there are therefore no questions about the origins

of the resulting communications (son et al., 1995).

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