A Primer for School Psychologists and Counselors

By Peter R. Breggin, M.D.

Dr. Peter Breggin, M.D., is a psychiatrist on the Division of Education faculty at John Hopkins University, Editor-in-chief of Ethical Human Sciences and Services: An International Journal of Critical Inquiry, and was selected by NIH to serve as the expert presenter on “Risks and Mechanisms of Actions of Stimulants” at the November 1998 “NIH Consensus Development Conference on Diagnosis and Treatment of ADHD.” He is author of numerous books and articles on stimulant medication and the drug treatment of children, including Toxic Psychiatry (1991) and Talking Back to Ritalin (1998).

School psychologists and counselors can play a pivotal role in decisions about appropriateness of prescribing stimulant medication to children. Advocates of stimulant medication frequently try to “educate” school mental health professionals to make them more enthusiastic about diagnosing Attention Deficit/Hyperactivity Disorder (ADHD) and encouraging medication. Most recommendations for stimulant drugs originate in schools. School psychologists and counselors therefore need a thorough understanding of the mechanism of action of stimulants, as well as their many adverse effects.

Until recently, most of the information has been generated by individuals with strong vested interests in what may be called the “ADHD/stimulant lobby.” As a psychiatrist, my own research into the mechanism of action and adverse effects of drugs dates back several decades. I first wrote extensively about ADHD and stimulant drugs in Toxic Psychiatry (1991) and then again inTalking Back To Ritalin (1998). In November of this year I was invited by NIMH and NIH to be the scientific expert on “Risks and Mechanism of Action of Stimulant Drugs” at the “Consensus Development Conference on ADHD and its Treatment,” sponsored by the two government agencies. This paper draws on the research presented in my books and at that conference (Breggin, 1999, in press). In addition to my clinical work, it also draws on my faculty position at the Johns Hopkins University Department of Counseling in the Division of Education.

Based largely on double-blind placebo-controlled clinical trials and on animal laboratory research, this paper will focus on the emotional and behavioral effects of dextroamphetamine (e.g., Dexedrine, Adderall), methamphetamine (Desoxyn, Gradumet) and methylphenidate (Ritalin). Emphasis will be placed on two relatively ignored areas: the mechanism of action that enforces specific behaviors and adverse drug effects on the central nervous system, mental life and behavior of the child. An overview of all adverse reactions will also be provided.

The Mechanism of Action: Effects on Animals

Stimulant drugs lend themselves readily to suppressing behaviors that are unwanted in the classroom or highly controlled family situations, and for enforcing obsessive-compulsive behaviors that adults desire in the classroom or the controlled family. Animals, like children, have spontaneous tendencies to move about, to explore, to innovate, to play, to exercise and to socialize. Dozens of studies have shown that stimulant drugs suppress all of these spontaneous tendencies, sometimes completely inhibiting them (Arkawa, 1994; Hughes, 1972; Randrupt & Munkvad, 1967; Schiorring, 1971, 1981; Wallach, 1974). In effect, the animals lose their “vitality” or “spirit.” They become more docile and manageable.

Animals, like children, resist boring, routine, rote or meaningless tasks. Stimulant drugs enforce these behaviors in animals, producing what is called stereotypy or perseveration in animal research (Bhattacharyya et al., 1980; Costall & Naylor, 1974; Koek & Colpaert, 1993; Kuczenski & Segal, 1997, Mueller, 1993; Randrup & Munkvad, 1967; Rebec & Segal, 1980; Rebec & Bayshore, 1984; Segal, 1975; Segal et al., 1980; early studies reviewed in Wallach, 1974 and Schiorring, 1979). In human research, it is called obsessive-compulsive or over-focused behavior (see below). For example, instead of struggling to escape a cage, the animal will sit relatively still carrying on rote, useless behaviors, such as compulsive grooming, chewing on its paws or staring in the corner. If the drugged animal does move about, it will pace a constricted area in a purposeless manner.

In summary, in animals stimulant drugs (1) suppress spontaneous and social behaviors, rendering them more submissive and manageable, and (2) enforce perseveration or obsessive-compulsive over-focusing.

The Mechanism of Action: Emotional and Behavioral Effects on Children

The effects of stimulants on children are identical to those in animals. This is not surprising since the basic biochemical or neurological impact is the same. Similarly, the effects on children are the same regardless of the child’s mental state or diagnosis.

Drawing on double-blind studies, Table 1 (insert section) lists the adverse drug reactions (ADRs) of stimulant drugs that lend themselves to being easily mistaken for improvement in the child. The chart is divided into three categories of stimulant ADRs: (1) Obsessive-compulsive ADRs, such as over-focusing, cognitive perseveration, inflexibility of thinking and stereotypical activities; (2) social withdrawal ADRs, such as social withdrawal and isolation, reduced social interactions and responsiveness, and reduced spontaneity and behaviors that are subdued, depressed, apathetic, lethargic and bland.

Firestone et al. (1998) found that 0.5mg/kg of methylphenidate caused marked “deterioration” compared to placebo in several variables, including “sad/happy” (69% of children) and “uninterested in others” (62%). Mayes et al. (1994) found that 18.5% of children on methylphenidate became “lethargic,” displaying symptoms such as “tired, withdrawn, listless, depressed, dopey, dazed, subdued and inactive.” Barkley et al. (1990) found an increased proneness to crying in 10% of children on a low dose of methylphenidate. Schachar et al. (1997) documented that more than 10% of children dropped out due to methylphenidate-induced ADRs, including serious behavioral aberrations such as “sadness and behavior deterioration, irritability, withdrawal, lethargy, violent-behavior,” “withdrawal and mild mania,” and “withdrawal and dysphoria.” Stimulants commonly cause obsessive-compulsive behaviors, including over-focusing, that are similar to stereotypy in animals. In a study of single small doses of methylphenidate on the day of the experiment, Solanto and Wender (1989) found “cognitive perseveration” (over-focusing) in 42% of children. Castellanos et al. (1997) found that 25% of children on methylphenidate developed obsessive-compulsive ADRs. In the most thorough study of the subject, Borcherding et al. (1990) found that 51% of children taking methylphenidate and dextroamphetamine developed obsessive-compulsive ADRs. Some children exhausted themselves raking leaves or playing the same game over and over again. The authors note that these behaviors were sometimes considered improvements in the classroom.

These data in this section, derived from several controlled clinical trials, further confirm the emotional and behavioral suppression caused by stimulant drugs.

