Saturday, July 01, 2000

ADHD: Serious Psychiatric Problem or All-American Cop-out?

A Debate Between Richard J. DeGrandpre, PH.D., and Stephen P. Hinshaw,, PH.D.

By: Richard DeGrandpre Ph.D. and Stephen P. Hinshaw Ph.D.

Psychologists DeGrandpre and Hinshaw debate ADHD and the pervasive treatment (or quick fix?), Ritalin.

Little more than a decade ago, parents and teachers began to hear about an affliction called “attention deficit hyperactivity disorder” or ADHD. The name was new, although the same cluster of symptoms had been described with other labels: minimal brain dysfunction, hyperactivity, and attention deficit disorder. ADHD rang a loud bell. Kids in school were misbehaving more and more instead of paying attention. Many were acting in more extreme ways than had been seen a generation or two earlier. Psychiatrists were suggesting that the cause might be a brain disorder—and that a pill called “Ritalin” could control it.

ADHD has now become a diagnosis applied to millions of American children, some as young as two. But even as ADHD and Rital­in became household words, critics began challenging their validity. Was there indeed a brain disorder behind the defiance and over-activity or were they just the latest symptoms of an American society sliding into apathy and egocentrism? Was Ritalin a needed treatment or merely a quick fix for parents too busy, too confused, or too meek to control their kids?

Richard J. DeGrandpre, Ph.D., a visiting psychologist at St. Michael’s College, Vermont, presented the case for the critics in Ritalin Nation: Rapid-fire Culture and the Transformation of Human Consciousness, published in 1999 by W. W. Norton. In the debate that follows, DeGrandpre and Stephen P. Hinshaw, Ph.D., a psychologist and professor at the University of California, Berkeley, and author of Attention Deficits andHyperactivity in Children (Sage Publications, 1994), examine these questions.

 

In the next issue of Cerebrum we will publish comments from readers. Your letters of up to 500 words are welcome.

DEGRANDPRE

STATEMENT

In 1940, a Gallup poll of schoolteachers in the United States reported the two greatest difficulties with children: chewing gum in class and cutting in line. Today, four million or so American children are taking Ritalin or other psycho-stimulant drugs, supposedly to treat severe behavioral and cognitive problems known collectively as attention deficit hyperactivity disorder, or “ADHD.” About 1,400 new children are being put on stimulants every day.

The “ADHD” label is at best a poor description of a cluster of developmental and psychological problems stemming from myriad causes; at worst, it is a pseudo­scientific explanation standing in for a real explanation that would link symptoms to independent causes and point the way to real solutions. For this reason, I put “ADHD” in quotation marks.

In the United States, “ADHD” and psycho-stimulant drugs such as Ritalin cannot be considered independently because these drugs are used in about 90 percent of all cases in which an “ADHD” diagnoses is made, and because response to treatment with stimulants is used to define the syn­drome of “ADHD.” In some parts of the country, as many as 20 percent of the boys aged 5 to 14 are receiving stimulants. The fastest-growing segments of the population receiving stimulants are now at the extremes of that age range: preschoolers and adolescents. Among children under age six, use of stimulants increased almost sixfold from 1995 to 1999. Even though Novartis, the manufacturer of Ritalin, does not recommend the drug for children under age six, a rise has also been reported for children under age two.

Outside the United States (excepting Canada) the situation looks dramatically different. More Ritalin is consumed in the United States than in all the other countries of the world combined; North America accounts for about 96 percent of the world’s Ritalin consumption. While use of stimulant drugs in the United Kingdom increased as much as fiftyfold in the 1990s, per capita use there still remains a small fraction (less than one-tenth) of that in the United States. The United Kingdom is among countries identified by the UN’s International Narcotics Control Board as showing a troubling increase in childhood use of stimulant drugs. Spain also shows rapid growth, whereas medium growth has occurred in Australia and Israel, and little or no growth in countries such as France and Germany. In France, a country of 57 million people, about 100,000 Ritalin pills were dispensed in 1998, compared with 56.5 million pills in Canada, a country of only 31 million people.1 These differences correlate with differences in how often “ADHD” is diagnosed; it is essentially unheard-of in France, where family structure is more nearly intact and child development is still viewed as a psycho-social rather than a biomedical matter.

