The use of a dietary supplement combination and an essential fatty acid as an alternative and complementary treatment fo...


Material Information

The use of a dietary supplement combination and an essential fatty acid as an alternative and complementary treatment for children with Attention Deficit Hyperactivitiy Disorder (ADHD)
Physical Description:
ix, 261 leaves : ; 29 cm.
Brue, Alan W
Publication Date:


Subjects / Keywords:
Foundations of Education thesis, Ph.D   ( lcsh )
Dissertations, Academic -- Foundations of Education -- UF   ( lcsh )
bibliography   ( marcgt )
non-fiction   ( marcgt )


Thesis (Ph.D.)--University of Florida, 1999.
Includes bibliographical references (leaves 211-259).
Statement of Responsibility:
by Alan W. Brue.
General Note:
General Note:

Record Information

Source Institution:
University of Florida
Rights Management:
All applicable rights reserved by the source institution and holding location.
Resource Identifier:
aleph - 030471118
oclc - 42450629
lcc - LD1780 1999 .B889
System ID:

This item is only available as the following downloads:

Full Text








Thank you to my doctoral committee members for their

assistance during the completion of this dissertation,

especially my committee chair, Dr. Thomas Oakland, for his

help and guidance throughout my graduate studies. His

untiring work ethic is an inspiration. Drs. John Kranzler,

Mary Kay Dykes, and Barry Guinagh were helpful and

supportive. Their insightful comments were very useful in

preparing my dissertation, and I appreciate their


Thanks to Dr. Robert Evans, Bonnie Snyder, and other

members of the study team for their assistance throughout

this project. And special thanks to the children, parents,

and teachers who participated in the study, for without them

this research would not have been possible.

Most of all I would like to thank my friends and

family, and especially my wife, Dawn, for their support

throughout my graduate studies.



ACKNOWLEDGMENTS ............................... ..... .....

LIST OF TABLES..........................................

ABSTRACT ................................................


ONE INTRODUCTION ....................................

Statement of the Problem......
Purpose of the Study..........
Trial I Hypotheses............
Trial II Hypotheses...........


Historical Views............
Theoretical Views...........
Etiology ....................

Problems Associated with ADHD Symptoms..........
Pharmacological Intervention....................
Reasons For Not Using Medication as an Initial
Treatment.................................. ..
Combining Medication with Other Interventions...
Opposition to the Use of Medications............
Alternative Treatments .........................



.................... 11
.................... 13
.................... 15

.................... 17
.................... 18
.................... 32
.................... 37


Classroom- and Home-based Interventions......... 91
Purpose of the Study..... ....................... 107

THREE METHODOLOGY..................................... 109

Selection of Participants....................... 112
Procedures. ..................................... 114
Instrumentation................................. 117
Assignment of Participants...................... 123
Treatments....................................... 124
Administration .................................. 128
Trial I Hypotheses ............................ 129
Trial II Hypotheses .......................... 130
Data Analysis Procedures........................ 132

FOUR ANALYSIS OF THE DATA............................ 134

Trial I Results.................................. 134
Trial II Results................................. 141
Additional Findings .............................. 150


Discussion of the Results....................... 155
Study Limitations............................... 167
Recommendations for Future Research............. 170


A ADHD RESEARCH PROTOCOL.......................... 172



BOARD APPROVAL ................................ 190


F INFORMED CONSENT FORM........................... 204

REFERENCES ................................... ........... 211

BIOGRAPHICAL SKETCH .... ................................ 260


Table Page

1 Feingold Diet, Stage 1 .......................... 72

2 Feingold Diet, Stage 2........................... 74

3 Application of and Results from Neurofeedback
Treatment..................................... 80

4 Effective Interventions for Children with
Attention Deficits............................ 93

5 DSM-IV Criteria for a Diagnosis of ADHD,
Combined Type.................................. 110

6 Participants by Assignment, Age Group, and
Gender After Attrition........................ 112

7 Parent and Teacher Data Collections by
Participants' Age Group and Gender............ 115

8 DSM-IV: Inattentive Subscale Items from the
CRS-R :L....................................... 116

9 DSM-IV: Hyperactive-Impulsive Subscale Items
from the CRS-R:L .............................. 118

10 Psychometric Properties of the CRS-R:L.......... 122

11 Number and Mean Age of Participants in Each
Group After Attrition......................... 124

12 Trial I Parent Results From the DSM-IV:
Inattentive Subscale for Children Not Taking
Ritalin....................................... 135

13 Trial I Teacher Results From the DSM-IV:
Inattentive Subscale for Children Not Taking
Ritalin....................................... 135

14 Trial I Parent Results From the DSM-IV:
Inattentive Subscale for Children Taking
Ritalin....................................... 136

15 Trial I Teacher Results From the DSM-IV:
Inattentive Subscale for Children Taking
Ritalin....................................... 137

16 Trial I Parent Results From the DSM-IV:
Hyperactive-Impulsive Subscale for Children
Not Taking Ritalin............................. 138

17 Trial I Teacher Results From the DSM-IV:
Hyperactive-Impulsive Subscale for Children
Not Taking Ritalin ........................... 139

18 Trial I Parent Results From the DSM-IV:
Hyperactive-Impulsive Subscale for Children
Taking Ritalin................... ............. 140

19 Trial I Teacher Results From the DSM-IV:
Hyperactive-Impulsive Subscale for Children
Taking Ritalin ............................... 141

20 Trial II Parent Results From the DSM-IV:
Inattentive Subscale for Children Not Taking
Ritalin....................................... 142

21 Trial II Teacher Results From the DSM-IV:
Inattentive Subscale for Children Not Taking
Ritalin....................................... 143

22 Trial II Parent Results From the DSM-IV:
Inattentive Subscale for Children Taking
Ritalin....................................... 144

23 Trial II Teacher Results From the DSM-IV:
Inattentive Subscale for Children Taking
Ritalin....................................... 146


24 Trial II Parent Results From the DSM-IV:
Hyperactive-Impulsive Subscale for Children
Not Taking Ritalin ............................ 147

25 Trial II Teacher Results From the DSM-IV:
Hyperactive-Impulsive Subscale for Children
Not Taking Ritalin ............................ 148

26 Trial II Parent Results From the DSM-IV:
Hyperactive-Impulsive Subscale for Children
Taking Ritalin ............................... 149

27 Trial II Teacher Results From the DSM-IV:
Hyperactive-Impulsive Subscale for Children
Taking Ritalin ................................ 150

28 Ritalin vs. Non-Ritalin Group Comparisons for
the DSM-IV: Inattentive and DSM-IV:
Hyperactive-Impulsive Subscales............... 152

29 Treatment vs. Control Group Comparisons for the
DSM-IV: Inattentive and DSM-IV: Hyperactive-
Impulsive Subscales............................. 154


Abstract of Dissertation Presented to the Graduate School
of the University of Florida in Partial Fulfillment of the
Requirements for the Degree of Doctor of Philosophy



Alan W. Brue

August 1999

Chairman: Thomas D. Oakland, Ph.D.
Major Department: Foundations of Education

The study investigated the efficacy of the use of a

dietary supplement combination (i.e., Ginkgo biloba, Melissa

officinalis, Grapine, dimethylaminoethanol, and L-Glutamine)

and an essential fatty acid (i.e., flaxseed) as a treatment

for qualities relevant to attention deficit hyperactivity

disorder (ADHD) (i.e., inattentiveness and hyperactivity-

impulsivity). Its goal was to provide empirical evidence

regarding their effectiveness in reducing ADHD-related

behaviors in children diagnosed with this disorder.

Sixty participants initially were chosen to participate

in two 12-week trials. Thirty participants were chosen


randomly from those not taking Ritalin, and thirty

participants were chosen randomly from those taking Ritalin.

After attrition, fifty-one children completed both trials,

among whom 25 were in the non-Ritalin group and 26 were in

the Ritalin group.

During Trial I, the dietary supplement combination was

not more effective than a placebo at ameliorating children's

inattentiveness and hyperactivity-impulsivity. Results from

Trial II were mixed. Among children taking Ritalin, those

who received the double dietary supplement combination

displayed less inattentive behaviors than those who received

the double dietary supplement combination plus an essential

fatty acid based on teacher reports. Also, among children

not taking Ritalin, those who received the double dietary

supplement combination plus an essential fatty acid

displayed less hyperactive-impulsive behaviors than those

who received the double dietary supplement combination based

on parent reports. However, those who received the double

dietary supplement combination displayed less hyperactive-

impulsive behaviors than those who received the double

dietary supplement combination plus an essential fatty acid

based on teacher reports. Thus, these ingredients may not be

a reliable and effective alternative to or complementary

treatment of ADHD.


Most children are active, energetic, and move from one

activity to the next. They may become bored easily with

tasks offering no reward, and often require considerable

self-discipline to sit still and finish them. However, some

children live in a world of disorganized and frenzied

activities. They display levels of activity that far exceed

their age group. Their ability to sustain interest or

persistence as well as their peers is a challenge. Many

of these children have been diagnosed with an attention

deficit hyperactivity disorder (ADHD).

Statement of the Problem

Stimulant medication (e.g., Ritalin, Dexedrine, Cylert)

is the most commonly used treatment for ADHD (Epstein,

Singh, Luebke, & Stout, 1991). Ritalin is prescribed in more

than 90% of children with ADHD who receive stimulant

medication (DuPaul & Stoner, 1994; Goldman, Genel, Bezman, &

Slanetz, 1998). The number of people taking Ritalin doubled

between 1993 and 1995, and about three-fourths of the 2.6

million consumers of Ritalin are children aged 5 to 12 with

ADHD (Price, 1996). The United States Drug Enforcement

Administration (DEA) has expressed alarm at the large

increase in the number of prescriptions for stimulant

medications in recent years (Haislip, 1996).

While 70% to 80% of the children taking stimulant

medications will find them somewhat effective (Buncher,

1996), the majority will experience mild to severe adverse

drug reactions (Efron, Jarman, & Barker, 1997). Severe

adverse reactions may include liver dysfunction (Barkley,

1995; Jordan, 1998; Tan & Schneider, 1997), glaucoma

(Armstrong, 1995), symptoms of psychosis (Braswell &

Bloomquist, 1991), anorexia (Physicians' Desk Reference,

1999), heart problems leading to sudden death (Armstrong,

1995), and permanent facial tics (Breggin & Breggin, 1995;

Reichenberg-Ullman & Ullman, 1996; Tan & Schneider, 1997).

Parents increasingly are seeking effective, natural

alternative or complementary treatments for their children

with ADHD. Many do not wish to expose their children to

medications whose adverse reactions may lead to irreversible

health problems. The Physicians' Desk Reference (1999)

acknowledges there are insufficient data on the safety of

long-term stimulant use by children.

Purpose of the Study

The purpose of this study was to investigate the

efficacy of the use of a dietary supplement combination

(i.e., Ginkgo biloba, Melissa officinalis, Grapine,

dimethylaminoethanol, and L-Glutamine) and an essential

fatty acid (i.e., flaxseed) as a treatment for qualities

relevant to ADHD (i.e., inattentiveness and hyperactivity-

impulsivity). Its goal was to provide empirical evidence

with respect to their effectiveness in treating children

with this disorder.


Parents of children ages 4 through 12 were invited as

potential participants. They were self-referred or referred

by pediatricians, psychologists, psychiatrists, or

educators. Children were required to have a previous

diagnosis of ADHD, Combined Type as established by the

Diagnostic and Statistical Manual of Mental Disorders, 4th

Edition (DSM-IV) (American Psychiatric Association, 1994).

Those receiving medication for their ADHD must have been

taking Ritalin.

Parents of candidates completed a Study Participant

Information Form. This form was used to obtain information

in many areas, including developmental, medical, and

nutritional histories. Those candidates with other pre-

existing diagnoses (e.g., asthma, depression) were not

considered, as pre-existing conditions often require regular

use of medication as a treatment.

Sixty candidates initially were chosen to participate.

Thirty participants were chosen randomly from those not

taking Ritalin, and thirty participants were chosen randomly

from those taking Ritalin. The medical record of each

participant was reviewed by the study physicians. Parents of

children whose primary care physician were treating them

were asked to request a blood analysis and to provide a copy

of the child's last physical examination. Participants

taking Ritalin continued to receive it as prescribed by

their physicians.

It was explained to parents that they could withdraw

their child from the study at any time. Parents also were

told to notify the physician in charge of the study if their

child's Ritalin dosage was modified or if medication was

changed from Ritalin to any other medication to treat ADHD.

These conditions led to an administrative withdrawal of

children from the study.

Participants' parents were asked to complete a Conners'

Parent Rating Scale-Revised: Long Form (Conners, 1997a). The


teachers with whom participants spent most of their school

day were asked to complete a Conners' Teacher Rating Scale-

Revised: Long Form (Conners, 1997a).

The intervention consisted of two 12-week trials,

hereafter called Trial I and Trial II. Within each trial

were two experimental and two control groups. Prior to the

beginning of Trial I, participants not taking Ritalin were

assigned randomly to either the non-Ritalin treatment group

or the non-Ritalin control group. Participants taking

Ritalin were assigned randomly to either the Ritalin

treatment group or the Ritalin control group.