More Extreme Emotional and Behavioral Effects

Swanson et al. (1992) reviewed “cognitive toxicity” produced by methylphenidate. They summarize the more extreme effects on children:

In some disruptive children, drug-induced compliant behavior may be accompanied by isolated, withdrawn, and over-focused behavior. Some medicated children may seem “zombie-like” and high doses, which make ADHD children more “somber,” “quiet,” and “still” may produce social isolation by increasing “time spent alone” and decreasing “time spent in positive interaction” on the playground. (p.15)

Arnold and Jensen (1995) also comment on the “zombie” effect caused by stimulants:

The amphetamine look, a pinched, somber expression, is harmless in itself but worrisome to parents, who can be reassured. If it becomes too serious, a different stimulant may be more tolerable. The behavioral equivalent, the “zombie” constriction of affect and spontaneity, may respond to a reduction of dosage, but sometimes necessitates a change of drug. (p.2307)

The “zombie” effect is mentioned by a number of other investigators (e.g., Fialkov & Hasley, 1984, p. 328; Swanson et al., 1992, p. 15). It is a more extreme manifestation of the supposedly “therapeutic” effect that makes a child more compliant, docile and easier to manage. When a child seems more compliant in class or seems to attend more readily to boring, rote activities, the child is experiencing an adverse drug reaction. The seeming “improvement” is an expression of a continuum of drug toxicity with the zombie effect at one extreme. The toxicity is considered “therapeutic” unless it becomes so extreme that the child seems bizarre or disabled.

Excitatory Adverse Effects

As already described in detail, routine stimulant doses given to children or adults commonly cause ADRs that seem paradoxical, such as depression, lethargy and apathy (Tables 1 and 2; see insert). It is uncertain why stimulants at clinical doses so commonly cause these suppressive effects. Stimulants also cause more classic signs of over-stimulation or excitation, such as anxiety, agitation, aggression and insomnia, as well as manic psychoses the more suppressive effects, as in a mixture of agitation and depression.

Frequently stimulants cause tachycardia and cardiac arrhythmias and can even weaken heart muscle (Ishiguro & Morgan, 1997; Henderson et al., 1994). The FDA has received many reports of methylphenidate-induced heart attack (Food and Drug Administration, 1997).

The overall list of stimulant ADRs is much too extensive for inclusion in this paper. Table 2 (insert) draws on several independent sources to present an overview. More detail and further documentation for all of the adverse drug effects mentioned in this paper can be found in my reviews (Breggin, 1998; 1999, in press). Many doctors seem unaware of the varied nature of stimulant ADRs. Often they mistake these drug reactions for the surfacing of new psychiatric disorders in the child and mistakenly increase the dose or add further medications, instead of stopping the stimulants.

Gross and Irreversible Brain Dysfunction

In addition to the many serious central nervous system ADRs that are apparent in the child’s behavior, stimulants also cause gross brain dysfunction. Methylphenidate, for example, in routine doses caused a 23%-30% drop in blood flow to the brain in volunteers (Wang et al., 1994). All stimulants directly disrupt at least three neurotransmitter systems (dopamine, norepinephrine and serotonin). There is strong evidence that stimulant-induced biochemical changes in the brain can become irreversible, especially in regard to amphetamine and methamphetamine, which can cause permanent neurotransmitter system changes and cell death (Battaglia et al., 1987; Melega et al. (1997a, b; Wagner et al., 1980). One study demonstrated that adults can develop atrophy of the brain after being treated with stimulants as children (Nasrallah et al., 1986). These potentially disastrous irreversible effects have been ignored in most reviews (see details in Breggin, 1998; updated in 1999, in press).

Through a combination of anorexia and disruption of growth hormone, stimulants also inhibit growth, including the growth of the brain (reviewed in Breggin, 1998; 1999, in press; Dulcan, 1994; Jacabvitz et al., 1990). Bathing a child’s growing brain in toxic chemicals must ultimately impair its development.

Stimulants are highly addictive. The U.S. Drug Enforcement Administration (DEA) places methylphenidate, amphetamine and methamphetamine into Schedule II along with cocaine and morphine as the most addictive drugs used in medicine. The DEA and the International Narcotics Control Board have both issued warnings about the danger of widespread stimulant prescription in North America (Drug Enforcement Administration, 1995; International Narcotics Control Board have both issued warnings about the danger of widespread stimulant prescription in North America (Drug Enforcement Administration, 1995; International Narcotics Control Board, 1996; 1997). The United States uses 90% of the world’s methylphenidate. Typical of addictive drugs, they often cause withdrawal or rebound. Rebound commonly occurs after only one or two doses in normal children, and it can last many hours and even more than a day (Rapport et al., 1978). During rebound, the child’s original ADHD-like symptoms may become worse than before the drug was ever taken, including hypomania and mania. Even when children do not become addicted to stimulants, they sometimes give them away or sell them to friends who abuse them.

Stimulants commonly cause tics and other abnormal movements, and sometimes these become irreversible (Lipkin et al., 1994). Often the tics occur along with obsessive-compulsive symptoms. Too often, drug-induced ADRs lead mistakenly to the prescription of other psychiatric drugs rather than to the termination of the stimulant.

ADHD and the Rationalization of Stimulant Effectiveness

The concept of ADHD was developed to rationalize a pre-existing motivation with medicine and psychology to use stimulant drugs to control the behavior of children. From the beginning, the focus was on classroom settings in which one-to-one attention is not available. ADHD as a diagnosis evolved as a convenient list of various behaviors that tend to disrupt a classroom and to require additional or special attention from teachers or other adults (Armstrong, 1995; Johnson 1998). Almost every behavior that tries a teacher’s ability or patience, or drains a teacher’s energy and attention, has been put into the diagnosis.

A simple reminder about the official criterion for ADHD in the Diagnostic and Statistical Manual (American Psychiatric Association, 1994, p. 84) should make clear how the list focuses on behaviors that interfere with an orderly, quiet, controlled classroom. The first criterion under hyperactivity is “often fidget with hands or feet or squirms in seat” and the second is “ often leaves seat in classroom or in other situations in which remaining seated is expected.” The first criterion under impulsivity is “ often blurts out answers before questions have been completed” and the second is “ often has difficulty awaiting turn.” Under inattention the first criterion is “often fails to give close attention to details or makes careless mistakes in schoolwork, work, and other activities.”

None of the ADHD criteria are relevant to how the child feels . Mental and emotional symptoms, such as anxiety or depression, are not included. All of the behaviors in the ADHD diagnosis are commonly displayed by children in groups where they are frustrated, anxious, bored or receive too little attention. Individually, each of the behaviors represents normal developmental stages. Of course, the behaviors can become exaggerated. A child can become extremely hyperactive, impulsive or inattentive. These behaviors, even when extreme, do not constitute a syndrome—-a consistent pattern of symptoms related to a specific cause.

In Talking Back to Ritalin , I have catalogued dozens of “causes” for ADHD-like behavior. Most commonly it is the expression of a normal child who is bored, frustrated, frightened, angry, emotionally injured, undisciplined, lonely, too far behind in class, too far ahead of the class or otherwise in need of special attention that is not being provided. More rarely, the child may be suffering from a genuine physical disorder, such as a head injury or thyroid disorder, that requires special medical attention rather than stimulant medication.

ADHD as Conflict

ADHD-like behaviors in a child almost always indicate a conflict between the child and adults in the child’s life, especially adult expectations for submissive, conforming or compliant behavior. But instead of being used as a signal for the need for conflict resolution, the diagnosis is used as a justification for drugging the diagnosed member of the conflict, the powerless child.