The stunning rise in Ritalin use began in the United States in the 1970s, and so-called experts have attributed it to advances in medical understanding of childhood disorders. They believe that children once considered stupid or spaced-out are now appropriately diagnosed and treated. Indeed, many of these experts, while acknowledging that “ADHD” can be misdiagnosed and Ritalin overused, still consider that many children, especially girls, are not properly diagnosed. The few times when interna­tional comparisons are made, however, these assessments take on a different tone, suggesting as they do that professionals and parents in other countries are neglecting millions of children, failing to diagnose and treat them and, instead, blaming the children for their behavioral difficulties.

Given the cross-cultural differences in the rate of “ADHD” diagnosis and stimulant treatment, combined with the relatively brief period in which stimulant use has gone in the United States from several thousand to several million children, the opposite conclusion (and the one drawn in 1999 by the International Narcotics Control Board) seems more realistic: Children in the United States have been experiencing an epidemic of behavioral and emotional problems. This by itself is disturbing. Even more disturbing is that the United States is in almost complete denial about the meaning and source of this development. That denial has incapacitated us as a society to understand, treat, and, most important, prevent these problems. 

SHADOWS AND FOG: THE MEANING OF “ADHD”

The researcher who suggests that a brain scan might be developed to distinguish “ADHD” children from non-“ADHD” children, like the parent who wants to know in black-and-white terms whether a child has “ADHD,” is assuming it is a single disorder with a single cause. Anyone who has been around ADHD-diagnosed children, however, has seen considerable differences among them, both of severity and kinds of problems experienced. The difficulties experienced by the ADHD-diagnosed child vary across several dimensions, and each dimension—behavioral, cognitive, experien­tial—has its own continuum of severity. It is a mistake to try to flatten this multidimen­sional picture into a simple yes or no—as does the DSM (Diagnostic and Statistical Manual of Mental Disorders) in its diagnostic criteria for “ADHD.” Such over-simplification is designed not to clarify and address these problems but to label children medically and then, as occurs in the vast majority of cases, “manage” their symptoms with psy­chiatric medications. A billion-dollar industry has grown up with the explicit function of carrying out this scheme. One of the leading experts on “ADHD,” Russell Barkley, has compared “ADHD” to a physical handicap, with Ritalin being the equivalent of a wheelchair.

No matter how severe the symptoms, the so-called diagnosis of “ADHD” should be viewed as only a description of the problem, not an explanation. From the parent’s point of view, a child who is diagnosed and treated has had a problem solved. This view is reinforced when adults interpret the drug’s effect as evidence that children must be “ADHD” if a stimulant calms them down. The truth, of course, is that these drugs have calming effects in almost any child, whether overactive or not.

The ready acceptance of the label “ADHD” also reveals how the syndrome has come to be conceived as something that lies within the child. For a medical illness diagnosed by a blood test or biopsy this would be valid logic: Observation of X explains symptoms Y and leads to diagno­sis Z. But when the only measure of the problem is symptoms themselves, the logic goes awry—observation of Y explains the symptoms of Y and leads to a diagnosis of Y—and the diagnosis of “ADHD” becomes based on the very symptoms it is supposed to explain. It also overlooks the differences among children so diagnosed and the different origins of their symptoms. If stimulatant drugs have similar “manag­ing” effects on them, why bother to deter­mine whether or not the source of their problems is the same? 

ALL THE KING’S MEN: NATURE AND NURTURE

As more and more children experience dif­ficulties with attention, impulse, and hyper­activity, it becomes harder to distinguish the occasional rowdy or spoiled child of yesteryear from the scores of dazed and hyperactive children of today. One reason is the near total failure of funding institutions to encourage research on the developmental and social origins of these problems. Instead, research has been dominated for more than 30 years by a biomedical view­point, with little to show in return.2 When there has been research into nonbiological origins, the evidence has not supported this biomedical view.3 For example, Deborah Jacobvitz, Alan Sroufe, and their colleagues tracked several dozen children from birth through middle childhood, and found that “in early childhood, quality of caregiving more powerfully predicted distractibility, an early precursor of hyperactivity, than did early biological or temperamental factors.”4 Indeed, the parents’ marital status at the time of the child’s birth, the level of emotional support received by the caregivers, and caregiving style were shown to be pre­dictors of later problems with distractibility and hyperactivity.

