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Posted by Dad on August 24, 2000 at 06:10:46:

FEAT DAILY NEWSLETTER Sacramento, California
"Healing Autism: No Finer a Cause on the Planet"
August 23, 2000


Dr. Lovaas Comments on the Mistaking of his Work - Part 2

Dr. Ivar Lovaas is the UCLA scientist who developed a treatment
sometimes labeled ABA-DTT, Applied Behavior Analysis utilizing a defined
Discrete Trial Training format. It is also known as the UCLA Model. Dr.
Lovaas has written this report to answer a variety of questions and
assertions about his work.

In this, the second installment, Dr. Lovaas addresses:
* Do treatment outcomes from TEACCH and the Neuropsychiatric
Institute (UCLA-NPI) or other centers equal the outcome from the Young
Autism Project in the Department of Psychology at UCLA (UCLA YAP)?
* Do alternate forms of treatment provide comparable outcomes?
* Do the best-outcome subjects show residual signs of autism?
* Have the outcome data been distorted?

The complete report, with references, will be made available on the
FEAT website at the conclusion of the series.

Ivar Lovaas, Ph.D. August 2, 2000

F. Do treatment outcomes from TEACCH and the Neuropsychiatric
Institute (UCLA-NPI) or other centers equal the outcome from the Young
Autism Project in the Department of Psychology at UCLA (UCLA YAP)?
(1) Lovaas (1987) compared children in his intensive treatment group with
two other groups: (a) a group that received minimal treatment from UCLA YAP
and (b) a group of 21 children seen at UCLA-NPI by Freeman et al. (1985)
never referred to Lovaas (1987). TEACCH also presented data on children of
the same age as those in the Lovaas and Freeman studies (Lord & Schopler,
1989). The IQ scores were as follows:

Treatment IQ at Age 2-3 IQ at Age 7
Intensive Tx (UCLA YAP) 63 83
Minimal Tx (UCLA Therapy) 57 52
UCLA NPI (Freeman et al.) 59 58
TEACCH (Lord & Schopler) 57 64

Regarding the UCLA-NPI group, Freeman et al. noted that twelve of the
fifty three children in their study showed improvements in their IQ
classification (low, medium, or high), while five showed decreases. They
further noted that "no known special medical, behavioral, or educational
interventions" accounted for the changes in status. Regarding TEACCH, Lord
and Schopler noted that most of the improvements occurred with the lowest
functioning children (those who were initially nonverbal and had an IQ
50). Lord and Schopler noted that no child with an initial IQ above 50
gained 20 IQ points or more. Overall, then, the intellectual functioning
most children at UCLA-NPI and TEACCH remained stable. This is in contrast
to the intellectual functioning of children who received intensive
behavioral treatment at UCLA YAP: Their functioning increased