With more concern for the child, the very same behaviors in any child could be used to focus attention on the need for change in the behavior of the adults in the conflict. The seemingly exaggerated hyperactivity, impulsivity or lack of attentiveness in the child can and should become a signal for the adults in the child’s life to find, identify and respond to the child’s genuine needs for rational discipline, unconditional love, play, exercise and engaging education. An effective teacher, parent or coach would do exactly that. Signs of hyperactivity, impulsivity and inattention in a youngster are used to indicate the need for greater, more focused attention to the child.

Stimulant drugs, as we have seen, flatten the child’s behavioral signal system. The child literally becomes neurologically unableto express feelings of boredom, frustration, distress or discomfort by displaying hyperactivity, impulsivity or inattention. Adults can then feel justified in teaching the class or managing the group without attending to the child’s individual and often varied needs.

Evidence for Effectiveness

Reviews by stimulant drug advocates routinely demonstrate that stimulants have no positive long-term effects whatsoever on any aspect of a child’s behavior. Short-term (a few weeks or months), they can suppress behavior, but they do not improve academic performance or learning. Based on the most extensive review in the literature, Swanson (1993) concluded:

Long-term beneficial effects have not been verified by research. Short-term effects of stimulants should not be considered a permanent solution to chronic ADD symptoms. Stimulant medication may improve learning in some cases but impair learning in others. In practice, prescribed doses of stimulants may be too high for optimal effects on learning to [to be achieved] and the length of action of most stimulants is viewed as too short to affect academic achievement. (p. 44)
Swanson (1993) defined “short-term” as 7-18 weeks. He also summarized:

No large effects on skills or higher order processes— Teachers and parents should not expect significantly improved reading or athletic skills, positive social skills, or learning of new concepts.

No improvement in long-term adjustment— Teachers and parents should not expect long-term improvement in academic achievement or reduced antisocial behavior. [italics in original] (p. 46)

Swanson is not alone in his conclusions. Popper and Steingard (1994) state:

Stimulants do not produce lasting improvement in aggressivity, conduct disorder, criminality, education achievement, job functioning, marital relationships, or long-term adjustment. (p. 745)

Richters et al. (1995) from NIMH conclude: “The long-term efficacy of stimulant medication has not been demonstrated for anydomain of child functioning” (italics in original, p. 991). They conclude that there is no evidence for even short-term positive effects on academic performance.

Conclusion

Stimulant drugs have two basic effects on animals and children regardless of their mental status. First, stimulants reduce all spontaneous and social behavior. This makes the child more docile, submissive and manageable (compliant). Second, stimulants enforce perseverative, obsessive-compulsive or over-focused behavior. This makes the child more easily led or compelled to do rote, boring activities. These twin toxic effects are readily misinterpreted as “improved behavior” in highly structured or controlled environment where children are given insufficient or inappropriate attention and where their genuine needs are being ignored. As a result of toxicity, stimulants suppress a child’s behavior in a global fashion that has nothing to do with any diagnosis or disorder.

Stimulant drugs also produce a wide variety of other adverse effects. By causing anorexia and by disrupting growth hormone, they suppress the growth of the body, including brain size and development. They cause severe biochemical imbalances in the developing brain that can become permanent. They often worsen ADHD-like symptoms and can cause psychoses.

The ADHD diagnosis is tailored to justify the use of stimulants for the behavioral control of children in groups. It enumerates behaviors that healthy children often display in structured-over-controlled groups in which their individual needs are unmet.

Ultimately, by suppressing emotional and behavioral signals of distress and conflict, stimulants allow adults to ignore the needs of children in favor of creating a controlled environment. Meanwhile, stimulants do not improve academic performance and provide no long-term improvement in any aspect of a child’s behavior or life.

School psychologists and counselors should strongly discourage the use of stimulant drugs for treating “ADHD” and other emotional or behavioral problems that surface in the classroom. Instead, more effort should be made to identify and to address the genuine individual needs of the children in our schools whether or not they are signaling their distress or conflict with ADHD-like behaviors.

Abbreviated Bibliography*

Borcherding, B.V., Keysor, C.S., Rapoport, J.L., Elia, J., Amass, J. (1990). Motor/vocal tics and compulsive behaviors on stimulant drugs: Is there a common vulnerability? Psychiatric Research , 33, 83-94

Breggin, P.R. (1998). Talking back to Ritalin . Monroe, ME: Common Courage Press

Breggin, P.R. (1999, May, in press). Psychostimulants in the treatment of children: Risks and mechanism of action. Ethical Human Sciences and Services, 1 (1).

Firestone, P., Musten, L.M.,Pisterman, S., Mercer, J., & Bennett, S. (1998). Short-term side effects of stimulant medications in preschool children with attention-deficit/hyperactivity disorder. A double-blind placebo-controlled study. Journal of Child and Adolescent Psychopharmacology, 8, 13-25.

Melega, W.P., Raleigh, M.J., Stout, D.B., Huang, S.C., & Phelps, M.E. (1997a). Ethological and 6-[18]fluoro-L-DOPA-PET profiles of long-term vulnerability to chronic amphetamine. Behavioural Brain Research , 84, 258-268.

Melega, W.P., Raleigh, M.J., Stout, D.B., Lacan, G., Huang, S.C., & Phelps, M.E. (1997b). Recovery of striatal dopamine function after acute amphetamine- and methamphetamine-induced neurotoxicity in the vervet monkey. Brain Research , 766, 113-20.

Nasrallah, H., Loney, J., Olson., S., McCalley-Whitters, M., Kramer, J., & Jacoby, C. (1986). Cortical atrophy in young adults with a history of hyperactivity in childhood. Psychiatry Research , 17, 241-246.

Schiorring, E. (1981). Psychopathology induced by “speed drugs”. Pharmacology Biochemistry & Behavior , 14, Suppl. 1, 109-122.

Swanson, J.M., Cantwell, D., Learner, M., McBurnett, K., Pfiffner, L & Kotkin, R. (1992, fall). Treatment of ADHD: Beyond medication. Beyond Behavior 4, 13-16 and 18-22.

Wang, G-J, Volkow, N., Fowler, J., Ferrieri, R., Schlyer, D., Alexoff, D., Pappas, N., Lieberman, J., King, P. Warner, D., Wong, C., Hitzemann, R., & Wolf, A. (1994). Methylphenidate decreases regional cerebral blood flow in normal human subjects. Life Sciences , 54, 143-146.

National Association of School Psychologists Psychostimulant Effects on Children

Peter R. Breggin, 1998                             

 

Table 1: Adverse Drug Reactions From Stimulants

Mistakenly Identified As “Beneficial.”