During Trial I, participants in the treatment groups

received a dietary supplement combination with the following

ingredients and dosages: Ginkgo biloba 10 mg, Melissa

officinalis 200 mg, Grapine 30 mg, dimethylaminoethanol 35

mg, and L-Glutamine 100 mg. Participants in the control

groups received an inactive slippery elm supplement (220 mg)

as a placebo.

Trial II was implemented following the completion of

Trial I, using the same subjects from the first trial.

Subjects remained in their cohort group; only the treatment

changed. During Trial II, all participants received a

dietary supplement combination whose concentration was

doubled. Additionally, the two treatment groups (formerly

control groups) received an essential fatty acid (i.e.,

flaxseed) with their combination. The double dietary

supplement combination, a uniform intervention received by

all participants, helped to detect any significant

differences in the groups of participants who received this

essential fatty acid.

Nine children were withdrawn from the study during

Trial I. The reasons for withdrawal were: parental choice (n

= 6), change in Ritalin dosage (n = 1), and participants

stopped taking Ritalin (n = 2). After attrition during the

first trial, 51 children remained with the study until it

ended (i.e., they completed both trials). Females comprised

14% (n = 7) of the remaining participants. The mean age of

all remaining participants was 8.4 years.

Trial I Hypotheses

The study proposed the following hypotheses for Trial I

in reference to the display of inattentiveness:

1. Participants receiving the dietary supplement

combination were expected to display less inattentiveness

than those receiving the placebo, based on parent and

teacher reports.

2. Participants receiving Ritalin plus the dietary

supplement combination were expected to display less

inattentiveness than those receiving Ritalin plus the

placebo, based on parent and teacher reports.

The study proposed the following hypotheses for Trial I

in reference to the display of hyperactivity-impulsivity:

3. Participants receiving the dietary supplement

combination were expected to display less hyperactivity-

impulsivity than those receiving the placebo, based on

parent and teacher reports.

4. Participants receiving Ritalin plus the dietary

supplement combination were expected to display less

hyperactivity-impulsivity than those receiving Ritalin plus

the placebo, based on parent and teacher reports.

Trial II Hypotheses

The study proposed the following hypotheses for Trial

II in reference to the display of inattentiveness:

1. Participants receiving the double dietary supplement

combination with an essential fatty acid were expected to

display less inattentiveness than those receiving the double

dietary supplement combination, based on parent and teacher


2. Participants receiving Ritalin plus the double

dietary supplement combination with an essential fatty acid

were expected to display less inattentiveness than those

receiving Ritalin plus the double dietary supplement

combination, based on parent and teacher reports.

The study proposed the following hypotheses for Trial

II in reference to the display of hyperactivity-impulsivity:

3. Participants receiving the double dietary supplement

combination with an essential fatty acid were expected to

display less hyperactivity-impulsivity than those receiving

the double dietary supplement combination, based on parent

and teacher reports.

4. Participants receiving Ritalin plus the double

dietary supplement combination with an essential fatty acid

were expected to display less hyperactivity-impulsivity than

those receiving Ritalin plus the double dietary supplement

combination, based on parent and teacher reports.


A review of relevant research and related literature on

ADHD is presented in Chapter Two. A detailed description of

the study's methodology is included in Chapter Three.

Results of this study are presented in Chapter Four. A

discussion of the results, study limitations, and


recommendations for future research are included in Chapter



Historical Views

The roots of ADHD can be traced back thousands of

years. The ancient Greeks described the disorder's common

features (i.e., inattentiveness and hyperactivity) (Husain &

Cantwell, 1991). German physician Heinrich Hoffman described

these ADHD characteristics in 1845 (Cantwell, 1975). Our

present concept of ADHD has its foundation in the work of

George Frederic Still and Alfred Tredgold (Sandberg &

Barton, 1996).

Still (1902) described an ADHD-type cluster of

behaviors that included hyperactivity, inattention, and

conduct disturbance in children. He attributed hyperactive

behavior to a defect of moral control. This theory is

supported by the proposal that suggests ADHD is a deficit in

sensitivity to reinforcement (Haenlein & Caul, 1987) or

rule-governed behavior (Barkley, 1981, 1989b). A theory of

deficient attention, inhibition, and arousal, and preference

for immediate reward also provides evidence for this claim

(Douglas, 1972, 1983). Still's research parallels many of

the facets of our current knowledge of ADHD, namely a

heredity component of the disorder, and the possibility that

ADHD occurs from acquired nervous system injury (Barkley,


Extreme defects observed in Still's sample of children

were due more to biological factors than environmental

factors. ADHD was thought to be caused by genetic

transmission, central nervous system damage, or certain

brain diseases or infection (Mellor, Storer, & Brown, 1996).

Tredgold (1908) adopted the theory that damage, often mild

and undetected, occurred in the early stages of an

individual's development. Damage resulted in behavioral

problems or hyperactivity. This belief gained support

following the 1917-18 encephalitis epidemic when children

began suffering from both behavioral and cognitive problems

(Sandberg & Barton, 1996).

Theoretical Views

Several theories to explain ADHD have been postulated.

One theory suggests a central deficiency in inhibitory

processes is present in persons with ADHD (Schachar & Logan,

1990). This theory proposes that an event or stimulus is

hypothesized to trigger an activating or primary response

and an inhibitory response. As a result, there is

competition between the two with reference to which will be

executed first. Disinhibited children (e.g., those with

ADHD) have a slower start of inhibitory processes compared

to normal children (Schachar, Tannock, & Logan, 1993).

Another theory conceptualizes persons with attention

deficits as hunters in a farmer's world (Hartmann, 1997).

That is, those with the disorder are "hunters," while those

without it are "farmers." Individuals with attention

deficits are considered leftover hunters whose ancestors

evolved and matured thousands of years ago in hunting

societies. Their characteristics (i.e., impulsivity,

distraction, and even aggression) make them ideal for

hunting. However, the criteria for this theory may have been

developed from observations of individuals with ADHD rather

than hunters, since some hunters never display the clinical

symptoms of ADHD (Shelley-Tremblay & Rosen, 1996).

A recent theory centers around the assumption that the

impairment in ADHD is a deficit in response inhibition

(Barkley, 1997b). Developmental failure in the circuitry

underlying inhibition and self-control is believed to be the

cause of ADHD (Barkley, 1998). The theory's model postulates

a link between response inhibition and four executive

neuropsychological functions: working memory, self-

regulation of affect-motivation-arousal, internalization of

speech, and reconstitution (behavior analysis and

synthesis), which depend on this inhibition for effective

performance. Evidence suggests deficits in behavioral

inhibition, working memory, and regulation of motivation are

most prominent in persons with ADHD.


ADHD is a treatable but not curable complex disorder.

Children and adolescents comprise the ages most

predominantly affected. The disorder typically occurs in

children between ages 3 and 7 (Loeber, Green, Lahey, Christ,

& Frick, 1992), and is diagnosed using criteria established

in the DSM-IV (American Psychiatric Association, 1994).

The incidence of ADHD-related behaviors, while low in

preschool and kindergarten, increases dramatically in first

grade and remains fairly stable thereafter (Pellegrini &

Horvat, 1995). Symptoms diminish by approximately 50% every

five years between the ages of 10 and 25 (Goldman et al.,

1998). Up to 50% of children with ADHD display significant

symptoms at age 25 (Mannuzza, Klein, Bonagura, Malloy,

Giampino, & Addalli, 1991; Weiss, Milroy, & Perlman, 1985),

and some believe the syndrome never disappears with maturity

(Gittelman, Mannuzza, Shenker, & Bonagura, 1985; Gross,

1997; Hechtman, 1992; Klein & Mannuzza, 1991; Weiss et al.,

1985). ADHD usually is characterized by serious and

persistent difficulties resulting in inattention,

hyperactivity, and impulsivity (American Psychiatric

Association, 1994).


Inattention comprises a main characteristic of children

with ADHD. Teachers often note these children do not listen

as well as they should, cannot concentrate, daydream, and

change activities more than others. Inattention is a multi-

dimensional construct referring to problems with alertness,

arousal, selectivity, sustained attention, and

distractibility (Hale & Lewis, 1979). Inattention is seen

most often in activities requiring children to sustain

attention to dull, boring, repetitive tasks (e.g.,

schoolwork, homework, chores) (Luk, 1985; Milich, Loney, &

Landau, 1982; Ullman, Barkley, & Brown, 1978). Inattention

also is seen in children who are more disorganized,

forgetful, and distracted than their peers.


Hyperactivity typically is the most visible and

observable characteristic of children with ADHD. Hyperactive

children often fidget, are noisy, and engage in nervous

habits (e.g., finger tapping, hair twirling). They become

easily over-excited and loud when externally over-

stimulated. They frequently change activities without fully

completing them. Many children exhibit hyperactive symptoms,

but it is the frequency, duration, and intensity with which

they occur that determine a diagnosis of ADHD.


Children with ADHD act impulsively, showing little

regard for the consequences of their actions. Students

encounter trouble because they make decisions and act too

quickly without allowing sufficient time between

presentation of the stimulus and their response (Lerner,

Lowenthal, & Lerner, 1995). Displays of impulsivity in

school--shouting out remarks without waiting for their turn,

answering questions before hearing or reading the entire

problem, or interrupting others--can lead to deficient

academic attainment and inadequate social relationships.


ADHD is the most common chronic behavioral disorder in

children (Johnson, 1997). It is not limited to one

particular group. Children who are gifted and talented also

may exhibit symptoms of ADHD. The disorder also occurs

across cultures and ethnic groups.

The prevalence of ADHD, the proportion of the

population affected, is estimated between 6 and 8% of

school-aged children (Baren, 1995). Depending on the

criteria used for diagnosis, the prevalence rate may be as

high as 10% (Tan & Schneider, 1997). Disagreement about the

prevalence of ADHD is due, in part, to lack of agreement

among professionals as to which neurological dysfunctions

characterize the syndrome (Gross, 1997).

The disorder is more common in boys. The male-female

ratio ranges from 2:1 to 10:1 (Szatmari, Offord, & Boyle,

1989). The greater frequency with which it occurs in males

may be attributed to the fact that boys are far more likely

than girls to be referred for evaluation, especially if they

display oppositional or conduct disorders (Barkley, 1996;

Swanson, Sergeant, Taylor, Sonuga-Barke, Jensen, & Cantwell,

1998). Although boys evidence more neuropsychological

disorders, gender differences and neuropsychological

performance of children with ADHD remain largely unexamined

(Arcia & Conners, 1998).

Girls with ADHD may be more likely to go undetected

(Berry, Shaywitz, & Shaywitz, 1985; Hinshaw, 1994; Szatmari

et al., 1989). Since girls are less aggressive, they are

more likely to mask symptoms of ADHD (Bain, 1991; Buncher,

1996). More females are likely to be diagnosed as

"predominantly inattentive" following the publication of the

DSM-IV (Boliek & Obrzut, 1997).


ADHD affects approximately 2 to 3 million school-aged

children in the United States (Ricchini, 1997). Every

classroom from kindergarten through 12th grade in the U.S.

on average has one of two students who has been diagnosed

with the disorder (Schneider & Tan, 1997). While some claim

ADHD is over-diagnosed, research suggests this may not be

the case (Goldman et al., 1998). Researchers found that

although some children are being diagnosed with ADHD without

a sufficient evaluation, there is little evidence of

widespread over-diagnosis of the disorder.

The number of children identified with ADHD recently

has increased dramatically. It is difficult to determine

whether the increase in the prevalence of ADHD is the result

of clearer clinical diagnosis or better recognition of the

disorder over the past four decades (Scahill & deGraft-

Johnson, 1997). Increases also may be attributed to

different methods for selecting subjects for research

studies (Barkley, 1996), the key symptoms emphasized

(Sherman, McGue, & Iacono, 1997), who reports the occurrence

of behaviors (Sherman et al., 1997), and age ranges of

samples (Barkley, 1996).


The study of the causes of hyperactivity has occurred

in distinct periods (Williams & Cram, 1978). Before World

War II, hyperactive behaviors were believed to be related to

brain damage. From World War II to 1960, attention was

placed on the symptomatology of minimal brain dysfunction.

Severely overactive and disruptive children were believed to

have a central nervous system deficit in the thalamic area

of their brain, resulting in cortical overstimulation. Since

1960, deficits in sustained attention and impulse control

have been considered more likely to account for


The etiology of ADHD remains unclear. Precipitating

factors often are unknown and the cause typically is

considered idiopathic (Boris & Mandel, 1994). Symptoms of

ADHD may result from a variety of causal mechanisms, such as

pre- and postnatal factors, neurological variables,

neurochemicals, genetics, diet, candidiasis, temperament,

and lead exposure.

Pre- and Post-natal Factors

Prenatal factors can put a fetus at risk. Absence of

prenatal care, inadequate maternal nutrition, infections,

stress, and metabolic or toxic factors may impact a

developing fetus. Anepartum hemorrhage and length of labor

have been associated with ADHD (Chandola, Robling, Peters,

Melville-Thomas, & McGuffin, 1992). Prenatal exposure to

alcohol and tobacco smoke is related to inattention and

hyperactivity (Bennett, Wolin, & Reiss, 1988; Milberger,

Biederman, Faraone, & Jones, 1998; Nichols & Chen, 1981;

Shaywitz, Cohen, & Shaywitz, 1980; Streissguth, Martin,

Barr, Sandman, Kirchner, & Darby, 1984), and children born

with fetal alcohol syndrome were found to exhibit symptoms

of hyperactivity, impulsivity, and inattention (Frederick,


Acquired medical problems and extensive post-natal

trauma to the nervous system can result in ADHD or ADHD-like

behaviors (Silver, 1992). An association between otitis

media in infancy and later development of ADHD has been

discovered (Adesman, Altshuler, Lipkin, & Walco, 1990;

Weintraub, 1997). Effects of viral encephalitis can include

hyperactivity, distractibility, and impulsivity (Tredgold,

1908). Children and adolescents with a history of a closed

head injury also may display these behaviors.