G. Do alternate forms of treatment provide comparable outcomes?
A prepublication paper circulated by Drs. Dawson and Osterling and
at a tele-conference to medical personnel in the Northwest was brought to
our attention by parents who questioned the correctness of the data
in their paper. The paper was also presented at a conference in Chapel
Hill. We wrote Dr. Dawson March 19, 1996 to inform her of mistakes in her
reporting of the outcome data from the UCLA Project, Project TEACCH and
the Colorado Health Sciences. Dawson had reported that 3- and 4-year old
children in the TEACCH program gained an average of 15-24 IQ points. We
indicated to her that this statistic applied to only 44 of the 142 children
in the study (those who attained IQs under 50 and were classified as
nonverbal at intake) and was not representative of the sample as a whole.
The remaining 98 children showed IQ changes of 0 to -4, and, collectively,
the 142 children in the study averaged an IQ change of +5.
In a letter of April 19, 1996, Dr. Dawson informed us that she had
corrected these errors and promised to send us the final version of her
chapter when it became available. However, she continued to describe the
TEACCH data as indicating that children typically made large improvements.
Because this is not what their data show, we wrote to her on May 21, 1996,
to request a clarification. We did not receive a reply nor the promised
final version from her. However, we did see a preprint of the chapter. In
it, she had mostly corrected her description of the UCLA data, though she
continued to omit the McEachin, Smith, and Lovaas (1993) follow-up data and
did not report accurately on the number of intensively treated children
normal IQs, giving us credit for having one more child with average IQ at
follow-up than we actually had reported. Unfortunately, the description of
the TEACCH data, while different from the earlier draft, continued to have
major inaccuracies. To their credit, Lord and Schopler did not hide the
absence of changes in test scores in their original report (e.g., their
title refers to the stability of these scores).
Dawson and Osterling also reported on the claim by Rogers and
colleagues from the Colorado Health Sciences that children in that program
made significant increases in their rate of cognitive, language, and other
skills. Instead of reporting IQ scores, Rogers and colleagues reported
children's developmental ages at follow-up, as well as the developmental
ages they would have been expected to have without treatment. However,
data pertaining to cognitive skills are converted to ratio IQ scores, the
gains did not support significant increases but appear quite small, ranging
from 3 to 9 points for the 10 reported pre-post treatment comparisons and
apparently lower for the 2 unreported comparisons. Thus, substantial
inaccuracies pervade Dawson and Osterling's review. Also, they attributed
data to peer-reviewed publications when in fact most (LEAP, Princeton and
Walden) actually appeared in non-peer reviewed forums.
Essentials of the paper were subsequently published in the 1996 NIH
State-of-the Science in Autism conference (Alexander, D., Cowdry, R.W.,
Hall, Z.W., & Snow, J.B., 1996. The state of the science in autism: A
from the National Institutes of Health). The paper was also published in a
comprehensive volume on early intervention (Guralnick, M.J. (Ed.). The
effectiveness of early intervention. Baltimore, MD: Paul Brooks Publishing
Co., 1996 and was presented at a conference at Chapel Hill (North
The widely circulated misleading information in the Dawson and
Osterling article risks having an adverse effect on professionals and
parents seeking adequate and truthful information to help guide them in
their search for effective treatments for their children. For example, Dr.
Gerald Mesibov cited the Dawson and Osterling data in a Fair Hearing to
argue against parents' requests of using the UCLA program to help their
young autistic child (Sherman v. Pitt County).

H. Do the best-outcome subjects show residual signs of autism?
A total of ten out of the nineteen subjects in the experimental group
obvious signs of autism and mental retardation in the McEachin et al.
follow-up. Some investigators have expressed concern that the nine
best-outcome subjects in the experimental group may evidence residual signs
of autism that escaped observation in our previous follow-ups (e.g., Mundy,
1993). (See also Lovaas, 1987 "...certain residual deficits may remain in
the normal functioning group...answers...will soon be forthcoming in a more
comprehensive follow-up."). As described earlier, the McEachin et al.
(1993) follow-up study used comprehensive assessment batteries that allowed
for multiple opportunities to detect signs of autism.
In addition, these batteries were administered by examiners blind to
the purpose of the assessment. However, subtle signs of autism may still
have escaped attention (or may have become more obvious as subjects grew
older). Also, many assessment instruments designed to test for residual
signs of autism were not available when NIMH approved funding for the
McEachin et al. (1993) study (MH 11440-15 "Experimental Studies in Child
Schizophrenia"). The recently awarded grant (1 R01 MH51156-01A1 "Long-Term
Outcome of Early Intervention For Autism") is specifically designed to
detect residual signs of autism in the best-outcome group. The assessments
involved were referred to in paragraph D.