This severe imbalance of the research is just one barrier to our understanding of “ADHD.” A larger problem is the assumption that a biological basis has been established. Seeing nature and nurture as two opposing forms of explanation has encouraged several scientific fallacies. To illustrate, I focus here on two blunders in biomedical research on “ADHD.”

On the heels of a 1998 National Institutes of Health Consensus Conference report on “ADHD”—which concluded that it was both overdiagnosed and unreliably diagnosed, and was not clearly biological in origin—an article appeared in the Proceedings of the National Academy of Sciences stating that, using functional magnetic resonance imaging (fMRI), researchers had found differences in the brain functioning of ADHD-diagnosed children compared to controls. These differences could be useful, the authors said, in developing what the article called “biologically valid criteria” for “ADHD.”5 The study was hailed by the media as establishing a biological basis for “ADHD,” implying that a diagnostic test was on its way.6 The Associated Press story that appeared in the Boston Globe had the headline “Test Found to Identify Attention Deficit.” In truth, the differences between the two groups of children were only statistical. The fMRI scans in the study were no more effective in reaching a diagnosis than are traditional paper-and-pencil methods. Two of the 10 boys diagnosed with “ADHD” did not fit the fMRI criteria for it, and three of the nine boys not diagnosed with “ADHD” did fit the fMRI criteria.

Another problem was the article’s assumption that the differences detected in the scans were evidence of a biological cause of “ADHD.” This is a major blunder, since the differences are likely to represent othing more than the underlying physiological correlates of the behavior already observed—all behaviors have physiological correlates, no matter what their ultimate cause. Physiological correlates must be, but have not been, distinguished from organic, pathophysiological causes of the behavior, to the extent that such causes even exist. In fact, there are studies that explicitly show changes in both behavior and physiology as a result of psycho-social interventions.7 Thus, the claim that the results might be useful as a diagnostic tool was extremely misleading for parents reading the newspaper accounts, who equated a brain scan for “ADHD” with an X-ray for a broken arm. Would it not be absurd to spend thousands of dollars to conduct a diagnostic test that can be as easily (and reliably) done with a behavioral checklist?

A second blunder of the same type, involving cause and effect, has been made in other neuroscience research on “ADHD,” which seeks anatomical differences in individuals with the diagnosis. There is the disturbing possibility that these anatomical differences are not the cause of behavioral and cognitive differences but the result of their “treatment” with psycho-stimulant drugs. As a 1986 study acknowledged (reluctantly, at the end of the article), “since all of the [ADD] patients had been treated with psycho-stimulants, cortical atrophy may be a long-term adverse effect of this treatment.”8 Other studies have consistently refused to stress this interpretation, however, or to follow up with valid studies of the long-term effects of psycho-stimulant treatment on the developing brains of children.

A major rise in the percentage of very young children in the hands of babysitters or nannies and the time constraints of their harried, overworked parents, may turn out to have more to do with the exponential increase in children labeled “ADHD” than any biological factor.

One example is Russell Barkley’s 1998 article on the biological basis of “ADHD,” which appeared in Scientific American.9 Here Barkley interprets anatomical differences as evidence of a biological basis for ADHD, making no mention that, in these studies, the ADHD-diagnosed children (or adults) all had a history of chronic use of Ritalin or other stimulants (as did children in the Stanford study (noted above). Barkley also hails genetic research, citing a study from Norway that suggests a heritability of .80 for “ADHD,” meaning that 80 percent of the variance in the symptoms in the population studied is

accounted for by variance in the genes. Aside from wrongly describing “heritability” as a universal statistic (it is a population based statistic), Berkeley makes no effort to explain how this “.80”accounts for the dramatic differences in prevalence of “ADHD” in Norway versus the United States. Cross-cultural differences play no role in his assessment. 