Data From 20 Controlled Clinical Trials

Obsessive Compulsive ADRs	Social Withdrawal ADRs	Behaviorally Suppressive ADRs
Stereotypical activities (1,3)Obsessive-compulsive behavior (1,3,7,17)Cognitive perseveration (7)Inflexibility of thinking (9) Over-focusing or excessive focusing (7, 9)	Social withdrawal and isolation (3, 12, 14)General dampening of social behavior (19)Reduced social interactions, talking, or sociability (3, 8, 10*, 15*, 18**, 19)Decreased responsiveness to parents & other children (10*, 18**, 19)Increased solitary play (4, *8)Diminished play (15*)	Compliance, especially in structured environments (4*, 8*, 10*, 11*)Reduced curiosity (7)Somber (2)Subdued (3)Apathetic; lethargic: “tired, withdrawn, listless, depressed dopey, dazed subdued and inactive” (3; also 12, 20)Bland, emotionally flat, affectless (5, 16)Depressed, sad, easy/frequent crying (3, 4, 12, 13, 18**, 20) Little or no initiative or spontaneity (5) Diminished curiosity, surprise, or pleasure (5) Humorless, not smiling (5) Drowsiness (18) Social inhibition—passive and submissive behaviors (6)

*Considered positive or therapeutic by the source

** Considered possibly positive or therapeutic by source

1. Borcherding et al. (1990) 11. Cotton and Rothberg (1988)

2. Tannock et al. (1989) 12. Schachar et al. (1997)

3. Mayes et al. (1994) 13. Barkley et al. (1990)

4. Schleifer et al. (1975) 14. Handen et al. (1990)

5. Rie et al. (1976a) 15. Barkley and Cunningham (1979)

6. Granger et al. (1993) 16. Whalen et al. (1989)

7. Solanto and Wender (1989) 17. Castellanos, et al. (1997)

8. Cunningham and Barkley (1978) 18. Firestone, et al (1998)

9. Dyme et al. (1992) 19. Buhrmestar, et al. (1992)

10. Barkley et al. (1985) 20. Gittelman-Klein et al. (1976)

 

Table 2: Adverse Effects Caused by Methylphenidate and Amphetamines

 

 

Cardio- Vascular	Central NervousSystem	Gastro- Intestinal	Endocrine/ Metabolic	Other	Withdrawal & Rebound
PalpitationsTachycardiaHypertensionArrythmiasChest Pain [Cardiac Arrest]	Psychosis with hallucinations(skin crawling or visions)[mania]Excessive CNS stimulation[convulsions]Drowsiness, “dopey,”less alert Confusion Insomnia Agitation, anxiety, irritability, nervousness [hostility] Dysphoria (esp. at higher doses) Impaired cognitive test performance (esp. at higher doses) Dyskinesias, tics, Tourette’s Nervous habits (e.g. picking at skin, pulling hair) Stereotypy and compulsions Depression, emotional oversensitivity, easy crying Decreased social interest Zombielike constriction of affect and spontaneity* Amphetamine look (pinched, somber expression)**	AnorexiaNauseaVomitingStomach ache, crampsDry mouth Constipation Bad taste**** Diarrhea****	pituitary dysfunction, including growth hormone and prolactin]Weight lossGrowth suppressionGrowth retardationDisturbed sexual function****	Blurred vision HeadacheDizzinessHypersensitivityReaction with rash, conjunctivitis, or hives[hair loss]*** Exforiative Dermatitis*** Anemia*** Leukopenia*** Enuresis*** Fever *** (unexplained) Joint pain*** Unusual sweating***	InsomniaEvening crashDepressionOveractivity and irritabilityRebound ADHD Symptoms

Sources Combination of Dulcan (1994. table 35-6. p. 1217). Arnold and Jensen (1995. Table 38-5. p. 2306). Maxman and Ward (1995. pp 365-6). And Drug Enforcement Administration (1995B. p 23) Any additional material indicated by brackets

*”Zombie” references from Arnold and Jensen (1995. Table 38-5. p 2306. Table 38-7. p 2307. and column 2. p 2307).

Swanson. et al. (1992. p 15). Fialkov and Hasley (1984. p 328)

**Arnold and Jensen (1995)

***For methylphenidate only

****For dextroamphetamine only

Responses to Common Professional Statements Made to Parents About Their Children Doctors, mental health professionals, and educators often say things about “Attention Deficit Hyperactivity Disorder” (ADHD) that are unproven. These same professionals often say things about drugs that are supposed to treat “ADHD” that are not true. This brochure reveals and responds to six common lies or misleading statements you might be told.

1. “ADHD” is a brain-based biological disorder, caused by a chemical imbalance in your child’s brain. The simple fact is that there is absolutely no reliable test that accurately distinguishes between children that are supposed to have “ADHD” and those that are not. The simplest way to counter this statement is to ask for a medical test to prove that your child has “ADHD.” Many physicians will respond to your request by saying that the test is too expensive. You must persevere and ask that your insurance company pay for those tests. You can also ask any professional to show you the article or articles in the scientific literature that proves the existence of a confirmatory physical or chemical abnormality that validates the existence of ADHD as a medical disease. The plain truth is that no such article exists. If someone gives you an article, please share and discuss it with someone who can critically analyze it.

2. The symptoms are clearly printed in a book called the DSM-IV which stands for the Diagnostic and Statistical Manual of the American Psychiatric Association, Fourth Edition. Yes, the “symptoms” are printed there, but as described in point 1, these alleged “symptoms” in no way prove that ADHD is a disease. Furthermore, these “symptoms” are actually nothing more than someone’s observations of your child’s behavior, and the truth is they are not even reliable as behavioral observations. To be reliable, people must agree that your child has “ADHD.” An article in the prestigious Journal of the American Academy of Child and Adolescent Psychiatry , printed in September 2000, says that the diagnosis is very unreliable. Many children who are supposed to be “ADHD” are not identified, and many children who are identified as not having ADHD are identified as having it. This means that research done to support the identification and treatment of ADHD that uses the DSM-IV definition totally lacks support. It also means that no medical person correctly diagnoses ADHD . ADD and ADHD are politically manufactured concepts, created by committees of the American Psychiatric Association. ADD was created in 1980, ADHD in 1987. The plain truth is that they are not real diseases in any legitimate scientific meaning of the term disease. To declare otherwise is not medicine; it is fraud.

3. Medication (such as Ritalin) corrects the chemical imbalance. Remember first there is no demonstrated chemical imbalance (see point 1). The brain does have chemicals that help cells “talk” to each other that are called neurotransmitters. However, when a professional says that one of these chemicals, usually a variety of something called Dopamine, needs some kind of correction, and that they have just the right kind of medicine to do this, you are being misled. This idea assumes that nerves only “talk” to nerves that use the same chemicals. That is absolutely positively false. It is a lie at worst, a gross over simplification at best. It is unethical for a medical professional to state or imply otherwise.

4. The medication (e.g., Ritalin) is a mild stimulant with few or no side effects. “Side effect” is a euphemism; all drugs (alleged medications) have a variety of effects. It is vitally important that you personally research the effects of any drug you might consider for your child. Go to the Physicians Desk Reference (PDR), ask your neighborhood pharmacist to print you a list of side effects, and/or get the references listed at the end of this brochure. You need to find out about all possible effects — those considered common (such as nervousness, insomnia, and loss of appetite, and those considered rare (such as toxic psychosis and death). The lie that Ritalin is a mild stimulant is even more difficult to maintain since a recently concluded study at the Brookhaven National Laboratory (BNL), and published in the Journal of the American Medical Association, not only confirmed the similarities of cocaine and Ritalin, but found that Ritalin is more potent than cocaine in its effect on the dopamine system in the brain. Referring to Ritalin as “kiddy cocaine” is not a joke.