Neurological Variables

A neurological basis of ADHD has been suggested

(Rosenberger, 1991). The early onset and persistent nature

of ADHD support this neurological origin. The belief that

dysfunction in the brain or central nervous system causes

ADHD has been held for almost a century (Lerner et al.,

1995). Frontal lobe underactivity is associated with ADHD

(Chelune, Ferguson, & Richard, 1986; Lou, Henriksen, &

Bruhn, 1984). Findings of deficient performance on

neuropsychological tests associated with prefrontal lobe

functions (e.g., inhibition, persistence, working memory)

further support a neurological basis (Barkley, 1990;

Barkley, Grodzinsky, & DuPaul, 1992; Goodyear & Hynd, 1992).

Brain damage

The purpose of the brain is to control movement, sleep,

hunger, thirst, and nearly every other vital activity

necessary for survival. It also receives and interprets

countless signals sent to it from other parts of the body

and from the external environment. Thus, proper functioning

of the brain is critical.

The first neurological theory hypothesized children

with ADHD had structural brain damage that contributed to

their attention and behavior difficulties (Anastopoulos &

Barkley, 1988). Current evidence suggests most children with

ADHD do not have structural defects in the central nervous

system. Thus, structural brain damage is no longer

considered a primary cause of ADHD (Barkley, 1990).

Reticular activating system

The lower portion of the brain contains the Reticular

Activating System (RAS), the attention center in the brain.

The purpose of the RAS is to regulate the level of alertness

and arousal and filter out irrelevant distractors in the

environment. When functioning properly, the RAS provides the

neural connections needed to attend to a task. If the RAS

does not excite the neurons of the cortex as much as it

should, underarousal results in a lack of self-control, poor

memory, and learning difficulties. An excited RAS leads to

an overarousal of the cortex and other brain systems. This

can cause an individual to talk too much, become restless,

and act hyperactive. A dysfunction in the RAS has been

proposed as a neurological basis for ADHD (Nussbaum &

Bigler, 1990).


The purpose of neurotransmitters is to facilitate

communication among cells. An imbalance or deficiency in

certain neurotransmitters has been studied as an etiological

variable (Raskin, Shaywitz, Shaywitz, Anderson, & Cohen,

1981). Children with ADHD are believed to possess an

insufficient amount of necessary chemicals in their brains

(Friedman & Doyal, 1992; Goldstein & Goldstein, 1990).

Studies of monoamines have received the most attention as a

possible cause of ADHD (Kado & Takagi, 1996; Silver, 1992).

Monoamines are comprised of the catecholamines (e.g.,

dopamine and norepinephrine) and the indoleamines (e.g.,

serotonin). Metabolic studies have shown that glucose

(Zametkin, Nordahl, Gross, King, Semple, Rumsey, Hamburger,

& Cohen, 1990), norepinephrine (Shekim, Javaid, Davis, &

Bylund, 1983; Shekim, Javaid, Dekirmenjian, Chapel, & Davis,

1982), dopamine (Shaywitz, Yager, & Klopper, 1976),

adrenaline (Weintraub, 1997), and thyroid dysfunction

(Hauser, Zametkin, Martinez, Vitiello, Matochik, Mixson, &

Weintraub, 1993) are related to ADHD.

Dopamine and norepinephrine are the two most important

chemicals in the attentional system (Goldstein & Goldstein,

1990). These neurotransmitters affect the regulation of

attention, inhibition, and motor responses. They are

presumed to be deficient in certain regions of the brain,

thus contributing to symptoms of ADHD (DuPaul & Stoner,


Research on cerebral glucose metabolism has provided

strong evidence of a biological basis for ADHD (Zametkin et

al., 1990). Glucose promotes human cell development. Rates

of metabolism are significantly slower in those with ADHD.

Researchers also discovered a relationship between the areas

of the brain affected and the nature of the symptoms of

hyperactivity in adults.

Genetic Influence

Some have postulated a genetic contribution to ADHD

(Cantwell, 1972; Hechtman, 1993; Fouse & Brians, 1993;

Rutter, Macdonald, LeCoutier, Harrington, Bolton, & Bailey,

1990; Sherman, lacono, & McGue, 1997; Stevenson, 1992). The

discovery of an association with a single dopamine

transporter gene (Cook, Stein, Krasowski, Cox, Olkon,

Kieffer, & Leventhal, 1995) and a variation in the D4

dopamine receptor gene (LaHoste, Swanson, Wigal, Glabe,

Wigal, King, & Kennedy, 1996; Swanson, Sunohara, Kennedy,

Regino, Fineberg, Wigal, Lerner, Williams, LaHoste, & Wigal,

1998) has increased the interest in a genetic basis. Genetic

studies may provide evidence for an underlying genetic

relationships between clinical phenotypes, thus leading to

biologically based understanding of the diagnosis and

treatment of ADHD (Levy, Barr, & Sunohara, 1998).

Family studies

Results of behavioral genetic studies have provided

additional evidence supporting a hereditary contribution

(DuPaul & Stoner, 1994; Faraone, Biederman, Keenan, &

Tsuang, 1991; Gross-Tsur, Shalev, & Amir, 1991). Immediate

family members of children with ADHD have a higher rate of

concurrent and past ADHD symptoms than their non-ADHD

counterparts (Anastopoulos & Barkley, 1988). Up to 20% of

mothers (Silver, 1992), up to 30% of fathers (Silver, 1992),

and up to 35% of biological siblings (Biederman, Faraone, et

al., 1991; Biederman, Faraone, & Lapey, 1992; Pauls, 1991;

Silver, 1992; Welner, Welner, Stewart, Palkes, & Wish, 1977)

of children with ADHD have the disorder. Second-degree

relatives also display a higher incidence of ADHD (Faraone,

Biederman, & Milberger, 1994). However, it often is

difficult to accurately identify the contributing effects of

genetics and environment, inasmuch as the two co-occur.

Twin studies

Monozygotic twins display higher rates of ADHD when

compared to dizygotic twins (Cunningham & Barkley, 1978;

Heffron, Martin, & Welsh, 1984; Lopez, 1965; Sherman, McGue,

et al., 1997). There is a high concordance for hyperactivity

and inattention in monozygotic pairs (51 to 100%) and

dizygotic pairs (17 to 33%) (Gillis, Gilger, Pennington, &

DeFries, 1992; Goodman & Stevenson, 1989; O'Connor, Foch,

Sherry, & Plomin, 1980; Willerman, 1973).

Adoption studies

The adoption study method is regarded as one of the

most powerful tools for studying complex human behavioral

disorders (DeFries & Plomin, 1978). Studies of adopted

children with hyperactivity report higher rates of

hyperactivity in the biological parents than in the adoptive

parents (Alberts-Corush, Firestone, & Goodman, 1986;

Cantwell, 1975; Morrison & Stewart, 1971, 1973). A strong

genetic component also has been shown for attention problems

among biologically-related adoptees (van den Oord, Boomsma,

& Verhulst, 1994).

Diet Factors

The role of diet in behavior has been investigated for

many years. Early research suggested that behavior and

learning can be affected by diet (Shannon, 1922). In a

majority of studies, a significant change in behavior was

noted with dietary intervention (Breakey, 1997). Certain

foods have been shown to alter brain electrical activity

(Uhlig, Merkenschlager, Brandmaier, & Egger, 1997), and

children on an elimination diet exhibited normalization in

previous EEG abnormalities (Kittler & Baldwin, 1970). In

addition, food allergies and sensitivities and food

additives have been cited as affecting behavior.

Food allergies

Reports since the 1920s have linked hyperactive

behavior with food allergies (Crook, 1997; Ross & Ross,

1976). Food allergies may be related to the onset or

exacerbation of ADHD. It has been suggested that two-thirds

of children with ADHD would not need pharmaceutical

intervention if their food allergies were detected and

treated (Rapp, 1998). Symptoms of irritability, fatigue, and

behavior problems have been attributed to an allergic

response to foods (Randolph, 1947).

Food allergies may have a cumulative effect, causing a

child with a weak sensitivity to certain foods to become

hyperactive if a large amount of these foods are consumed

within a short period of time (Conners, 1980b). The

relationship between food allergies and hyperactivity is

strongest in hyperactive children who also exhibit evidence

of learning disabilities and minimal brain dysfunction

concurrently (Trites, Tryphonas, & Ferguson, 1980). However,

empirical data do not support the claim that food allergies

play a role in ADHD (Palmer, Rapoport, & Quinn, 1975; Trites

et al., 1980; Tryphonas & Trites, 1979; Varley, 1984).

Food sensitivities

Response to food dyes and additives is considered a

sensitivity, not an allergy, since the primary symptoms are

behavioral disturbances (e.g., short attention span,

nervousness) rather than physical disturbances (e.g., hives,

respiratory problems (Swanson & Kinsbourne, 1980a).

Sensitivities to food dyes have been reported since 1940

(Weintraub, 1997). Clinical cases of hypersensitivity are

noted with dyes commonly ingested from foods and medicines

(Lockey, 1971, 1977). This sensitivity may lead to an

intolerance of different foods, resulting in hyperactivity,

aggression, mood swings, and rebellion (Jordan, 1998).

Food dyes, additives, and natural salicylates are

implicated as a cause of ADHD (Feingold, 1973a, 1975a,

1975b). A relationship was first noted when a patient's

hostile and aggressive behavior ceased following a diet that

excluded artificial colors and flavors (Harley & Matthews,

1980). Sensitivity to artificial colors is caused by a

pharmacological response, similar to a sensitivity to

aspirin (Feingold, 1975a, 1975b).

Thirty-four synthetic food colors, 1,610 synthetic

flavors, and 1,120 other chemicals (e.g., preservatives)

added to foods are believed to cause hyperactivity once

ingested (Feingold, 1973b). Natural salicylates also have

been targeted in the belief that they cross-react with

additives (Swanson & Kinsbourne, 1980a). The increased

incidence of hyperactivity is related to an increase in

consumption of food colorings, flavorings, and preservatives

(Feingold, 1975a, 1975b). Removal of the substances

reportedly terminates the hyperactive symptoms.

Evidence suggests that children affected by food dyes

and additives differ biochemically from those who remain

unaffected (Brenner, 1979). Some researchers believe

children are born with a genetic predisposition for

hyperactivity that is triggered by these substances. For

example, Erythrosin B (i.e., Red No. 3) often is used in

candies, powdered desserts, and beverages. Concentrations of

this dye partially prevents brain cells from taking in

dopamine (Augustine & Levitan, 1980; Lafferman & Silbergeld,

1979). The blocking of dopamine by the food dye is

consistent with the theory that the dye can cause

hyperactivity in some children.


Symptoms of ADHD have been attributed to Candida

albicans, a common yeast in the human body (Bell & Peiper,

1997; Crook, 1983, 1997). Candidiasis, an overgrowth of this

yeast, causes a release of toxins in the intestines that

results in hyperactivity, irritability, anxiety, and other

symptoms (Rapp, 1991). Yeast interferes with the formation

of fatty acid conversions and can overwhelm and damage the

immune system, especially when using antibiotics.

Antibiotics increase the growth of yeast, which in turn

increase the absorption of food antigens, putting a child at

risk for food sensitivities. This may play an important role

in causing ADHD and other behavior and learning problems

(Weintraub, 1997).


Children's temperament may contribute to their ADHD

symptoms (Friedman & Doyal, 1992). Studies of temperament in

hyperactive children indicate its importance in the

development of hyperactivity (Prior & Griffin, 1985).

Temperament patterns differ for hyperactive and control


subjects (Dudding & Dudding, 1995; Lambert, 1982). Children

with hyperactivity are characterized by low adaptability,

low persistence, high activity, and high negativism (Carey &

McDevitt, 1980). An effort must be made to determine whether

hyperactivity is a reflection of ADHD, an expression of

temperament characteristics, or a combination of the two

(Friedman & Doyal, 1992).

Temperament was only one of three factors to contribute

to hyperactivity (i.e., pre- and peri-natal factors, family,

and home environmental characteristics). Its contribution

has been found to be more significant than the others

(Lambert, 1982; Lambert & Hartsough, 1984). Differences in

temperament between hyperactive and non-hyperactive children

of the same age, gender, and social class are noted for

children as young as preschoolers (Prior, Leonard, & Wood,


The diagnosis of ADHD among school children may be

attributed to personality type (Provost, 1994), and its

diagnosis may be related to an insufficient appreciation of

normal temperament variations (Carey, 1998). Type

preferences of teachers and parents predisposes them to

conflict with children who manifest ADHD symptoms (Johnson,

1995). For example, introverted parents or teachers may view

children with an extroverted personality as more likely to

possess the disorder.