CHILDREN OF A LESSER SOCIETY

Wholesale prescribing of psychiatric drugs to children speaks not to medical progress but to society’s regress.10 Some oppose stimulant treatment of ADHD-diagnosed children on moral grounds. But we can also oppose their use simply because they are both too effective and too ineffective. They are too effective in the sense that they have untoward effects on the adults who hand them out, serving as a quick fix for an unruly or inattentive child. At the same time, they are too ineffective because they do not result in the anticipated long-term effects: improved academic performance, social skill development, and overall good comportment when the drug is stopped.11 Even Barkley has admitted this, writing in 1978 that: “Stimulant drug studies based primarily on measures of teacher opinion have frequently concluded that these drugs improve the achievement of hyperkinetic children. How­ever, a review of those studies using more objective measures of academic performance revealed few positive short-term or long-term drug effects on these measures.”12

Perhaps the contribution of cultural transformations to child-development problems in America today has yet to be examined. A major rise in the percentage of very young children in the hands of babysitters or nannies and the time constraints of their harried, overworked parents, may turn out to have more to do with the exponential increase in children labeled “ADHD” than any biological factor. One day the real causes and solutions may be found. Meanwhile, millions of children are abandoned to the halls of medicine. 

HINSHAW

STATEMENT

During the last century, ADHD has appeared under several different labels, including mini­mal brain dysfunction, hyperkinesis, hyperac­tivity, and attention deficit disorder. Whatever the name, the condition refers to a set of problems in three interrelated cognitive and behavioral systems. The first has to do with attention—specifically the inability to focus attention for long periods. The second has to do with inhibition—specifically difficulties with controlling impulses and responses. The last has to do with failure to regulate movement— specifically “extraneous motor activity.” As knowledge about the brain regions and cogni­tive mechanisms that underlie these three sys­tems has raced ahead, research on the under­pinnings of ADHD has become a growth industry.1 One target of this research has been the so-called executive functions of the brain’s frontal lobes and how they guide behavior in conection with other brain regions.2

We must realize that all three major features of ADHD are part of normal devel­opment. Anyone entering an elementary school classroom will observe plenty of inattention, impulsivity, and hyperactivity, particularly among the boys. A valid diagnosis of ADHD requires that:

  • The problems must be extreme for the child’s age or level of development.
  • They must be persistent across time, and begin before age seven. (Parents of children with ADHD typically report that problems became evident in the earliest years.)
  • They must be pervasive across situations, in school as well as at home and when the child is among peers.
  • They must significantly impair the child’s development of normal competencies.

Thus, a high level of activity alone may fit quite well into a child’s life (particularly if cognitive skills are good); a diagnosis of ADHD should be considered only when activity and impulse control are highly dysregulated, so that the child cannot focus in class, cannot get around without risk of injury, cannot obey reasonable requests, or cannot get along with other children. (There is an interesting parallel here with depression. Everyone feels some sadness or irritability at times, but major depression is diagnosed only when there is persistent, impairing unhappiness.)

Also, there appear to be subtypes of ADHD, notably an “inattentive” type (for­merly called ADD or “ADD without hyper­activity”), in which the chief problem is focusing attention, and another type marked by salient impulsivity and hyperactivity, termed “hyperactive/impulsive” or “com­bined.” Although boys outnumber girls by at least 3 to 1 in the hyperactive/impulsive subtype, the ratio is closer to 2 to 1 for the inattentive type. Girls with ADHD remain an understudied population.

IS ADHD A VALID DIAGNOSIS?

At least four kinds of observations tend to make critics skeptical that ADHD is a serious psychiatric problem:

  1. The commonness of the symptoms among all children
  2. The popularity of the diagnosis over the past decade
  3. The inconsistent nature of the behavior patterns (inattention is not always present in a diagnosed child, and, in fact, video games and frequent rewards can temporarily diminish symptom display)
  4. The current demand for improved standardized test scores.