It is important to know that the use of stimulant medication can mask the symptoms of potentially fatal disorders that could be causing your child’s problems with inattention or activity. It is also important to know that if your child really is having problems with attention and concentration, this could be caused by problems within the class environment (no work breaks, poor environmental temperature regulation, poor acoustics, poor lighting, poor teaching, etc.) or within other areas of your child’s life (nutrition, TV and video overstimulation, family stress and conflict, etc.).

5. If your child had diabetes, you would give him insulin, wouldn’t you? This is one of the most common, and heinous statements that doctors and other professionals make to parents. It is a heavy guilt trip telling parents they are negligent and irresponsible if they don’t go along with the pressure to drug their children. Remember clearly, as described in point 1 above, that ADHD is in no way a real disease; to imply otherwise is a lie. The truth is that protecting your children from toxic drugs is being completely responsible. It is those who advocate these drugs for children who are abdicating responsibility and avoiding the challenge of truly meeting the needs of our children.

6. You are going against medical advice . Physicians work for you. There is something called informed consent. If they have given you false or inaccurate information, or attempted to deceive you in any way, then the advice that they have given is faulty and you can justifiably take matters (concerning “ADHD”) into your own hands. It is your responsibility to protect the short and long-term health, well-being and development of your child.

Steve Edelman, M.A.

John breeding, PhD.

 

Please copy and distribute widely.

 

Resources

Breeding, J. The Wildest Colts Make The Best Horses . Bright Books, 1996.

Breggin, P. Talking Back To Ritalin . Common Courage Press, 1998.

 

 

ADHD Classification

I am Dr. Dave Walker from the International Center for the Study of Psychiatry and Psychology (ICSPP) founded by Peter Breggin, MD.

Along with a group of 11 psychologist/members of the American Psychological Association, we recently sent a letter to directors of a ‘brochure project’ on ADHD in Division 29, the division of psychotherapy (of all places!).

The gist of this letter was to refute 3 deceptive statements within this brochure and to seek revision of the brochures before they are released to the public.

Our letter was received respectfully and our request to revise the brochures appears to be ignored.

Therefore, we are seeking to post and distribute our letter and its objections to the statements as widely as possible

May 15, 2003
Dear Dr. Rubenstein:

This is a reply to your letter of March 17, 2002. The letter you sent was a reply to Dr. Galves’ letter of February 16, 2002 in which he expressed concern about the following three statements that are included in the brochures on ADHD that were published by Division 29 (Psychotherapy) in conjunction with Celltech Pharmaceuticals Inc:

1. “ADD/ADHD is generally considered a neuro-chemical disorder.”

2. “Most people with ADD/ADHD are born with the disorder, though it may not be recognized until adulthood.”

3. “ADHD is not caused by poor parenting, a difficult family environment, poor teaching or inadequate nutrition.”

Dr. Galves’ basic objection to these statements was that there is no scientific evidence to support them.

In your letter to Dr. Galves, you included information and references that were provided to you by Dr. Robert J. Resnick and Dr. Kalman Heller. We have reviewed the information and references you sent and continue to find that they do not contain scientific evidence for the statements in question. We submit to you the following analysis of the information and references you provided as well as additional information and references.

“ADD/ADHD is generally considered a neuro-chemical disorder”

Although ADD/ADHD may be generally considered by popular opinion to be a ‘neuro-chemical disorder,’ there is no scientific evidence to back this claim. The scientific evidence to which you refer (which is in itself inconsistent), merely suggests that the biochemistry and brain physiology of individuals diagnosed with ADD/ADHD is different from that of individuals not diagnosed with the disorder (Goldstein and Goldstein, 1998; Barkley, 1990; Ross and Ross, 1982 ). However, the statement you have made in your letter implies that ADD/ADHD is caused by these biological dynamics. Elsewhere, you also state that “evidence to date suggests a biological cause.” Again, our review of the same references you have cited does not support either of these claims.

All that we can derive from our careful review of these citations is that there is evidence of a correlation between the biological dynamics and the ADHD category. Because this evidence is entirely correlational and the brain is a living, functioning organ constantly responding to its environment with complex neurochemical and other neurofunctional changes, it is just as likely (and perhaps more likely) that the biological dynamics are a result of an interplay of emotions, thoughts, intentions and behavior experienced by the diagnosed individuals. Please consider the following research findings in relation to this perspective:

• Jeffrey Schwartz et.al of UCLA (1996) found that a group of people suffering from obsessive-compulsive disorder had “abnormalities” in their brains. Half of the group received drug therapy; the other half received cognitive behavioral “talk therapy.” All of the patients improved and, when Schwartz checked their brains, he found that their brains had changed in the same ways. Presumably, the cognitive-behavioral therapy had the same impact on the physiology of the brain as did the biological therapy.
• Mark Rozensweig et.al. (1972) found that the brains of monkeys raised in rich environments had a greater number of neurons and more complex interneuronal connections than the brains of monkeys raised in more impoverished environments.
• Franz Alexander (1984) found the people who had been deprived of support, affirmation and ample time while growing up were much more likely to suffer from overactive thyroids than people who were brought up in more nourishing environments
• James Pennebaker (2000) found that students who were assigned the task of writing about traumas they had suffered and about their fears, relationships and desires had stronger immune systems and were healthier than students who were assigned to write about less emotionally charged topics.

Studies have demonstrated a relationship between vulnerability to depression and the following psychological variables:

• Suffered trauma at an early age (Kramer, 1993);
• Have a high need for and/or lost an important relationship (Johnson and Roberts, 1995);
• Use a ruminating style of thinking (Lehmicke & Hicks, 1995);
• Score low on self-esteem and high on stress (Kreger, 1995);
• Have lost control over important variables in their life (Jensen, Cardello & Baun, 1996);
• Hold a stable rather than flexible attributional style (Seligman, 1975).
• Score high on a scale of self-defeating personality (McCutcheon, 1995).
• A recent study by Cornell researchers found that a two-week course in remedial reading significantly changed the brainphysiology of dyslexic students (Rappaport, 2003).
• A recent study by Seattle psychiatrist Arif Khan (Khan et al., 2002) indicated a large overlap in effect between placebo and antidepressants in the original FDA trials of these drugs. Leuchter and fellow UCLA researchers (Leuchter et al., 2002) found that these placebo effects result in detectable changes in brain function. Similar studies have not been undertaken with ADD/ADHD subjects nor are individuals who may have already experienced temporary or permanent brain changes as a result of stimulant treatment typically excluded or controlled for in ADD/ADHD research (Leo & Cohen, 2002).
• Baumeister and Hawkins (2001) undertook an exhaustive review of efforts to substantiate a neuroanatomical site or sites related with ADD/ADHD through structural and functional neuroimaging techniques such as PET, single positron scanning, MRI, and electrophysiological measurement. These researchers stated that while “[t]here seems to be a consensus among experts today that ADHD is associated with structural and/or functional abnormalities in the brain”, they could only conclude that “the present review indicates that the neuroimaging literature provides no convincing evidence for the existence of abnormality in the brains of persons with ADHD” (p. 7-8).