Lead Exposure

Exposure to lead is one the nation's most serious

environmental threat to children's health. Factory exhaust,

urban topsoil, water pipes, metal food containers, fruits

and vegetables, and paint may contain high levels of lead.

Many of the children affected are from economically-

impoverished families. In the United States, half a million

children on Medicaid ages five years and under have harmful

levels of lead in their blood ("Lead Screening," 1998).

The neurotoxic effects of lead affects brain function

and is associated with a number of neurological and

psychological disorders, including ADHD (Baloh, Sturm,

Green, & Gleser, 1975; David, 1974; de la Burde & Choate,

1972, 1974; Walker, 1996; Weintraub, 1997). Exposure to lead

is linked to disruptive behavior, distractibility,

impulsivity, poor school performance, and low IQ (Fergusson

& Horwood, 1993; Fergusson, Horwood, & Lynskey, 1993;

Needleman, Schell, Bellinger, Leviton, & Allrich, 1990;

Thomson, Raab, Hepburn, Hunter, Fulton, & Laxen, 1989; Yule,

Lansdown, Millar, & Urbanowicz, 1981). Lead poisoning also

has been shown to be associated with ADHD (David, Clark, &

Voeller, 1972; Rummo, Routh, Rummo, & Brown, 1979).

Treatment to reduce the levels of body lead has accounted

for behavioral improvements in hyperactive children (David,

Hoffman, Sverd, Clark, & Voeller, 1976; Eppright, Sanfacon,

& Horwitz, 1996).


A diagnosis of ADHD requires a comprehensive and

detailed evaluation. Diagnosing hyperactivity and

impulsivity remains subjective, despite sophisticated

assessment techniques (Johnson, 1997). A diagnosis comes

from a number of sources, based on an evaluation of the

intensity and duration of symptoms (Buncher, 1996). An

appropriate assessment includes a medical, behavioral, and

educational history, evidence of normal vision and hearing,

recognition of systemic illness, and a developmental survey

(National Attention Deficit Disorder Association, 1998).

ADHD is diagnosed exclusively on the basis of observable

behavior patterns, since it is difficult to determine

specific biochemical or neuropsychological tests that

contribute to a more accurate diagnosis (Kuperman, Johnson,

Arndt, Lindgren, & Wolraich, 1996). The delineation from

normals is partially determined by local cultural factors

since no biological markers for general use exist (Lou,


Specifying symptoms to ADHD has not been demonstrated

(Halperin, Matier, Bedi, Sharma, & Newcorn, 1992).

Confounding diagnosis is the problem of other conditions

sharing similar symptoms (Buncher, 1996). These include

processing disorders (e.g., language disorders), medical

disorders (e.g., hyperthyroidism, infections, seizure

disorders), chromosomal or genetic abnormalities (e.g.,

Turner's syndrome, Tourette's syndrome, sickle-cell anemia),

emotional disorders (e.g., depression, anxiety, manic-

depression), and environmental factors (e.g., dysfunctional

family dynamics, abusive home situations, school placement).

Studies attempting to distinguish children with ADHD from

other patient groups, based on measures of attention, have

yielded negative results (Koriath, Gualtieri, Van

Bourgondien, Quade, & Werry, 1985; Shapiro & Garfinkel,

1986; Werry, Elkind, & Reeves, 1987). Although behaviors

from these disorders may be similar to ADHD, their causes

and treatments are different.

DSM-IV Criteria

The main feature of ADHD, as outlined in the DSM-IV, is

a persistent pattern of inattention or hyperactivity-


impulsivity that occurs more frequently and severely than in

a child's same-age peers. The symptom pattern must have

appeared before age 7 years and the impairment must be

observed in at least two settings (e.g., school and home).

Children with ADHD differ from their peers only in the

intensity, persistence, and clustering of symptoms (Lin-

Dyken & Wolraich, 1992).

The diagnostic criteria of ADHD are empirically-based.

They were derived from leading experts, literature reviews,

an informal survey of rating scales assessing the behavioral

dimensions related to ADHD, and statistical analyses from a

field trial of items (Barkley, 1996). The DSM-IV outlines

distinct subtypes of ADHD to help aid in the diagnosis of

the disorder. These subtypes are: predominantly inattentive

type, predominantly hyperactive-impulsive type, and combined


Predominantly inattentive type (ADHD-PI)

Specific symptoms of inattention, hyperactivity, or

impulsivity must be displayed in academic, social, or

occupational situations. In their schoolwork, children with

ADHD may demonstrate characteristics of inattention by not

paying attention to details and making careless mistakes.

They find it difficult to persist with tasks, act as if they

are not listening, shift from one uncompleted task to the

next, and fail to complete their assignments, even if

instructions were understood (Boliek & Obrzut, 1997).

Homework assignments are avoided because they require

sustained attention and organization. Six of nine

inattention characteristics from the DSM-IV must be present

and considered deviant.

Predominantly hyperactive-impulsive type (ADHD-PHI)

Children who are hyperactive can be viewed as having

excessive amounts of locomotion, such as excessive movement

in their seat, running or climbing at inappropriate times,

talking indiscriminately, or poor control of motor system.

Toddlers and preschoolers display the same behaviors,

although less frequent and less intense. Adolescents and

adults may feel restless and find it difficult to

participate in sedentary activities.

Children described as impulsive lack patience and find

it difficult to delay responses to their external

environment. They may make comments out of turn or at

inappropriate times. Children with ADHD often interrupt

others, do not wait for instructions or directions, and

touch objects off-limits. Six of nine hyperactivity-

impulsivity characteristics from the DSM-IV must be present

and considered deviant. It is unclear whether children in

the ADHD-PHI category are separate from the ADHD-C (i.e.,

combined type) category or in an earlier developmental stage

of it (Barkley, 1996).

Combined type (ADHD-C)

The combined type is used if six or more symptoms of

hyperactivity-impulsivity, but fewer than six symptoms of

inattention, have persisted for the previous six-month

period. Children may have one subtype of the disorder at one

period of time and may develop another predominant subtype

at a later date. If specific criteria are no longer met for

the three subtypes, the diagnosis made is attention-

deficit/hyperactivity disorder, in partial remission.

Increased Diagnosis

Two federal government programs have been identified as

possibly increasing the diagnosis of ADHD (Merline, 1997).

In 1990, the federal Supplemental Security Income program

was created to provide money, as much as $560 per month for

each child, to low-income parents of children diagnosed with

ADHD. Special education grant money became available in

1991, with $400 in grant money being awarded to schools for

each student diagnosed with the disorder. The diagnosis of

ADHD was level prior to the inception of these two programs


but has increased 21% each year since (Merline, 1997). Other

factors also that may contribute to an increase in a

diagnosis include: increased public and physician awareness

and acceptance of the condition, acceptance of a broader

case definition, greater knowledge of the illness course,

fewer interruptions in treatment because of diminished

concerns regarding growth retardation, and increased

treatment of adults (Goldman et al., 1998).


Misdiagnosis of ADHD is a potential problem. In one

study, about half of the children at one military hospital

did not meet the standards in the DSM-IV, although all were

being given medication for their symptoms (Debroitner &

Hart, 1997). Misdiagnosis may occur because the symptoms of

ADHD are shared with other disorders. Therefore, it is

important that a comprehensive medical evaluation be

conducted before treatment begins.


School-based evaluation of ADHD is conducted in five

stages (Figure 1) (DuPaul & Stoner, 1994). The stages are

based upon an educational decision-making model. These five

stages include: screening, multimethod assessment,

Teacher Complaint of Inattention,
Impulsivity, and/or Overactivity

Stage 1: Screening
Teacher Ratings of ADHD Symptoms

Stage 2: Multimethod Assessment of ADHD
Parent and Teacher Interviews
Reviews of School Records
Behavior Rating Scales
Observations of School Behavior
Academic Performance Data

Stage 3: Interpretation of Results
Number of ADHD Symptoms
Deviance from Age and Gender Norms
Age of Onset and Chronicity
Pervasiveness Across Situations
Degree of Functional Impairment
Rule-out Other Disorders

Stage 4: Develop Treatment Plan, Based Upon:
Severity of ADHD Symptoms
Functional Analysis of Behavior
Presence of Associated Disorders
Response to Prior Treatment
Community-based Resources

Stage 5: Assessment of Treatment Plan
Periodic Collection of Assessment Data
Revision of Treatment Plan

Figure 1. Five Stages of School-based Assessment of ADHD
(adapted from DuPaul & Stoner, 1994).

interpretation of results, development of a treatment plan,

and assessment of the treatment plan.

The first stage includes the determination of whether a

student has problems related to ADHD. If so, a decision is

made in reference to the need for further assessment. A

teacher interview will help to specify the behavioral

concerns and to identify environmental factors that may

contribute to problem behavior. The interview will provide

information on the frequency, intensity, and duration of

these behaviors, and whether environmental factors (e.g.,

method of instruction, transition) act as an antecedent or

consequent event for behavior. Teacher ratings of ADHD

symptoms also are obtained.

Multiple assessment techniques are utilized during the

second stage. Parent and teacher interviews are conducted to

specify behaviors and the factors maintaining them. They

also will complete questionnaires to provide information

regarding the frequency and severity of behaviors. School

records and academic performance data are reviewed to

provide historical and current data. Direct observation of

the child across settings can provide further evidence of

the frequency and duration of target behaviors.

Assessment results are interpreted during the third

stage. The goal is to obtain a consistent picture of the

frequency and severity of ADHD behaviors across settings,

including possible causes. A child's behavior is evaluated

using DSM-IV criteria. Both parents and teachers provide

information about the number of symptoms, deviance from age

and gender norms, age and onset of chronicity, pervasiveness

across situations, and degree of functional impairment.

Other causes (e.g., poor or inconsistent instruction or

behavior management) are ruled out before a diagnostic

decision is reached.

A treatment plan is developed during the fourth stage.

Interventions are designed to target behaviors across

academic and social domains. The severity of a child's

symptoms must be considered, as more severe symptoms

increase the likelihood the child will be referred to a

physician. The presence of additional behavior or learning

disorders must be considered when developing treatment

strategies, and these strategies are contingent upon the

child's response to previous interventions. The availability

of treatment resources must be considered. This will decide

whether the child is referred to a community-based

professional (e.g., child psychologist) or whether home-


based interventions designed by the school psychologist are


An assessment of treatment is conducted during the

fifth stage. The student acts as his or her own control, and

behavioral change is evaluated in comparison to

nonintervention conditions. Assessment data are repeatedly

acquired across settings at different points in the

intervention program. If reliable behavior change occurs, it

can be assumed that the intervention was successful. If no

change occurs, the intervention, or the way it is

implemented, must be changed. Thus, ongoing assessment is

very important.

Assessment Techniques

Over half of all children with ADHD are diagnosed in

their elementary school years (Quinn, 1997). Consequently,

with the exception of parents, teachers often are the first

persons to observe the characteristics of ADHD. Children

with ADHD are more inattentive, overactive, and impulsive

than normal children. Measures of these constructs include

observational procedures (Abikoff, Gittelman-Klein, & Klein,

1977; Atkins, Pelham, & Licht, 1985; Milich et al., 1982),

behavior rating scales (Conners, 1969; McGee, Williams, &

Silva, 1984), psychometric tests (Campbell, Douglas, &


Morgenstern, 1971), and continuous performance tests (Klee &

Garfinkel, 1983; Sykes, Douglas, Weiss, & Minde, 1971).

Observational procedures

A behavioral observation assessment approach typically

is used to evaluate ADHD. Multiple methods of data

collection are employed with different observers across

different settings (DuPaul & Stoner, 1994). Emphasis is

placed on obtaining reliable information about a child's

behavior from parents and teachers. The evaluation should

include interviews with the child's parents and teachers,

questionnaires completed by parents and teachers, and

observations on the child's behavior in different settings.

Behavior rating scales

Behavior rating scales completed by parents and

teachers provide important details about the severity of a

child's symptoms. From this information we are able to

determine the degree to which a child's characteristics are

also exhibited by his or her peers. Rating scales collapse

information across situations and time, thus providing

information from persons who live and work with a particular

child (Landau & Burcham, 1995).

Caution must be used since behavior rating scales may

measure teacher and parent tolerance or intolerance of

children instead of the child's disability (Patterson,

1996). They also represent only opinions others have of the

child rather than the child's strengths and uniqueness

Landau & Burcham, 1995). However, a diagnosis of ADHD should

never be made based solely on rating scales (National

Attention Deficit Disorder Association, 1998). Examples of

behavior rating scales include: ADD-H: Comprehensive Teacher

Rating Scale (Ullman, Sleator, & Sprague, 1991), ADHD Rating

Scale (DuPaul, 1991), Attention-Deficit/Hyperactivity

Disorder Test (Gilliam, 1995), Attention Deficit Disorders

Evaluation Scale (McCarney, 1995a), Behavioral Assessment

System for Children (Reynolds & Kamphaus, 1992), Child

Behavior Checklist (Achenbach, 1991a), Comprehensive

Behavior Rating Scale for Children (Neeper, Lahey, & Frick,

1990), Conners' Rating Scales-Revised (Conners, 1997a),

Early Childhood Attention Deficit Disorder Evaluation Scales

(McCarney, 1995b), Teacher's Report Form (Achenbach, 1991b),

and Youth Self-Report (Achenbach, 1991c). Rating scales used

to assess comorbid symptoms and disorders include: Beck

Depression Inventory-II (Beck, Steer, & Brown, 1996),

Children's Depression Inventory (Kovacs, 1980/81), Revised

Behavior Problem Checklist (Quay & Peterson, 1987), and

Social Skills Rating System (Gresham & Elliott, 1990).