Indeed, in a society characterized by relentless pressure on children to succeed, it may be tempting to label any child who fails to conform to social or school norms or who has difficulty focusing on class work as suffering from an underlying attention deficit.

A crucial point, however, is that when clinicians follow established guidelines, the diagnosis of ADHD is reliable.3 Considerable evidence shows that ADHD is a persistent, impairing condition that runs strongly in families, that has clear psychological and biological roots, and that unfortunately has a poor prognosis. In other words, it is a valid psychiatric diagnosis when cases are rigorously assessed. How does the careful clinician distinguish ADHD from inattention or problems in adjusting to school that fall within the normal range?

First, she must examine the child’s behavior patterns in light of norms for development; only problems that are truly extreme compared to those of same-age youngsters are pertinent for diagnosis. It is essential to use standardized checklists and structured interviews with parents and teachers. Next, the clinician must get a thorough history of the child’s development to document that the problems are long standing and occur in many different situa­tions; she must consider whether other factors (child abuse, a recent move, chaotic classroom environments) better account for the symptoms. Third, she must request a medical evaluation of the child. This is not to “rule in” ADHD—there are no definitive physical signs of ADHD at present, making it similar in this regard to depression and other major psychological disorders—but to “rule out” conditions that may mimic its symptoms (for example, seizure disorders or neurological injuries). Finally, the clinician must use cognitive testing to measure the child’s basic intellectual and academic skills. What is absolutely clear is that a 10-minute pediatric examination cannot hope to yield an accurate, valid diagnosis; practice standards must be upgraded and enforced to prevent “shotgun” diagnosis of ADHD.

A child who meets the full diagnostic criteria is far more than just a bothersome youngster who fails to meet adult expecta­tions. Indeed, impairment is typically severe in just those domains of functioning that are crucial developmentally.4 Children with ADHD (even those without coexisting learning disabilities) show extremely high rates of school failure. Family relationships are often severely strained, and evidence points to family disharmony as following from rather than preceding the symptoms. Peers, too, severely reject youngsters with ADHD, often within minutes or hours of meeting them. Such social deficits have devastating consequences. Peer rejection in the elementary school years is the strongest known predictor of such negative outcomes as school dropout, delinquency, and mental health problems in adulthood. Finally, rates of accidental injury are alarmingly high with ADHD, and potentially serious consequences may follow, such as head injuries, emergency-room visits, and driving accidents in adolescence and young adulthood. In addition, contrary to former beliefs, ADHD does not disappear with the onset of puberty. Attention deficits and inhibitory problems (and associated impair­ments) are highly likely to persist through adolescence and even beyond.5

ADHD is associated with major problems in the attainment of crucial devel­opmental competencies; it can lead to serious consequences for health; and it is likely to be a lifelong condition. With accurate diagnosis, the prevalence is 3 to 7 percent of the school-aged population, not 15 to 20 percent or more, as has been claimed. Evidence is mounting that ADHD is a grave concern in nations far beyond the United States. With appropriate assessment, ADHD is not simply a problem of irritating, nonconforming behavior in a postindustrial society but rather a valid diagnostic category that poses a serious public health concern.

THE CAUSES OF ADHD

Strong evidence exists that the constituent symptoms of ADHD are extremely heritable —even more so than the symptoms of major depression or schizophrenia.7 Thus, individual differences in inattention, impulsivity, and hyperactivity are largely the products of genes rather than environments. At the molecular level, several candidate genes (most notably, the gene responsible for coding for a key brain receptor for the neurotransmitter dopamine, known as “DR4R”) have been identified. Note that these are not “dominant” genes but rather “susceptibility” genes, which may interact with one another and with a child’s envi­ronment to create the potential for ADHD. Other biological risk factors (low birth weight, a mother who smoked during preg­nancy) stand out for some cases of ADHD, particularly among boys. Deficient parenting alone does not seem to be a cause of ADHD, although negative parenting may accentuate the symptoms.