The above evidence contradicts your premises. The scientific principle of parsimony compels us to arrive at a completely different set of conclusions than you have—in which the biological dynamics you cite as correlating with ADD/ADHD at the brain level can be more accurately depicted as a result of psychological and environmental variables than a neurodevelopmentally damaged, diseased, or dysfunctional brain. The mind-body dynamic that has been most thoroughly researched in this regard is the human stress response. The human stress response is a profound, complex biochemical and physiological dynamic that is preceded by a perception of threat and a cognition that the threat is real and needs to be dealt with. The psychological variables of the human stress response precede and likely cause the physiological variables, rather than the converse (Everly, 1989; Selye, 1974).

Calling ADHD a “neurochemical disorder” with a “biological cause” implies that it has nothing to do with how a child thinks, feels, reacts, intends, perceives, adjusts and responds. It implies that the behaviors are not under the control of the child or those within the child’s world and have nothing to do with how the child finds and makes meaning in that world. That is a fundamental error contradicted by those of us who, like you, also work very closely with children and families everyday.

“Most people with ADD/ADHD are born with the disorder, though it may not be recognized until adulthood.”

The implication here is that ADD/ADHD is a genetic disorder. There is a body of research that purports to demonstrate that this disorder is essentially a result of genetic factors. Most of that research has used studies that compare interclass correlations between the rates of the disorder in monozygotic twins and dizygotic twins. Virtually all of this research has found significantly higher correlations between monozygotic twins than between dizygotic twins (Goodman & Stevenson, 1989; Pauls, 1991; Biederman et al., 1992; Gillis et al., 1992; Edelbrock et al., 1995; Sherman et al., 1997). However, this kind of research suffers from the following serious deficiencies:

• All of this research is based on the assumption that monozygotic twins and dizygotic twins are raised in equivalent environments. That assumption is erroneous. As Jay Joseph (2003) has explained:
• Identical twins spend more time together than fraternals, and more often dress alike, study together, have the same close friends and attend social events together. James Shields, in his 1954 study of normal twin school-children found that 47% of the identical twins had a ‘very close attachment’ which was true for only 15% of fraternal twins . . . According to Kringlen’s (1967) survey, 91% of identical twins experienced ‘identity confusion in childhood’ which was true for only 10% of fraternal twins. Kringlen also found that identical twins were more likely to have been considered as alike as two drops of water (76% vs. 0%), ‘brought up as a unit’ (72% vs. 19% and ‘inseparable as children’ (73% vs. 19%). Sixty-five percent of identical twins were found to have an ‘extremely strong’ level of closeness which was true for only 19% of the fraternal pairs (p. ).

Since the equal environment assumption is not valid, the correlations between monozygotic twins are just as likely a result of environmental factors as of genetic factors.

Findings of genetic influence over behavior are confounded by the fact that genes direct the synthesis of protein and protein synthesis can be affected by environmental factors such as stress, trauma and lack of parental responsiveness (Hubbard & Wald, 1993). The process of gene expression is much more complex than is suggested by stories in the popular press (Commoner, 2002). Thus, the process through which genes influence the behavioral characteristics of a person is itself greatly influenced by environmental factors.

In order to scientifically demonstrate genetic etiology for any trait, the precise genetic mechanism involved must be identified. As Ross and Ross (1982) point out:

“The only procedures that can precisely define a genetic mechanism are segregation studies which could only be done with humans under very unusual circumstances and linkage studies which would require the identification of the genetic marker associated with hyperactivity….and these are possibilities for which there is as yet no evidence.” (p. 73, 74)

These flaws cast doubt on the validity of the research that purports to show a genetic etiology for ADD/ADHD. Even without considering these powerful contaminating factors and obstacles, the research on genetic factors in ADHD accounts for no more than 50 % of the variance. This is hardly a reasonable basis for your declaration that ADD/ADHD is present at birth.

A second approach to demonstrating genetic etiology is by using research on the correlation between infant temperament (Thomas and Chess, 1977) and later diagnosis of ADD/ADHD. Some theorists have suggested that such temperament factors as activity level, threshold of responsiveness, intensity of reaction, distractibility and attention span and persistence of these elements might be associated with characteristics of behavior disorders such as ADD/ADHD later on. Thomas and Chess (1977) indicated, for example, that “features of temperament played significant roles [emphasis ours] in development of childhood behavior disorders.” However, those same researchers concluded that, “in no case did a given pattern of temperament, as such,result in [emphasis ours] behavioral disturbance. Deviant development was always the result of the interaction between a child’s individual makeup and significant features of the environment.” (p. 40). Indeed, the most carefully administered study of this factor found that “the contributions of family characteristics and pre-natal/perinatal characteristics are outweighed by the contribution of constitutional factors (hyperactivity in the family, chronic illness as a child and temperament characteristics) and by the home environment domain (measures of achievement press, provision of early learning activities and parent-child interactions) [emphasis ours]” (Lambert & Harsough, 1984 )

A third approach to inferring genetic etiology of ADHD is research that compares the incidence of ADHD and other psychiatric disorders in the relatives of children diagnosed with ADHD with the incidence of such disorders in relatives of children not diagnosed with ADHD (Safer, 1973; Biederman et al., 1986; Pauls, 1991). This research is confounded by the failure to control for the many environmental factors that could also explain the intergenerational transmission of mental disorders in families. Research on attachment dynamics and trauma demonstrate the profound influence that parent-child relationships in the first months of life have on the mental health of individuals. (Holmes, 1995; Bretherton, 1995; Crittenden, 1995; Lewis, Amini & Lannon, 2000; Herman, 2000; van der Kolk, McFarlane & Weisath, 1996). None of the research on the incidence of ADHD in families controls for these crucial factors.

Research and common sense confirm that genetic inheritance must have some influence over temperament and, therefore, over the behaviors that characterize ADHD. However, research also demonstrates that genetic influence is not a major factor. As three psychiatrists Lewis, Amini and Lannon (2000) put it:

Genetic information lays down the brain’s basic macro-and microanatomy; experience then narrows still-expansive possibilities into an outcome. Out of many, several; out of several, one……While genes are pivotal in establishing some aspects of emotionality, experience plays a central role in turning genes on and off. DNA is not the heart’s destiny; the genetic lottery may determine the cards in your deck, but experience deals the hand you can play…..Like most of their toys, children arrive with considerable assembly required…A child’s brain cannot develop normally without the coordinating influence that limbic communication furnishes. The coos and burbles that infants and parents exchange, the cuddling, rocking, and joyous peering into each other’s faces look innocuous if not inane; one would not suspect a life-shaping process in the offing. But from their first encounter, parents guide the neurodevelopment of the baby they engage with. In his primal years, they mold a child’s inherited emotional brain into the neural core of the self.” (, pp. 149-153)

A balanced review of this research indicates that there is no scientific evidence that ADD/ADHD is present at birth as you have claimed and that genetic factors are, at best, a minor influence over the behaviors that characterize ADD/ADHD.