Psychometric tests

Results from cognitive, neuropsychological, and

educational tests usually are not helpful in assessing a

child for ADHD (DuPaul & Stoner, 1994). No individually

administered test or group of tests has an acceptable level

of validity (Barkley, 1991). Children often display

appropriate behavior and attention when task conditions are

highly structured and include one-on-one interaction,

typically found with these testing situations (Barkley,


Continuous performance test

Standard measures of sustained attention and impulse

control often are included in an evaluation. Frequently used

standardized measures include the Conners' Continuous

Performance Test (Conners, 1994), Gordon Diagnostic System

(Gordon, 1986a), and Test of Variables of Attention

(Greenberg, 1993). They provide data that are less

influenced by factors that may bias parent and teacher

reports (Barkley, 1987; Gordon, 1986b).

Problems Associated with ADHD Symptoms

Taken as a group of symptoms, ADHD may lead to complex

or secondary difficulties (Green & Chee, 1994). A child

often becomes the center of family and classroom problems.


These problems include insatiability (e.g., nags and never

lets a matter drop), social clumsiness (e.g., misreads

social cues), poor coordination (e.g., poor flow of

movement), disorganization (e.g., blind to mess), and

variability (e.g., mood swings).

Symptoms of ADHD can have a profound effect on a child.

They often lead to disturbed peer relationships (King &

Young, 1982; Pelham & Bender, 1982; Scahill & deGraft-

Johnson, 1997), negative interactions with teachers (Whalen,

Henker, & Dotemoto, 1980), and low self-esteem (Mellor et

al., 1996; Ricchini, 1997; Safer & Allen, 1976; Weiss,

Hechtman, & Perlman, 1978). Children with ADHD display these

social difficulties very soon after entering the primary

grades (Pellegrini & Horvat, 1995).

As many as 65% of children with ADHD have at least one

comorbid condition (Biederman, Newcorn, & Sprich, 1991).

They have higher than expected rates of conduct disorder

(Loney & Milich, 1982; Szatmari et al., 1989), affective

disorders (Biederman, Faraone, Keenan, Benjamin, Krifcher,

Moore, Sprich-Buckminster, Ugaglia, Jellinek, & Steingard,

1992), and tic disorders (Comings & Comings, 1984; DuPaul, &

Stoner, 1994; Gadow, Nolan, & Sprafkin, 1995; Pauls,

Leckman, & Cohen, 1993).


Academic Achievement

Children with ADHD are academic underachievers compared

to their peers (Barkley, 1990; Barkley, DuPaul, & McMurray,

1990; Scahill & deGraft-Johnson, 1997). As many as 80 to 90%

of children with ADHD exhibit some type of underachievement

(Cantwell & Baker, 1991; McEwan, 1998). They demonstrate

significantly lower rates of on-task behavior during work

than that of their classmates (Abikoff et al., 1977). The

cumulative effects of inattention can result in a drop of 7

to 15 IQ points (McEwan, 1998). Additionally, between 30 and

60% of children with ADHD also have learning disabilities or

language problems (Nemethy, 1997), the most common type

being dyslexia (Jordan, 1998). These children are considered

learning disabled because of deficits in the acquisition of

specific academic skills (DuPaul & Stoner, 1994).

Peer Relationships

It is difficult for children with ADHD to initiate and

maintain friendships with their classmates. Approximately

half may experience trouble making and keeping friends

(McEwan, 1995). They engage in more aggressive interactions

(Pelham & Bender, 1982), disruptions and interference in

group play (Prior & Griffin, 1985), and display more

controlling and dominating behaviors with their peers

(Cunningham, Siegel, & Offord, 1985) when compared with

normal children. In general, their peer interactions are

intrusive and often negative (Barkley, 1990).

A high rate of peer rejection exists for children

displaying ADHD-related behaviors (Milich & Landau, 1982;

Pelham & Bender, 1982). For example, they may encounter

trouble playing group sports if they ignore rules, do not

follow instructions, and possess possible visual-motor or

gross motor difficulties. About half of all children with

ADHD have poor motor coordination (Nemethy, 1997). As many

as 60% experience some form of social rejection from their

peers (Guevremont, 1990). Peer rejection is stable over

time, providing evidence of the chronic nature of

interactional difficulties (Parker & Asher, 1987).

Approximately 45% remain rejected one year later, and as

many as 30% maintain their rejected social status for up to

four years (Guevremont, 1990).


Low self-esteem frequently is reported by children with

ADHD. Self-esteem is particularly at risk at the elementary

school age, and children display low self-esteem as early as

the first or second grade (Campbell, Schleifer, Weiss, &

Periman, 1977). Low self-esteem can occur since children

with ADHD may not perform as well as their peers

academically (Barkley, 1990). In addition, self-esteem of

older children may be damaged when they realize their chance

for entering certain occupations (e.g., military) is reduced

because of prior use of stimulant medications (Johnson,

1998; "Ritalin Use," 1996). However, important short-term

gains from the medication may help to preserve the self-

esteem in some children with ADHD, and their parents,

teachers, and peers (Reichenberg-Ullman & Ullman, 1996).

Conduct Disorder

The presence of ADHD may trigger an early onset of

conduct disorder symptomatology (Hinshaw, Lahey, & Hart,

1993). As many as 50% of children with ADHD will display

enough signs of antisocial behavior to receive a diagnosis

of conduct disorder (Barkley, 1990; Klein & Mannuzza, 1991).

Lying, stealing, and truancy are the behaviors most commonly

occurring with conduct problems. Adolescents with ADHD

engage in activities that result in more school suspensions,

and have more adversarial relationships with police compared

to adolescents without the disorder (Goldstein, 1997). The

overlapping subgroup of children with both conduct disorder

and ADHD display a more destructive form of psychopathology

than does either single-diagnosis category (Hinshaw &

Anderson, 1996). They display more physical aggression and a

greater range and greater persistence of antisocial

behavior. Parent and teacher ratings of the symptoms of

conduct disorder correlate highly with each other (Hinshaw,


Affective Disorders

Disagreement exists with regard to the comorbidity of

affective or mood disorders with ADHD (Hinshaw, 1994). As

many as 20% of children have anxiety or mood disorders

(Goldman et al., 1998). Overlap has been found to occur in

community and clinic samples (Anderson, Williams, McGee, &

Silva, 1987; Biederman, Faraone, et al., 1991). Overlap

rates range from chance levels to over 70% in various

studies (Biederman, Newcorn, et al., 1991). Yet, other

studies have concluded that children with ADHD are not at an

increased risk for mood disorders (Gittelman et al., 1985;

Lahey, Pelham, Schaughency, Atkins, Murphy, Hynd, Russo,

Hartdagen, & Lorys-Vernon, 1988).


Children diagnosed with ADHD may actually be suffering

from depression (Block, 1996; Bloomfield & McWilliams,

1994). Chronic monopolar depression often is hidden by ADHD

(Jordan, 1998). As many as 75% of children with ADHD may

also suffer from depression (Armstrong, 1995).

A familial link between ADHD and depression has been

proposed (Faraone & Biederman, 1998). Adopted children with

ADHD have high rates of depression in their biological

relatives (Deutsch, Swanson, Bruell, Cantwell, Weinberg, &

Baren, 1982). Familial risk analyses suggest major

depression and ADHD may represent a variable expression of

the same etiological factors that cause ADHD (Biederman,

Mick, & Faraone, 1998).

Tic Disorders

Tics are sudden, involuntary, repetitive movements

involving a limited group of muscles. Still's (1902)

research may be the first of its kind to note a comorbid

condition of tics and ADHD. As many as 40 to 60% of children

with tic disorders have a history of ADHD symptomatology

(Comings & Comings, 1987; Goldman et al., 1998; Robertson,

Trimble, & Lees, 1988). Symptoms may worsen once tics begin,

as the child must now face another set of uncontrollable


Pharmacological Intervention

Stimulant medication currently is one of the most

common treatments for ADHD (Epstein et al., 1991). The


belief that ADHD has a biological basis is supported by the

positive effects of stimulant medications. Reportedly,

response rate to stimulant medications varies from 70 to 96%

(Elia, Borcherding, Rapoport, & Keysor, 1991). However, a

person's response to medication is not a valid justification

of the presence of ADHD (National Attention Deficit Disorder

Association, 1998).

Many parents support the notion that behaviors

associated with ADHD can be treated with medication (Mellor

et al., 1996). Successful medication use removes the focus

from other etiological factors (e.g., psychosocial factors).

A dysfunctional family relationship is thus eliminated as

the cause of a child's ADHD, since poor parenting often is

an underlying suspicion of many clinicians. Medications also

may have a significant positive effect by reducing stress in

parents (Swanson, McBurnett, Wigal, Pfiffner, Lerner,

Williams, Christian, Tamm, Willcutt, Crowley, Clevenger,

Khouzam, Woo, Crinella, & Fisher, 1993). Its use is

convenient and does not disrupt family schedules.

Stimulant Medications

Stimulant medication was first proposed as a treatment

for hyperactivity in the 1930s (Bradley, 1937), although

pharmacology was not introduced for another two decades

(Williams & Cram, 1978). Widespread use of stimulant

medication for children with hyperactivity occurred during

the 1960s. By the 1970s social concerns were raised with

regard to the use of stimulant medication (Weithorn & Ross,

1976). Some suggested hyperactivity was a label physicians

used to extend control over children's behavior through the

use of drugs (Conrad, 1975; Schrog & Divoky, 1975).

According to the Physicians' Desk Reference (1999),

reasons why stimulant medications are effective remain

unclear. Stimulants are believed to be associated with

increased levels of neurotransmitters, such as dopamine and

norepinephrine (Tan & Schneider, 1997). There is greater

activity of neurochemicals in the parts of the brain that

control the ability to attend and remain alert. Recent

evidence in mice studies suggests that Ritalin and other

psychostimulants may decrease hyperactivity by increasing

the levels of serotonin, a neurotransmitter, in the brain

(Gainetdinov, Wetsel, Jones, Levin, Jaber, & Caron, 1999).

Stimulants reduce distractibility, enhance concentration,

and decrease motor restlessness and hyperactivity, although

they do not boost IQ or long-term academic performance

(Merline, 1997). The three most commonly used stimulants are

methylphenidate (i.e., Ritalin), dextroamphetamine sulfate

(i.e., Dexedrine), and pemoline (i.e., Cylert).

Worldwide consumption of methylphenidate increased from

3 tons in 1990 to 5 tons in 1995, and was projected to reach

13 tons by 1997 (Ghodse & Kreek, 1998). The United States

produces and consumes five times more methylphenidate than

the rest of the world combined (Drug Enforcement

Administration, 1995). Other countries are beginning to

report an increase in the consumption of the drug as a

treatment for ADHD (Ghodse & Kreek, 1998).

The number of people taking Ritalin doubled between

1993 and 1995, and about three-fourths of the 2.6 million

consumers of Ritalin are ADHD children aged 5 to 12 (Price,

1996). It is prescribed in more than 90% of children with

ADHD who receive stimulant medication (DuPaul & Stoner,

1994; Goldman et al., 1998). The number of American children

taking stimulant medications has doubled every two years

since 1988 and should reach 8 million by the year 2000

(Guistolise, 1998). The United Nations is concerned about

Ritalin "being passed out as freely as candy in the United

States" (Light, 1997, p. 74).

Antidepressant Medications

Antidepressant medications, such as tricyclic

antidepressants and monoamine oxidase (MAO) inhibitors, also

are used to treat children with ADHD. Tricyclic

antidepressants have a well-demonstrated ability in treating

behavioral symptoms (Popper, 1997). Desipramine

hydrochloride (i.e., Norpramin) and imipramine hydrochloride

(i.e., Tofranil) may be used to treat ADHD.

Monoamine oxidase (MAO) inhibitors often are effective

for symptoms related to the disorder (Rapoport, 1986;

Zametkin, Rapoport, Murphy, Linnoila, & Ismond, 1985).

However, they have potentially greater adverse reactions

than tricyclic antidepressants and require dietary

restriction and monitoring (Sarason & Sarason, 1984). The

United States Food and Drug Administration (FDA) has not

approved either tricyclic antidepressants or monoamine

oxidase (MAO) inhibitors for treating ADHD (Tan & Schneider,


Antidepressants are not as widely used as stimulants

due to severe adverse reactions. One of the most serious

adverse reactions of tricyclic antidepressants is

tachycardia (Biederman, Gastfriend, Jellinek, & Goldblatt,

1985; Puig-Antich, Ryan, & Rabinovich, 1985), which can be

fatal with as few as 10 pills (Copeland & Copps, 1995).

Cardiac arrhythmias, anticholinergic effects, and sudden

death have also been reported (Ryan, 1990; Tan & Schneider,

1997). Desipramine hydrochloride also has been associated

with growth defects in children (Spencer, Biederman, Wright,

& Danon, 1992) and bone marrow depression (Block, 1996). The

long-term effectiveness of tricyclics in treating ADHD is

questionable (Copeland & Copps, 1995).