A persistent misconception—even among otherwise sophisticated scholars and clinicians—is that the strong genetic predis­position to ADHD means that parenting and schooling do not matter. On the con­trary, a child’s environment may powerfully influence even strongly heritable traits. How the family copes with and reacts to the “deficient” infant, toddler, and preschooler is crucial in shaping development. Difficult, hostile, or overly lax parenting may well exacerbate underlying tendencies and shape important problems (for example, aggressive behavior) that often accompany ADHD. Conversely, optimal parenting may well promote strengths in children with ADHD, including positive peer relations.6 Despite strong psycho-biological underpinnings of ADHD, psycho-social influences are key to the way it may emerge and develop. 

INTERVENTION

A host of mainstream and alternative treat­ments have been put forward for ADHD: play therapy, couples therapy for the parents, family therapy, diets of several types, homeopathy, biofeedback, and many more. Only two types of treatment are unequivo­cally supported by empirical evidence: treating behavior by such means as family management and school consultation, and teaching social skills using rewards; and stimulant medications, including methyl­phenidate (Ritalin) and dextroamphetamine (Dexedrine).9 Neither type of treatment is a “cure” for ADHD; rather, through active psycho-social intervention designed to establish more regular incentives or through drugs that target the chemical messenger dopamine in the brain, the aims are to enhance attention, improve inhibitory capa­bilities, and foster self-control.

Much of the current controversy surrounding ADHD focuses on medication. Doctors have been prescribing stimulants safely for ADHD for more than three decades, and many carefully controlled trials attest to their benefits in reducing core symptoms, enhancing school behavior, and improving interactions at home and, to some extent, with peers. They act quickly (improvement can usually be seen on the first morning of administration of an appropriate dose); they do not “tranquilize” the child (rather, they boost inhibitory control); and they do not pose the potential of side effects if they are carefully managed. Head-to-head comparisons consistently show that they are more effective (at least in the short term) than even the best-delivered behavioral/psycho-social treatments. Because, however, many families reject medication treatments (and up to 20 percent of children with ADHD do not show a positive response), we must continue to develop psycho-social alternatives or adjuncts.7

In addition, it is crucial to emphasize that stimulants are potential drugs of abuse. They are known to be capable of inducing tolerance and producing problems with withdrawal when used nonmedically. Further­more, given the large increases in prescription rates during the last decade, critics rightly ask whether ADHD has become a label of convenience for children who are not achieving or performing up to capacity and whether stimulants are being used indis­criminately, risking unknown, negative long-term consequences for both patients and society at large (which may come to depend on chemical solutions to solve problems in families and school). Clearly, data on the risk/benefit ratio of medication treatments are urgently needed, given the potential risks and problems.

A recent major clinical trial at several medical centers and universities, sponsored by the National Institute of Mental Health, found clear benefits of stimulant medications over a longer period of time (14 months) than usually studied.8 The children who showed the benefits were well-diagnosed children with ADHD who had their medication carefully managed (that is, initial dosage adjustment, monthly family visits to the doctors, and mandatory contact with school personnel). Indeed, such medication management procedures did better in reducing symptoms than an intensive psycho-social intervention that involved long-term parent training, school consultation, and summer behavioral treatment. This careful medication strategy was also superi­or to prescription of the same stimulant medications without the close monitoring. Yet combination treatment (medication management plus intensive behavioral treatment) fared best in terms of percentages of children ending treatment without significant symptoms. Furthermore, when combined medication/behavioral treatment led to improvement in parental discipline at home, the children’s disruptive behavior at school was brought into the normal range.9 This work has received international attention, with a call for greater acceptance of pharmacologic treatments in other countries.10

We still do not know the impact of years of stimulant treatment during childhood. For example, concerns have been raised that it may increase the risk for drug abuse in adolescence. The available data, however, suggest just the opposite— that successful medication treatment may prevent later substance abuse.3 Of equal concern is that we have no evidence that medication truly alters the course of ADHD. Instead, by lessening symptoms and enhancing performance, the medications pave the way for more adaptive functioning day by day, with the suggestion that, for many cases, long-term medication may be needed. In this way, stimulants are like medicine for major depression or schizophrenia; the medicine helps as long as patients take it, but does not appear to alter the depression or schizophrenia fundamentally. 