I. Have the outcome data been distorted?
(1) In addressing the Young Autism Project at an autism conference
("Autismus Heute") in Hamburg, Germany in 1988 attended by more than one
thousand parents and professionals from throughout the world, Professor
Ritvo stated that the results of the Lovaas (1987) study were "totally not
true," and added, "I regret that a lot of that stuff comes out under the
label of UCLA and it is unfortunately disseminated widely and untrue."
Professor Ritvo withdrew these remarks, however, when confronted with a
inquiry. Neither Professors Ritvo nor his colleague Dr. Freeman have
examined the best outcome children in the Lovaas (1987) study.
(2) Sometimes the accusations have been directed to others who
voiced support for the UCLA project. Dr. Gillberg, a well-known
psychiatrist from Sweden, resigned from Dr. Rimland's journal
Autism Research Review) after Dr. Rimland had written a positive review of
the UCLA program. Dr. Gillberg cited in his letter of resignation
(10/20/87) that "...I would not like to be associated with a publication
pushing negative reinforcement therapies in autism" and "...I certainly
don't agree with his (Lovaas) conclusion that autism couldn't be a brain
problem since it can be cured with behavior therapy."
The reader will recognize Dr. Gillberg's mistaken inferences about
supposed use of "cure." (See Section I for misunderstandings about "cure"
and paragraph (5) below. Negative reinforcement is involved whenever a
person (e.g. a parent) helps another person (e.g. a child) overcome stress
and fear. Behaviors (e.g. the child coming to the parent) are strengthened
because the latter removes an aversive event. All of us use negative
reinforcement in our interaction with others, including Dr. Gillberg.
exists hundreds of scientific studies on the properties of negative
reinforcement. It is regrettable that our position on an organic etiology
in autism and our reference to the plasticity of the young nervous system
and the effect of early environmental enrichment (conf. Lovaas, 1987 and
McEachin, Smith & Lovaas, 1993) was not familiar to him.
(3) In a conference sponsored by the Bancroft Foundation
New Jersey), Eric Schopler, Ph.D., who was then the director of a statewide
service agency for children with autism (Project TEACCH) and the editor of
the Journal of Autism and Developmental Disorders (JADD), remarked that he
had serious reservations about the Lovaas (1987) study because Dr. R (the
real name has been withheld), who was a former student of Dr. Lovaas, had
sought grant funding and dispensed grant moneys in a fraudulent manner.
Lovaas wrote Dr. Schopler that Dr. R had been an undergraduate student in
his classes at UCLA, one of several thousands such students over the last
years, and that Dr. R had worked much more closely with two colleagues of
Dr. Schopler. Dr. Schopler did not respond to Dr. Lovaas' corrections.
(4) An issue which surfaces periodically is the assertion that the
UCLA project claimed to "cure" autism. Gresham and MacMillan (1997)
"We argue in this article that the (UCLA project) is far from providing a
cure for autism. With the exception of (studies from UCLA) none claim to
have a cure (of) autism." They go on to cite Rutter (1996) to back up
accusation that the UCLA project has claimed a "cure." Referring to the
Lovaas (1987) and McEachin, Smith, & Lovaas (1993) studies, Rutter (1996)
argues that one of the reasons for being cautious about the acceptance of
the "strong claims" of these articles are based on "the claims of cure."
Rutter argues that the claims of cure run "counter to both clinical
experience and what might be expected on the basis of prevailing theories"
(p. 270). Answer: The UCLA project has never claimed to cure autism.
We have earlier warned that "certain residual deficits may remain in
the normal functioning group" (Lovaas, 1987, p. 8). The term "cure"
removal of the original cause of the problem and because the cause of
is unknown, claiming a cure would certainly be unjustified and unethical.
In contrast, it is possible to enable a child with autism to achieve normal
functioning without finding a cure for autism, just as it is possible for a
physician to recover patients to normal functioning without having found a
cure for their illness. Hodgkin's disease is a case in point. It can only
undermine parents' and professionals' confidence in the UCLA project to
imply that we have made unethical claims. Part of the problems of how to
describe the outcome may have come from the use of term "Recovered" in
3 of Lovaas (1987, p. 7). The term "normal functioning" was used and
in the title of Lovaas (1987) Behavioral treatment and normal educational
and intellectual functioning in young autistic children. We warned that
"...questions can be asked about whether the children truly recovered from
autism" (p. 8) adding that "...certain residual deficits may remain in the
normal functioning group that...can only be isolated on closer
assessment, particularly as these children grow older" (p. 8). Reference
was made to McEachin's Ph.D. thesis (1987) which formed the basis for
McEachin, et al. (1993) follow-up. Data from this follow-up were familiar
to Lovaas at the time of submitting the 1987 report.
(5) Gresham and MacMillan liken the UCLA project to Hooked on
Phonics, which, as they point out, made false claims of treatment gains and
was successfully sued by the Federal Trade Commission. (See Gresham &
MacMillan pre-publication copy (February 14, 1997, p. 28 & 29). They
provide no basis for this thinly-veiled accusation of fraud.

Ivar Lovaas, Ph.D.
University of California, Los Angeles
Department of Psychology
1285 Franz Hall
Box 951563
Los Angeles, California 90095-1563
FAX (310) 206-6380

Tomorrows Installment:
7 Is the treatment cost-effective?
7 Are parents satisfied with intensive behavioral treatment?
7 Does the UCLA project focus on stimulus control and functional
7 Do discrete trial procedures result in limited generalization?
7 Quality Control on Treatment.
7 Additional Misunderstandings.

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