Additional Medications

The need for a variety of medications may be warranted,

given the diversity of children who present with symptoms of

ADHD and the limitations of their response to

psychostimulants alone (Hunt, Lau, & Ryu, 1991). Adderall is

one of the latest drugs being used for ADHD (Block, 1996).

Fluoxetine hydrochloride (i.e., Prozac) has been tried both

alone (Barrickman, Noyes, Kuperman, Schumacher, & Verda,

1991) and in combination with methylphenidate (Gammon &

Brown, 1993). Bupropion hydrochloride (i.e., Wellbutrin) is

successful in treating ADHD (Barrickman, Perry, Allen,

Kuperman, Arndt, Herrmann, & Schumacher, 1995; Casat,

Pleasants, Schroeder, & Parler, 1989; Simeon, Ferguson, &

Van Wyck Fleet, 1986), exerting both antiaggressive and

antihyperactive effects in some children (Hunt, Lau, Ryu,

1991). Clonidine hydrochloride (i.e., Catapres) can be

beneficial in treating ADHD symptomatology (Hunt, Minderaa,

& Cohen, 1985; Hunt et al., 1991; Wilens, Biederman, &

Spencer, 1994); guanfacine hydrochloride (i.e., Tenex)

reportedly is effective, less sedating, and longer acting

than clonidine hydrochloride (Hunt, Arnsten, & Asbell,

1995). A combination of drugs for children's sleep disorders

recently has been shown to alleviate the symptoms of ADHD,

including impulsive behavior and restlessness ("Sleep

Disorder," 1998).

Reasons For Not Using Medication as an Initial Treatment

While effective in many cases, medication is not

necessarily the best option as a first-line treatment of

ADHD. Other consideration must be made before this

intervention is utilized. Seven reasons have been suggested

as a rationale for not choosing medication as an initial

course of treatment (Copeland & Copps, 1995):

1. If medication is successful, there is little
incentive to try other interventions that are needed
for the long-term benefit of the child but require more
investment of time and energy from parents and

2. Research suggests that those children receiving
medication alone did not have a better outcome by late
adolescence than those who never received treatment.


3. The amount of medication needed may be reduced after
a child's allergies are treated, stress is reduced,
organization, structure, and routine are implemented,
and behavior management strategies are used

4. Parents are more comfortable with medication after
other alternatives have been tried and their child
continues to need intervention.

5. Children who may have been misdiagnosed or who do
not need medication typically are very obvious after a
few weeks of the use of other treatment.

6. Delaying medication insures adequate time to try
other interventions.

7. Medication is less likely to be over-utilized or
abused if important safeguards (e.g., careful
assessment) are followed.

Combining Medication with Other Interventions

Current research does not support sustained treatment

of ADHD with medication alone (Jacobvitz, Sroufe, Stewart, &

Leffert, 1990). Many professionals believe medication should

be used only after other appropriate interventions have been

tried (Coleman & Levine, 1988), and never should be the sole

treatment for ADHD (American Academy of Pediatrics, 1996).

As the only method of management, the value of stimulants is

limited (Pelham, 1993; Weiss, Kruger, Danielson, & Elman,

1975). At best, it is a short-term solution for many

children (lalongo, Horn, Pascoe, Greenberg, Packard, Lopez,

Wagner, & Puttler, 1993). These limitations have led to an

adoption of multimodal treatment for children with ADHD

(Barkley, 1989a).

Evidence suggests that successful treatment of ADHD is

related to the extended use of multimodal treatment

(Rostain, Power, & Atkins, 1993). A combination of

pharmacological and psychosocial treatments or behavior

modification strategies is recommended since multiple

impairments require multiple treatment modalities (Bramlett,

Nelson, & Reeves, 1997; Swanson, Sergeant, et al., 1998).

Despite support for multimodal treatment among medical

practitioners, most children are prescribed Ritalin as their

only treatment (Price, 1996).

The two most commonly used paired treatments are

stimulant medication and behavior modification (Barkley,

1990). The combination of these two has been found to be

more effective than either used in isolation (Bramlett et

al., 1997; Pelham & Murphy, 1986), and has been described as

an optimal treatment approach for ADHD (Barkley, 1990).

However, some believe medication alone is as effective as

medication used in combination with any other treatment

(Dawson, 1996). In practice, medication frequently is

administered without any behavioral interventions (Evans,

Ferre, Ford, & Green, 1995).

While multimodal treatment can lead to good outcomes,

there often is a lack of personnel who can research and

implement them. Thus, some child and adolescent services

will not accept referrals for ADHD. In addition, two recent

well-controlled studies question the effectiveness of this

multimodal approach (lalongo et al., 1993; Pelham, Carlson,

Sams, Vallano, Dixon, & Hoza, 1993).

Opposition to the Use of Medications

Opposition to the use of medication to treat children

with ADHD arises from many sources. Adults feel apprehensive

about giving children drugs that affect brain functioning

and are used to control behavior (Copeland & Copps, 1995).

Medication may be used indiscriminately. For example,

children who are disruptive in the classroom may be treated

with Ritalin even though they do not have ADHD ("Are Too

Many Children," 1996). It appears the use of Ritalin may

depend on parents' and teachers' ability to tolerate

children's behavior (Bromfield, 1996a). Children who may

have been misdiagnosed or who do not need medication

typically are very obvious after a few weeks of other

treatment (Copeland & Copps, 1995). Methylphenidate

typically produces similar effects on children, even those

without ADHD (Breggin & Breggin, 1995). Many physicians are

using drugs as a diagnostic tool, believing that if the

child improves, he or she must have ADHD (Livingston, 1997).

This belief may lead a physician to prematurely end the

search for a more proper diagnosis without considering

disorders that coexist with ADHD and may jointly interfere

with a child's functioning (National Attention Deficit

Disorder Association, 1998).

Medication, and more specifically Ritalin, is the most

common treatment for children with ADHD (DuPaul & Rapport,

1993). Given recent trends in managed care, many primary

care physicians who prescribe medications often do not

consult with school personnel or other health care

professionals (McEwan, 1998). In addition, compliance with

pharmacologic treatment of ADHD often is inadequate

(Firestone, 1982; Sleator, 1985). Delaying medication

insures adequate time to try other interventions.

Several reasons have been given for not choosing

medication as an initial treatment (Copeland & Copps, 1995).

If medication is successful, there is little incentive to

try other interventions that are necessary for the long-term

benefit of the child but require more investment of time and

energy from parents and teachers. The amount of medication

needed may be reduced once a child's allergies are treated,


stress is reduced, organization, structure, and routine are

implemented, and behavior management strategies are used

effectively. And parents are more comfortable with

medication after other alternatives have been used and their

child continues to need intervention. Thus, many

considerations must be made before allowing a child to take

stimulant medication, including: adverse reactions, unknown

results from long-term use, abuse, ineffectiveness, and the

financial aspects of prescribing medication.

Adverse Reactions of Stimulant Medications

The majority of children treated with stimulants

experience some adverse reactions, ranging from mild to

severe (Efron et al., 1997). Insomnia, decreased appetite,

irritability, anxiety, headaches, and stomachaches occur in

20% to 50% of children treated with stimulant medication

(Goldstein & Goldstein, 1990). Some children may experience

a negative rebound effect at night once the medication wears

off, and symptoms often are worse than if the child had

never taken the medication (Reichenberg-Ullman & Ullman,

1996). Additionally, 3% of individuals cannot take Ritalin

because of biochemical intolerance (Jordan, 1998). Adverse

reactions are reversible with dosage reduction or drug

withdrawal (Bramlett et al., 1997), however, and all traces

of Ritalin are cleared from the brain within 24 hours of

cessation (Jordan, 1998). Many children must take multiple

medications in an effort to counteract chemically-induced

adverse reactions (Hunker, 1998).

The potential for severe adverse reactions from

stimulant medications must be considered. These may include

liver dysfunction (Barkley, 1995; Jordan, 1998; Tan &

Schneider, 1997), glaucoma (Armstrong, 1995), symptoms of

psychosis (Braswell & Bloomquist, 1991), anorexia

(Physician's Desk Reference, 1999), heart problems leading

to sudden death (Armstrong, 1995), leukopenia (Findling &

Dogin, 1998), depression (Breggin, 1998), motor and vocal

tics (DuPaul, Barkley, & Connor, 1998), and permanent facial

tics (Breggin & Breggin, 1995; Reichenberg-Ullman & Ullman,

1996; Tan & Schneider, 1997). The risk of triggering tics

associated with Tourette's Syndrome also is of major concern

(Cherkes-Julkowski, Sharp, & Stolzenberg, 1997; Shaywitz &

Shaywitz, 1991b), especially since this disorder is

irreversible (Patterson, 1996). However, stimulant

medications may only trigger tic disorders when a genetic

predisposition exists (Erenberg, Cruse, & Rothner, 1985).

The effect of stimulant medications on children's

height is another concern. A decrease in the rate of growth

occurs when Ritalin disrupts the cycles of growth hormone

released by the pituitary gland. This negative effect has

been recorded after only one or two years of treatment

(Greenhill, Puig-Antich, Chambers, Rubinstein, Halpern, &

Sachar, 1981). A significant decrease can occur after two to

four years of Ritalin use (Mattes & Gittelman, 1983). High

doses continuously consumed over a number of years are more

likely to suppress growth than lower doses (Sears &

Thompson, 1998). Nevertheless, height tends to normalize

during adolescence (Spencer, Biederman, Harding, O'Donnell,

Faraone, & Wilens, 1996).

Unknown Results From Long-term Use of Medications

The Physicians' Desk Reference (1999) acknowledges

there are insufficient data on the safety and efficacy of

long-term use of stimulants by children. Some children

receive drug treatment for extended periods of time without

proper evaluation by professionals (e.g., psychologists,

speech pathologists, educational diagnosticians) and without

continuing evaluation during their therapy (American Academy

of Pediatrics, 1996). Children in the United States also are

prescribed the drug for longer periods of time than children

in other countries ("Agency Survey," 1996).

The full effects stimulant medications will have on

children's bodies are unknown. There is concern that harmful

effects may occur many years after treatment ends. Few

children who were treated extensively with stimulant

medications have reached middle age (Jacobvitz et al.,

1990). Thus, follow-up research must be conducted to

determine possible deleterious effects.


Ritalin has become a popular recreational drug

(Reichenberg-Ullman & Ullman, 1996). It has been referred to

as pediatric cocaine (Block, 1996). Ritalin is regulated by

the DEA in the same category as cocaine, morphine, PCP,

codeine, and methadone (Price, 1996). Schedule II controlled

substances such as Ritalin, drugs for which prescriptions

are carefully monitored, "have a high abuse potential with

severe psychological or physical dependence liability"

(DiGregorio & Barbieri, 1998, p. 263). One physician notes

the extensive procedure involved in prescribing and filling

the prescription, given its dangerous potential:

Doctors who prescribe it are required to obtain an
expensive narcotic license, renew it every two years,
and write the prescription (with annoying perfection)
on special triplicate prescription pads provided by the
DEA. The doctor retains a copy, the pharmacy retains a
copy, and the DEA retains a copy. .. A prescription
for Ritalin cannot be called into the pharmacy over the

phone; instead, the completed official prescription
form must be mailed or handed directly to the patient.
If the doctor forgets to cross a t or dot an i, the
pharmacist must send it back, for fear that someone may
have tampered with the prescription. The point is,
everyone involved with prescribing Ritalin takes it
seriously, especially the doctor, the pharmacist, and
the DEA. So must everyone else. (Sears & Thompson,
1998, p. 232)

Prescriptions for Ritalin have increased 600% since

1990, with a large portion of the drugs diverted for illicit

use (Bailey, 1995). The DEA has received reports of street

sales, drug rings, illegal importation, and illegal sales by

health professionals (Goldman et al., 1998). Ritalin has

ranked in the top 10 most frequently reported controlled

pharmaceuticals stolen from licensed handlers (Drug

Enforcement Administration, 1995).

Drug abuse injury reports involving Ritalin for

children ages 10 to 14 have increased 1,000% (Haislip,

1996). Psychotic episodes and violent behaviors are

associated with chronic abuse of Ritalin (Merline, 1997).

Ritalin-related visits to emergency rooms for 10-14 year

olds have increased 10-fold and now are at the same level as

cocaine (Haislip, 1996). Hospital admissions have increased

fivefold since 1990 (Merline, 1997).

The United Nations International Narcotics Control

Board has reported an increase in the number of teenagers


inhaling Ritalin (Bromfield, 1996b). A survey of high school

students indicated that more seniors in the United States

abuse Ritalin than are prescribed legitimately (Drug

Enforcement Administration, 1995). The number of high school

seniors who admitted abusing the drug doubled to 350,000

from 1993 to 1994 (Reichenberg-Ullman & Ullman, 1997). White

and suburban abusers are more likely to snort Ritalin, while

African-American inner-city abusers are more likely to

inject it (Bailey, 1995). As many as 15 to 20% of the

children in some communities have been placed on Ritalin or

a similar stimulant; thus, "there is good reason to conclude

that this is a 'quick-fix', bogus medical practice which is

nevertheless producing large profits" (Haislip, 1996, p. 2).