“ADHD is not caused by poor parenting, a difficult family environment, poor teaching or inadequate nutrition. ”

In fact, a preponderance of the scientific evidence demonstrates that ADHD is significantly associated with poor parenting, difficult family environments and inhumane and oppressive school and community environments. Researchers have found an association between the behavioral characteristics of ADHD and the following characteristics of parenting and family environments:

• Family instability, differences in press for achievement in the family, provision for early learning, disciplinary practices, interest in the child’s schooling, negative and pessimistic perception by parents of the child’s academic and intellectual competencies accompanied by decreased expectation levels and decreased desire to participate with the child in learning activities. (Lambert and Harsough, 1984).
• Parents feeling threatened and inadequate; parents unconsciously rejecting the child and parents blaming children for the extra problems they present. (Lambert, 1982)
• Mothers’ use of criticism and general malaise in parenting. (Goodman and Stevenson, 1989).
• Father’s hypercritical and destructive attitude, inconsistent, impatient and pressuring parenting approach and mothers who are judged to be emotionally disturbed (Thomas and Chess, 1977).
• Maternal anxiety and attitude toward pregnancy (Sameroff & Chandler, 1975).
• Mothers who are more directive commanding and negative; parents with depression, alcoholism, conduct disorder, anti-social behavior and learning disabilities; mothers who are less responsive to positive or neutral communications of their children (Barkley, 1990)
• A negative, critical and commanding style of child management (Campbell, 1990)
• Parental distress, hostility and marital discord (Cameron, 1977)
• Greater familial anger during conflicts, more disengagement from each other and repeated disputes over school issues and issues pertaining to siblings; parents who adhered to rigid beliefs about their teens’ bids for autonomy and who attributed misbehavior to malicious intentions (Robin, Kraus, Koepke and Robin, 1987)
• Parents who use aggressive behavior, indiscriminate aversiveness and submissiveness or acquiescence toward their children during management encounters (Patterson, 1982).
• Disharmony in early mother-child relationships (Battle and Lacy, 1972).
• Experiences of high level of stress in parenting and feelings of lower self esteem (Goldstein and Goldstein, 1990)
• Mothers who were critical of their difficult babies during infancy and showed lack of affection for them continued to be disapproving and tended to use severe penalties for disobedience during the primary school years and assessed their children’s intelligence as low (Ross and Ross, 1982).

The authors and the research you cite fail to account for two rich areas of research that have clearly demonstrated the impact of early familial experience on the behaviors characteristic of ADHD: attachment and trauma.

Attachment researchers have found significant relationships between the quality of mother (and father) – child relationships in the first months of life, the quality of attachment (secure, disorganized or avoidant) at one year of age and the school performance, sociability, levels of anxiety and general health of children in primary and secondary school (Goldberg, Muir and Kerr, 1995). As J. Holmes (1995) puts it, “Attachment research has shown that a school-age child’s sense of security is greatly influenced by the consistency, responsiveness and attunement he or she experienced with his or her parents in infancy.” Certainly, the behavior that is used to diagnose ADHD can be seen as the normal and understandable reaction of an insecure child to a stressful situation.

Researchers who have studied trauma have found that traumatic experiences early in life have a great impact on the ability of victims to modulate their emotions and to react effectively and appropriately to stressful and frustrating experiences (van der Kolk, McFarlane & Weisaeth, 1996; Herman, 2000). Trauma victims tend to become easily activated by threat and adversity, to react impulsively; or they protect themselves by shutting down and retreating into themselves. Both of these are behaviors that are used to diagnose ADHD. Traumatic experiences do not have to be life-threatening to have such an impact. They can consist of deficits in love, support, nourishment, affirmation that are experienced as being life threatening.

Deutsch et al. (1982) found that adopted children are much more likely to be diagnosed with ADHD than non-adopted children. This is understandable in view of the fact that all adopted children have suffered the trauma of being ripped away from their birth mothers.

Your inattention to the two rich lodes of research regarding attachment and trauma in relation to early experience and the kinds of behavior used to diagnose ADHD are major deficiencies in the research that you cite.

The brochure draft you quote from also denies the impact of “poor teaching” on ADHD. While ‘poor teaching’ may, indeed, not be ‘to blame’ for the rise of ADD/ADHD, the inhumane, oppressive, absolutely stultifying environment of the typical public school as a primary factor is undeniable. Current educational curriculums appear designed to be stuffed down the passively-receptive throats of students through repetitive, boring worksheets, one-size-fits-all, standardized methodologies, and minimal or no opportunity for active learning. Seldom is a child asked what he or she wants to learn or how she or he wants to learn it. Children are subjected to a horribly skewed value system in which primary emphasis is placed on linguistic and mathematical intelligence at the expense of other intelligences that are just as important: musical, spatial, mechanical, kinesthetic, interpersonal and intrapersonal. If children become bored, frustrated, and complain about it, they are told to be quiet or go to the principal’s office. Worse than this, these children may be shuffled into the special education diagnostic category of ADD/ADHD and placed in ‘less over-stimulating’ classrooms. In such circumstances, it is the children who are now pathologized as the ‘problem’ and ‘abnormality’ rather than a major societal system that fails to serve them.

Many scholars have testified to the ways in which the typical school hurts children by failing to encourage them to develop into the unique, separate, creative beings they crave to be (Leonard, 1968; Holt, 2000; Gatto, 2001). Others have noted that ADHD is diagnosed by watching the behavior of children in a typical classroom and that, if you put those same children in a less oppressive environment, they don’t engage in such behaviors. So Alfie Kohn (2000) wonders if we are diagnosing the child or the learning environment. And Willerman (1973) asks, “Should we classify a high level of activity and a low tolerance for being forced to pay attention to something one doesn’t want to pay attention to as a disorder?”

Even the ADHD researchers you have cited have found evidence of the school environment’s impact on diagnosis of ADHD:

• Inattention is most dramatically seen in situations requiring the child to sustain attention on dull, boring, repetitive tasks in which there are minimal immediate consequences of completion (Barkley, 1990)
• Task failure or a sudden reduction in anticipated reward or reinforcing feedback may severely disrupt behavior (Barkley, 1990);
• Pre-school hyperactive children were notably more restless, difficult and off-task than their nonhyperactive peers when required to engage in academic-type pursuits such as sitting at a table and listening but were indistinguishable from their peers in free play (Ross & Ross, 1982);
• Onset of hyperactivity often coincides with the point of school entry (Ross and Ross, 1982);
• Hyperactive children perform best on self-paced tasks and their behavior often deteriorates on ‘other-paced’ tasks (Ross & Ross, 1982);
• Hyperactive children have a difficult time in school, particularly in adolescence, when school work becomes more demanding and achievement becomes an important goal–this situation improves in adulthood when they can select for themselves a job in which they can succeed. (Ross and Ross, 1982).