In the United States, ADHD is diagnosed most commonly

in wealthy suburbs where parents often expect their children

to be high academic achievers (Toufexis, 1989). There is the

potential for abuse by adolescents and their parents who

inappropriately seek stimulants to enhance the ability to

study for higher level exams (Mellor et al., 1996) or to

succeed in school (Debroitner & Hart, 1997). Abuse of

Ritalin can result in psychotic episodes, violent behavior,

tolerance, and severe psychological dependence (Price,



Not all children with hyperactivity respond to

stimulant medication. As many as 40% may show no response

(Reichenberg-Ullman & Ullman, 1996), and those who do

respond may not respond fully (Williams & Cram, 1978). This

lack of response to its use may be attributed to the finding

that half of every dose of Ritalin may contribute nothing to

its therapeutic effect (Wu, 1998). One of two molecular

forms found in Ritalin was shown to offer little benefit,

while contributing to the drug's adverse reactions.

Among children who respond to stimulant medication,

drug therapy rarely is sufficient to bring them within a

normal range of academic and social functioning (Pelham,

1993). Some studies have failed to confirm improvement in

ADHD symptoms (McGuiness, 1989; Baughman, 1993; Breggin &

Breggin, 1994; Walker, 1996), including improvement in

retention of learning, overall achievement, or control of

anger (Weintraub, 1997). Several reasons have been offered

to explain this phenomenon: studies may be short-term,

dosages may have been inadequate, and dose-response

relationships may be different for different domains

(Goldman et al., 1998).

Persons with a type of ADHD attributed to one etiology

do not respond to medication. Approximately 93% of children

with right hemisphere syndrome, one genetic form of ADHD,

display characteristics of ADHD (Voeller, 1986). Persons

with this common form of ADHD are very difficult to treat

with medications unless a drug-treatable comorbidity (e.g.,

conduct disorder, depression) exists (Popper, 1997).

Despite decades of research, no demonstrable long-term

benefits of stimulant medication have been noted (Swanson &

Kinsbourne, 1980a). A lack of data showing continued or

lasting effects from medication suggest its long-term

effectiveness cannot be supported (Jacobvitz et al., 1990).

In addition, the effects from long-term use of stimulants on

children's growing bodies are unknown (Ullman, 1988).

Several explanations have been offered to account for a

lack of long-term benefits from the use of stimulant

medication (Jacobvitz et al., 1990). Drug treatment alone

may be an adequate treatment for most children. A tolerance

for the medication may develop and drug effects may

disappear over time. Children with attentional and

behavioral problems represent a very heterogeneous group. If

a subset has a specific biochemical abnormality, positive

effects of medication may be obscured.

Financial Aspect

One cannot overlook the financial aspect of medication.

Medicating children with ADHD at an early age often gains a

customer for life. Stimulant medications have been over-

promoted, over-marketed, and over-sold, resulting in annual

profits of approximately $450 million (Haislip, 1996).

Because pharmaceutical companies are making large profits

from the diagnosis and treatment of ADHD, drug treatment is

unlikely to stop, even if drugs are found not to be the best

treatment (Block, 1996). There clearly is greater financial

profit in getting doctors, parents, and teachers to treat

the disorder with medication instead of other therapies

(Johnson, 1998).

Alternative Treatments

The popularity of complementary and alternative

medicines (CAM) has grown in recent years. The use of CAM

with children also is increasing (Spigelblatt, 1995). Visits

to alternative medicine practitioners in the United States

increased 47%, from 427 million in 1990 to 629 million in

1997 (Eisenberg, Davis, Ettner, Appel, Wilkey, Van Rompay, &

Kessler, 1998), compared to only 386 million visits to

primary-care physicians (Cowley & Underwood, 1998). Over

half of all conventional physicians in the United States use

or refer patients for alternative treatments (Astin, 1998;

Blumberg, Grant, Hendricks, Kamps, & Dewan, 1995; Ernst,

1995). An estimated $32.7 billion is spent annually on

services of practitioners of alternative therapies

(Eisenberg et al., 1998).

CAM are intended to be complementary and compatible

with conventional medicine. It includes practices requiring

highly specialized and competent practitioners, over-the-

counter products, and self-care techniques. Many patients

use alternative medicine either because they are attracted

to CAM philosophies and health beliefs, or because they are

not satisfied with the process or results of their

conventional care (Furnham & Forey, 1994).

Some believe every effort should be made to investigate

alternatives before beginning drug therapy (Friedman &

Doyal, 1992). In an attempt to find more natural treatments

for ADHD, many parents seek a complementary or alternative

treatment for their children (Spencer & Jacobs, 1999). A

number of these treatments for children with ADHD have been

utilized, with varying success, including iron treatment,

Feingold Diet, neurofeedback, homeopathy, herbal medicine,

and dietary supplements.

Iron Supplementation

Iron deficiency is the world's most prevalent

nutritional disorder (Weintraub, 1997). Evidence suggests

iron deficiency has behavioral effects (Sever, Ashkenazi,

Tyano & Weizman, 1997). A deficiency affects motor behaviors

and cognitive function, and iron level may play a part in

motor hyperactivity, poor cognitive learning, and attention

deficit. Many children with ADHD have low levels of iron and

other trace elements, and the use of iron treatment for a

deficiency significantly improves behavior and intellectual

attainment (Deinard, Murray, & Egeland, 1976; Pollitt &

Leibel, 1976; Weintraub, 1997; Yehuda, Youdim, & Matofsky,

1986). There also may be some benefit to iron

supplementation in ADHD children who are non-iron-deficient

(Sever et al., 1997).

Feingold Diet

The Feingold Diet was created to teach parents how

children with behavioral, learning, and health problems can

be helped by the elimination of certain foods and synthetic

chemicals. The two stage elimination diet was created by

pediatrician Ben Feingold (Feingold Association, 1983). The

first stage (Table 1) involves an initial period when foods

containing synthetic colors and flavors, antioxidant

Table 1

Feingold Diet, Stage 1

Initial period during which two groups of foods are

Group 1: Eliminate foods containing:

Synthetic colors. Listed as "U.S. Certified
Color," or by its FDA number, such as "FD&C Yellow
No. 5."

Synthetic favors. May be listed as "flavoring" or
"artificial flavoring."

Three antioxidant preservatives:
BHA (Butylated Hydroxyanisole)
BHT (Butylated Hydroxytoluene)
TBHQ (Monotertiary Butylhydroxylquinone)

Group 2: Eliminate foods containing natural
salicylates, such as:

Grapes and raisins

Green peppers

Aspirin and medication containing aspirin also are

Source: Feingold Association. (1983). Feingold handbook,
page 3. Alexandria, VA: Feingold Association.

preservatives, and natural salicylates are eliminated. The

second stage (Table 2) includes a reintroduction of foods

with natural salicylates. Foods are added and tested

individually to determine if the child can use some or all

of them without a negative change in behavior.

Feingold's proposed diet received widespread support

despite a lack of corroborating controlled clinical trials,

and many parents were convinced their children were reacting

adversely to ingested synthetic colorings (Rowe, 1988). Five

factors have been suggested to account for the

attractiveness of Feingold's hypothesis (Williams & Cram,

1978): it offers a natural alternative to drug therapy, it

alleviates the guilt parents feel by putting the blame on

food, it removes blame from the schools, it is consistent

with the growing awareness of ecology and pure foods, and it

allows parents to control their child's diet, thus enabling

them to become the primary therapeutic agents. In addition,

parents are attracted to the diet treatment because of

dissatisfaction with other therapies (Harley & Matthews,


Research investigating food additives as the cause of

hyperactivity or learning problems in children has been

mixed (Conners, 1980a, 1980b; Lipton & Mayo, 1983; Mattes,

Table 2

Feingold Diet, Stage 2

After a favorable response has been observed for four to six
weeks, the foods in Group 2 may be carefully reintroduced
and tested one at a time. Foods in Group 1, from Stage 1,
are never reintroduced.

Examples of Fruits Allowed:

Banana Limes
Cantaloupe Papaya
Dates Pears
Grapefruit Pineapple
Lemons Watermelon

Examples of Vegetables Allowed:

Asparagus Onions
Beans (all types) Peas
Broccoli Potatoes, white and sweet
Carrots Pumpkin
Celery Spinach
Lettuce Squash

Source: Feingold Association. (1983). Feingold handbook,
page 4. Alexandria, VA: Feingold Association.

1981; Wender, 1986). Empirical research (e.g., Boris &

Mandel, 1994; Carter, Urbanowicz, Hemsley, Mantilla,

Strobel, Graham, & Taylor, 1993; Egger, Carter, Graham,

Gumley, & Soothill, 1985; Egger, Stolla, & McEwen, 1992;

Kaplan, McNicol, Conte, & Moghadam, 1989a; Pollock & Warner,

1990; Rowe & Rowe, 1994; Salzman, 1976) and anecdotal

reports (e.g., Cook & Woodhill, 1976; Swanson & Kinsbourne,

1980b; Weintraub, 1997; Williams, Cram, Tausig, & Webster,

1978) support Feingold's theory. Evidence suggests from 30

to 50% (Feingold, 1976) of children on the Feingold diet

display behavioral improvement. However, many empirical

studies have either discredited this relationship or yielded

inconclusive results (e.g., Connors, Goyette, Southwick,

Lees, & Andrulonis, 1976; Cook & Woodhill, 1976; David,

1987a; Goyette, Connors, Petti, & Curtis, 1978; Gross,

Tofanelli, Butzirus, & Snodgrass, 1987; Harley, Matthews, &

Eichman, 1978; Harley, Ray, Tomasi, Eichman, Matthews, Chun,

Cleeland, & Traisman, 1978; Levy, Dumbrell, Hobbes, Ryan,

Wilton, & Woodhill, 1978; Mattes, 1980; Mattes, & Gittleman,

1981; Mattes & Gittelman-Klein, 1978; Rowe, 1988; Weiss,

Williams, Margen, Abrams, Caan, Citron, Cox, McKibben, Ogar,

& Schultz, 1980; Williams, Cram, Tausig, et al., 1978).

Ironically, while many are skeptical of the relationship

between artificial colors and ADHD, the Physicians' Desk

Reference (1999) notes Ritalin sustained-release tablets are

available in a color-additive free form.

These data may not offer an accurate interpretation.

Some results are questionable because of logistic and

methodologic problems (Conners, 1980b; National Advisory


Committee on Hyperkinesis and Food Additives, 1980; Rippere,

1983). Impediments include the lack of a control group

(Tryphonas, 1979), uncertainties about which part of the

diet is of significance (Rowe, 1988), parental

identification of differences between the Feingold and

placebo diets (Conners et al., 1976), dietary compliance

(Gross et al., 1987; Tryphonas, 1979), possible lack of

inertness of the control substance (Rippere, 1983), varying

diagnostic criteria for hyperactivity (American Psychiatric

Association, 1968, 1980, 1987, 1994; Biederman, Newcorn, et

al., 1991; Halpern et al., 1992; Hinshaw, 1987; Pliszka,

1992; Shaywitz & Shaywitz, 1991a; World Health Organization,

1978), identification of responding children from

heterogeneous populations (Rowe, 1988), placebo or

"Hawthorne" effect (Brenner, 1977; Spring & Sandoval, 1976;

Wender, 1977; Williams, Cram, Tausig, et al., 1978), the

expense and difficulty of satisfactorily implementing

double-blind conditions (Conners et al., 1976; Harley, Ray,

et al., 1978; Williams, Cram, Tausig, et al., 1978), doubts

about the validity and reliability of outcome measures (Rowe

& Rowe, 1992), insufficient dependent measures to assess

treatment effects (Trites et al., 1980), and detection of

treatment effects when only a small number of children

respond (Cox, 1981; Dews, 1982/1983; Harley, 1981; Rowe,

1988; Schwab & Conners, 1986).

Several concerns have been raised with regards to

children being placed on the Feingold Diet without physician

supervision (David, 1987b). Children have suffered

anaphylactic reactions to certain dietary elements that were

previously restricted from their diet. They may be starved

of essential nutrients by highly-restricted diets

implemented by parents. Dietary treatment is expensive and

requires the time of several medical personnel. In addition,

restricting the child's diet can be unrealistic and

impossible to monitor outside of the home.

Two groups worked independently to address the claims

of Feingold's hypothesis. The National Commission on

Hyperkinesis and Food Additives was established by the

Nutrition Foundation, a group formed by the food industries

in the United States. The Interagency Collaborative Group on

Hyperkinesis was created by the United States Department of

Health, Education and Welfare. The groups reached the

following conclusions (Williams & Cram, 1978): the

hypothesis was based on clinical findings and not on

rigorous clinical trials or experimental research, the

hypothesis was derived from intuitions and clinical

experience rather than being based on the scientific

principles of biochemistry and nutrition, and systematic

clinical trials and strict experimental designs were

required to test the hypothesis and the effectiveness of the



The term "biofeedback" was first used in the 1960s. It

describes procedures used to train research subjects to

alter their brain activity, blood pressure, heart rate, and

other functions not normally voluntarily controlled (Runck,

1983). The treatment technique allows individuals to improve

their health by using signals from their own bodies.

Neurofeedback, or EEG biofeedback, training has been

applied to a number of neurological, psychological, and

psychosomatic conditions (e.g., Hartje, 1980; James & Folen,

1996; Tansey, 1993). The goal of neurofeedback is to improve

mental flexibility so a person can produce a mental state

appropriate for a particular situation (e.g., completing

classwork) (Sears & Thompson, 1998). Research has

established the effectiveness of neurofeedback in treating

individuals with ADHD (Lubar & Shouse, 1976; Othmer, 1997).

It is one of the fastest-growing applications of biofeedback

and a relatively new approach to the treatment and long term

management of ADHD (Othmer, Kaiser, & Othmer, 1995), and

neurofeedback generally is accepted by allopathic physicians

(Laken & Cosovic, 1995).

Differences in EEG are present in children with ADHD

and those without the disorder (Kuperman et al., 1996;

Lazzaro, Gordon, Whitmont, Plahn, Li, Clarke, Dosen, &

Meares, 1998; Lubar, 1991; Othmer & Othmer, 1992a).

Neurofeedback has been found to remediate the underlying

condition of physiological underarousal in hyperactivity

(Lubar & Lubar, 1976). Thus, symptoms of ADHD may arise from

a disregulated EEG, in combination with genetics, trauma,

and other factors that can be attributed to the onset of the

disorder (Othmer & Othmer, 1992a).

Neurofeedback can help ameliorate the problems

associated with ADHD (Lubar, 1995) (Table 3). It is a method

for repeatedly exercising the pathways of attention and

impulse control, thereby facilitating their growth and

development (Sears & Thompson, 1998). The use of

neurofeedback has resulted in increased attention, impulse

control, and speed of information processing on the Test of

Variables of Attention (Cartozzo, Jacobs, & Gevirtz, 1995;

Kaiser, 1997; Kaiser & Othmer, 1997; Rossiter & LaVaque,

1995; Scheinbaum, Zecker, Newton, & Rosenfield, 1995) and

Table 3

Application of and Results from Neurofeedback Treatment

Anyone with a primary diagnosis of ADD or ADHD, between the
ages of 7 and 45, with low-average, average, or above-
average intelligence is a candidate. Neurofeedback treatment
should not be offered with comorbidity of:
Mental retardation
Childhood psychosis
Severe depressive or bipolar illness
Significant seizure disorder where medications
interfere with learning (i.e., sedating
Hyperkinesis, where multiple medications or high
dosage with monotherapy have been ineffective
Learning disabilities without ADD and ADHD as a
primary problem
Dysfunctional families who refuse to participate
in indicated therapy

Symptoms that can be improved with neurofeedback:
Attention, focus, and concentration
Task completion and organizational skills
Mild hyperactivity

Results of treatment:
Improved behavior and learning
Improvement in school grades
Increased self-esteem
Better job performance
Greater realization of innate potential
Higher intelligence test scores
Improved scores on parent-teacher rating scales

Source: Lubar, J. F. (1995). Neurofeedback for the
management of attention-deficit/hyperactivity disorders. In
M. Schwartz, Biofeedback: A practitioner's guide, pp. 506-
507. New York: Guilford Press.


improved scores on the Freedom from Distractibility factor

of the Wechsler Intelligence Scale for Children-Revised

(Cartozzo et al., 1995). Behavior Assessment Scale for

Children (BASC) questionnaires completed by mothers also

confirm a reduction in ADHD symptoms (Rossiter & LaVaque,

1995). Results indicating a significant reduction of

symptoms are consistent with other studies (Linden, Habib, &

Radojevic, 1996; Lubar, 1991; Lubar, Swartwood, Swartwood, &

O'Donnell, 1995). Research indicates the success rate for

biofeedback training is approximately 85% (Sears & Thompson,

1998). Although the treatment has been used successfully

with more than 3000 children in over 300 health care

organizations (Lubar, 1995), Russell Barkley, an expert in

the field of ADHD research, disputes the claims of

neurofeedback as an effective intervention (personal

communication, February 16, 1998).


Homeopathy is the method of using any of more than

2,000 remedies with the power to resonate with the illness,

in contrast with the more traditional method of opposing

symptoms with great force (Jacobs & Moskowitz, 1996). The

medical theory and practice developed in reaction to the

bloodletting, blistering, purging, and other harsh


procedures of conventional medicine as it was practiced 200

years ago (Stehlin, 1997). Samuel Hahnemann, an 18th century

German physician and chemist discouraged with these methods,

developed a theory based on three principles: the law of

similar, the minimum dose, and the single remedy (Jacobs &

Moskowitz, 1996).

The law of similar states that if a large amount of a

substance causes certain symptoms in a healthy person,

smaller amounts of the same substance can be used to treat

the symptoms in an ill person (Reichenberg-Ullman & Ullman,

1996). Since symptoms are defenses of the body, it is best

to aid rather than suppress them (Ullman, 1988).

Conventional medicine applies this principle to

immunizations and allergy treatments.

Homeopathic remedies stimulate an ailing self-healing

mechanism rather than correcting a specific problem; thus,

large doses rarely are required and may even spoil the

effect (Jacobs & Moskowitz, 1996). With a minimum dose, the

strength and effectiveness of a substance increases the more

it is diluted. Small doses decrease any chance that

dangerous adverse reactions will occur.

A single remedy generally covers all of the symptoms a

patient is experiencing (Stehlin, 1997). Remedies made from

a variety of sources (e.g., plants, minerals, animals) are

prescribed based on a person's symptoms. The use of multi-

ingredient remedies is recognized as part of homeopathic


Homeopathy is widely used to treat a variety of health

problems. Approximately 500 million people worldwide receive

homeopathic treatment (Burton Goldberg Group, 1997), and it

is the second most popular form of CAM used by children

(Spencer & Jacobs, 1999). Treatments have been shown to be

effective for both common and chronic ailments, such as

allergies (Reilly, Taylor, McSharry, & Aitchison, 1986;

Wiesenauer & Ludtke, 1995), asthma (Reilly, Taylor, Beattie,

Campbell, McSharry, Aitchison, Carter, & Stevenson, 1994),

childhood diarrhea (Jacobs, Jimenez, Gloyd, Gale, &

Crothers, 1994), fibromyalgia (Fisher, 1986; Fisher,

Greenwood, Huskisson, Turner, & Belon, 1989), hyperactivity

(Frederick, 1998; Reichenberg-Ullman, 1997; Ullman, 1988),

influenza (Davies, 1971; Ferley, Zmirou, D'Adhemar, &

Balducci, 1989), irritable colon (Owen, 1990), migraines

(Brigo & Serpelloni, 1991), and rheumatoid arthritis

(Gibson, Gibson, MacNeill, & Buchanan, 1980). Two doctors of

naturopathy claim a 70% success rate using homeopathic

methods for at least one year with nearly 1,000 children

with ADHD (Reichenberg-Ullman & Ullman, R., 1996). Evidence

supporting its efficacy in placebo controlled-trials is

surfacing (Linde, Clausius, Ramirez, Melchart, Eitel,

Hedges, & Jonas, 1997). A meta-analysis of 25 years of

controlled clinical studies using homeopathic medicines

produced the following results: 81 showed homeopathic

medicines were effective, 24 showed they were ineffective,

and 2 were inconclusive (Kleijnen, Knipschild, & ter Riet,


The use of homeopathy has increased over the last few

decades, and its popularity is evidenced throughout the

world, especially in Europe, Latin American, and Asia

(Jacobs & Moskowitz, 1996). One-fourth of all physicians in

Germany use homeopathy (Ullman, 1991), while one-third of

general practice physicians in France engage in its use

(Bouchayer, 1990). Sales of homeopathic remedies in the

United States increased by 1,000 percent during the 1980s

(Jacobs & Moskowitz, 1996). In 1995, retail sales of these

medicines were estimated at $201 million and growing at a

rate of 20 percent (Stehlin, 1997).

Herbal Medicine

Interest in and actual use of herbs has dramatically

increased during the last two decades. Fifteen years ago,

none of the top 250 pharmaceutical companies had a program

to investigate plant-based medicines, although over half now

have programs to examine their efficacy (Vincent & Furnham,

1997). Despite the utilization of a large number of herbal

medicines, less than 10% of the estimated 250,000 flowering

plant species have been investigated for their scientific

potential (Vincent & Furnham, 1997). Thus, choosing new

herbs for investigation can be difficult. Research continues

to uncover possible treatments and cures among these plants,

guided by knowledge of the plants currently used by

different cultural groups for medical purposes (Meserole,


Herbal remedies are growing in popularity in the United

States. Americans spent $12 billion for herbals, vitamins,

minerals, and sports and speciality supplements in 1997

("Herbal Rx," 1999). This figure is approximately 30%

greater than that from two years earlier.

Herbal medicines offer a viable alternative treatment

for a variety of disorders (Cassileth, 1998). They have

earned the attention of parents and medical professionals

interested in finding an alternative to pharmacological

treatment of ADHD (Weintraub, 1997). Researchers have

identified two particular herbs, Ginkgo biloba and lemon

balm, that are useful in treating symptoms commonly

associated with ADHD (Weintraub, 1997).

Ginkgo biloba

Ginkgo biloba is one of the oldest living tree species,

dating back over 200,000 years. Much of the tree's original

territory was wiped out during the last Ice Age, although

today the tree survives in northern China and Japan (Burton

Goldberg Group, 1997). In China, extracts of the fruit and

leaves of the Ginkgo tree have been used as a remedy for

over 1,000 years (Pang, Pan, & He, 1996).

In Germany, Ginkgo extracts are among the most widely

used herbal medicines (Jones, 1998). Because the extract

increases blood circulation to the brain and increase oxygen

levels in brain tissues, it is used primarily in an effort

to improve mental clarity and alertness (Hobbs, 1991). It

also has been shown to improve the cognitive function of

demented patients (LeBars, Katz, Berman, Itil, & Freedman,


The treatment is somewhat effective for disorders of

the brain, such as dementia and memory impairment ("Boost

Brain Power," 1998; Itil & Martorano, 1995; Kanowski,

Herrmann, Stephan, Wierich, & Horr, 1996; LeBars et al.,

1997; Oken, Storzbach, & Kaye, 1998; Pang et al., 1996; Rai,

Shovlin, & Wesnes, 1991; Soholm, 1998). In a review of 40

controlled trials, nearly all trials reported at least a

partial positive outcome in patients with cerebral

insufficiency (Kleijnen & Knipschild, 1992). Cerebral

insufficiency is a general term for a collection of symptoms

that include difficulties of concentration and memory,

absentmindedness, confusion, lack of energy, depressive

mood, anxiety, dizziness, tinnitus, and headache.

Melissa officinalis

Melissa officinalis, or lemon balm, contains nervine

principles that help restore the balance and function of the

brain and nerve cells. It has a mild relaxing effect, making

it a good treatment for children with hyperactivity

(Anderson & Peiper, 1996; Klein, 1998; Mendola, 1996) and

other symptoms related to ADHD (Bell & Peiper, 1997).

Dietary Supplements

Dietary supplements are used to treat a variety of

disorders and, because they are readily available, are used

by parents wishing to self-treat their children (Weintraub,

1997). Supplements do not cure a disorder; rather, they

treat the symptoms and underlying causes. Many dietary

supplements are used to treat ADHD symptomatology, and


popular choices include grapine, dimethylaminoethanol, L-

Glutamine, and an essential fatty acid.


Grapine is derived from both the bark of the French

Maritime Pine tree and grape seed (Elkins, 1995). Grapine is

very similar to Pycnogenol, a nutritional compound from

France once comprised only of the tree bark but now also

derived from grape seeds (Walji, 1996). Original research

showing the power of Pycnogenol was done with grape seed

extract and is essentially equivalent in function (Eidelman,


Children with ADHD have found grapine somewhat

effective in decreasing their symptoms by normalizing brain

function (Rapp, 1998; Weintraub, 1997). It is a high potency

antioxidant known to cross the blood-brain barrier to

facilitate the flow of oxygen to the brain and central

nervous system, improving problems with inattentiveness and

hyperactivity (Anderson & Peiper, 1996), as well as memory,

recall, and concentration (Bell & Peiper, 1997). It often is

used in France to control symptoms of ADHD. Many Americans

are using it as an alternative to Ritalin (Debroitner &

Hart, 1997).


Dimethylaminoethanol (DMAE) is a choline precursor that

easily crosses the blood-brain barrier. It normally is

present in small quantities in our brains and is thought to

improve memory and learning, intelligence, and to elevate

moods (Weintraub, 1997). Seafood (e.g., sardines, anchovies)

is naturally abundant in DMAE, supporting the notion that

fish is good "brain food". A diet high in seafood will

provide higher than average levels of DMAE and choline to

the brain, ingredients that serve as raw materials for the

production of the neurotransmitter acetylcholine.

Acetylcholine is responsible for conducting nerve impulses

within the brain.


L-Glutamine is an amino acid that penetrates the

barrier separating the brain from the rest of the body's

circulatory system. It helps create the transmitters in the

brain that enhances learning and memory, and has increase

the IQs of mentally impaired children (Rogers & Pelton,

1957). Once inside the brain, it has the unusual ability to

provide fuel for brain cells, thus improving mental

alertness, and clarity of thinking and mood (Cocchi, 1976).

Glutamine has been found to be deficient in children with

Full Text
xml version 1.0 encoding UTF-8
REPORT xmlns http:www.fcla.edudlsmddaitss xmlns:xsi http:www.w3.org2001XMLSchema-instance xsi:schemaLocation http:www.fcla.edudlsmddaitssdaitssReport.xsd