Are we diagnosing a child or are we diagnosing a learning environment that is intolerable and damaging to a particular cohort of children with certain characteristics who are then called ‘mentally ill’ (ADD/ADHD) only because some of us choose to call them that?

We can think of many reasons why a child would resist being forced to pay attention to something that doesn’t meet his or her need or that diverts him or her from something that is considered more important at that moment:

• She may have some deep concerns that are so troubling that she doesn’t have space for anything else:
• Will I ever have any friends that I can really depend on and feel safe with?
• Is there something I can do to help my parents be happier so they can do a better job of nurturing me?
• Why is it that I have so much trouble doing this work and the other kids seem to be able to do it with ease?

He may have a burning desire to express a talent or drive that is not being honored. When he was ten years old, Picasso’s teachers were concerned because all he wanted to do was paint.

For practitioners of professional psychology to treat such concerns as a ‘mental illness’ and respond with a ‘prescribing predisposition’ is a disservice to a child whose individual crisis needs to be understood and used as an opportunity for learning—not how to read, write and do math but how to manage his emotions, thoughts and intentions and how to get along with other children without losing himself.

That ADD/ADHD is generally considered to be a neuro-chemical, genetic disorder with little relationship to parenting and environment is a case of popular opinion being at odds with scientific evidence.

What are the implications of ‘buying into’ such popular opinion?

This is, unfortunately, not a new dilemma for our discipline. As thousands of ADD/ADHD evaluations continue to be undertaken by psychologists nationally, we would do well to recollect the early days of applied clinical psychology when culturally biased IQ testing of immigrants, African Americans and Native Americans was used to bolster conclusions regarding the genetic inheritance of “feeble-mindedness” on behalf of the American eugenics social movement. At that time, many psychologists were just as convinced of their methods and theories as many continue to be about ADHD currently. In fact, no less than six presidents of the American Psychological Association signed up in some advisory capacity with eugenics organizations and initiatives over a twenty-year period. That is about the same time period with which we have witnessed our field involved with ADHD.

It was only tolerance for a diversity of views and a critical minority of applied psychologists of that time that helped to gradually extricate our field from a morass of significant racist biases. There are recognized scholars inside and outside APA who would submit that the current ADHD diagnostic descriptor, as well as many others contained within the Diagnostic and Statistical Manual of Mental Disorders (DSM), was composed in a controversial manner (Caplan,1996) and that ADHD itself has been substantiated only through poorly conceived and implemented research procedures using instruments of questionable reliability and validity (Carey, 1998; Armstrong, 1997).

The rise in popularity of the ADHD diagnostic category appears to be occurring on behalf of an American cultural movement relevant to the rearing of children that arises from changing values, mores, and demands in work and family life, educational curriculum, media exposure, and perception of time and time management. We should be vigilant of the multitude of voices and perspectives relevant to these changes, rather than lending our credibility to a single perspective that disregards or minimizes such factors in favor of a suspect reductionist, biological explanation.

Let our letter sound a warning to you that much is at stake here. As the ADHD category has already begun to be exported from its current white, middle-class, male youth focus to children of color, who continue to grow up under conditions of abject poverty and oppression, the die is being cast for psychology’s complicity in fostering a new, modern class of eugenics survivors – the ADHD child of color, shuffled to special education rooms as an individual “behavior issue”. Thus, we rationalize away our failure to accurately identify and effectively address his or her problem as having a primary origin in inequity, injustice, poor parenting and the failures of American public education.

The matter we are discussing here is of the utmost importance to psychology and to the people who are treated by psychologists. If we see the hyperactivity, impulsivity and “disinhibition” that characterize ADHD as driven by genetics and random biological dynamics, we call it a disorder and treat it with drugs and techniques of operant conditioning. If we see that same behavior as a functional response of the child to a situation that is difficult, off-putting, oppressive, abusive, irrelevant, discounting, disaffirming, and/or inhumane, we can call it a normal and understandable reaction and treat it by helping the child, family, and caretakers to fashion a better, more adaptive and life-enhancing response.

What does it imply if psychologists such as ourselves do not agree as to the existence of biological or neurological causes of ADD/ADHD? What does it imply if they have witnessed misuse and abuse of the category of ADHD with defiant, traumatized, or disruptive children of color? What does it imply if psychologists question the reliability and validity of their own diagnostic procedures with respect to ADHD?

It does not mean that children are not having trouble sitting still or paying attention to teachers or caretakers.

All we wish to demonstrate is that there is no “true ADHD” but only debatable ADHD. And we wish to emphasize that you are creating an American Psychological Association brochure and not a brochure for the American Psychiatric Association. There are many clinicians who do not subscribe to the reductionist, medical model implied in your efforts to legitimize ADHD as a so-called “neuro-chemical disorder.” They have weighed the same evidence you have and have come to contrary conclusions. We submit that the American Psychological Association has an obligation to present a more balanced account of the professional views of its constituents. That includes yours—and ours.

Many of the statements you make in your letter are far from conclusive to the APA practitioners you are attempting to represent in the brochure program. How can we hand our clients any brochure that seems to favor the zealotry of biological psychiatric views about ADHD as somehow unquestionably true when this is far from so, while minimizing and even invalidating the value of psychosocial explanations we might offer? This is disenfranchisement of our particular perspective on ADHD from our own professional organization.

We ask that Division 29 immediately cease the distribution of these brochures and that other brochures be produced that reflect a more balanced account of the available scientific evidence and the wide diversity of views of practicing psychologists regarding ADHD. As the most visible national public body of psychologists, we strongly recommend that:

• We indicate in these brochures that neurobiological explanations for ADHD are based on limited and controversial research findings
• Professional psychologists hold a variety of perspectives and opinions about the diagnostic category of ADHD and its etiology
• ‘Best practices’ of professional psychologists serving children, youth, adults, and families in relation to the descriptor of ADHD will vary in their approach based on what makes sense to each of us as professionals, what we know about human beings, and what appears to be in the best interests of all our clients
• As a body of practicing psychologists, we acknowledge before the public and one another that what we believe about ADHD is based on neither adequate nor established scientific fact but is instead a reflection of cultural and societal forces that have influenced our theoretical, research, professional, and practicing agendas
• We should publicly urge all psychologists to keep an open mind as we continue to work on the controversies we have raised surrounding the ADHD issue together.

We submit this letter to you in the spirit of collaboration and consultation. Although some of our differences with your perspective are great, your views have challenged us and inspired deeper thought as we clarify our own for you here. For that, we are very grateful to you.

Sincerely,

Albert O. Galves, PhD

David Walker, PhD

David Cohen, PhD

Kirk J. Schneider, PhD

Thomas Greening, PhD

Bertram Karon, PhD

Michaele Dunlap, PhD

Norbert A. Wetzel, PhD

Harris Friedman, PhD

Barry Duncan, PhD

Thomas Johnson, PhD

. . . Members in Good Standing, American Psychological Association

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