AREAS OF CONTROVERSY

Critics worry that increasing numbers of children, inadequately diagnosed and not carefully monitored, are getting stimulant medications. In the case of Ritalin, some of this increase may be appropriate—for example, use of multiple daily doses and prescriptions beyond childhood. On the other hand, prescription rates vary dramatically by region, and in many areas the critical problems are underdiagnosis of children with ADHD and lack of access to high-quality treatment. Whether the problem is overdiagnosis, with too much medication, or underdiagnosis, with too little, the solutions are the same: holding clinicians to higher standards of accountability for accurate assessment and insisting that, when medications are used, the patients be monitored with far greater care than appears to be the current practice.

To dismiss the potentially dramatic benefits of pharmacologic treatment for ADHD risks withholding an effective, important treatment for a heritable behavioral disorder that can entail devastating impairments.

A related concern is that ADHD is not a “real” diagnosis but rather a label for children who simply do not fit society’s current mold. As I have argued, the evidence strongly sup­ports the reality of ADHD and its validity as a diagnosis—when careful assessments are per­formed. There are lots of reasons a given child may appear to have symptoms of ADHD, including stress reactions, intolerant schools, other medical conditions, or simply being at the far end of the normal curve of activity level. The job of clinical scientists and others who intervene—and the responsibility of society—is to ensure that only accurately diagnosed children become candidates for medication treatments. To dismiss the potentially dramatic benefits of pharmacologic treatment for ADHD risks withholding an effective, important treatment for a heritable behavioral disorder that can entail devastating impairments, often for many years.

A RELIABLE DIAGNOSIS OF A SERIOUS DISORDER

Despite our incomplete understanding of its underlying neural and social mechanisms, ADHD is a reliable, valid diagnosis of a serious disorder that can severely affect areas of functioning that are important to a child’s optimal development. Study of ADHD requires knowledge of how several influences interact (genetic, psycho-biological, cognitive, familial, peer-related). This is an exciting challenge to basic and applied scientists. Although it became an identified disorder only with the advent of compulsory education in the nineteenth century, ADHD is not a social construction. Like severe learn­ing disabilities, which also were unmasked only when society began demanding literacy from all citizens, ADHD is strongly heritable and appears related to core problems in inhibitory control (parallel to the heritable, underlying deficits in awareness of basic sounds that underlie reading disorders). We urgently need to ensure rigorous standards for making a diagnosis as well as guidelines for clinicians that demand careful monitoring of medication treatments, if prescribed. Ultimately, we must realize that ADHD is neither a figment of society’s imagination nor a condition threatening to undercut our social fabric. It is a disorder that requires the best of our scientific and clinical expertise.

DEGRANDPRE

REJOINDER

Imagine a giant elephant. The sun is setting, casting a long, extended shadow of the elephant across the ground. The animal is large, unruly, and three-dimensional, and its shadow is skinny, harmless, and two-dimensional. I suggest these images because they seem to capture the exchange thus far between myself and Stephen Hinshaw. There is the large, unruly, and three-dimen­sional reality of the “ADHD” epidemic in America today, and there is Hinshaw’s shadow of this reality: skinny, harmless, and two-dimensional.

Hinshaw gives a textbook summary of “ADHD.” In fact, his comments are in some ways more cautious than is typical for medical experts. Nevertheless, in presenting his opening statement, he makes two moves that reveal the shaky foundation upon which the medical model rests.

First he suggests that “ADHD” is both a reliable and a valid medical disorder, and that if physicians would simply respect appropriate diagnostic practices we would not be in the mess we are in today. This is the having-your-cake-and-eating-it-too response to the “ADHD” epidemic. “Having your cake” occurs when “experts” like Hinshaw acknowledge “ADHD” as a valid but overdiagnosed medical disorder. The “eating it too” occurs when individual parents and physicians acknowledge the problem of overdiagnosis in the abstract but insist that it in no way applies to them. The abstract acknowledgment captures the high moral ground; then (to continue the metaphor) the particular picnics on it.

As a result, growing concern with stimulant use in children over the past 25 years has been correlated not with a decrease but with an explosion in use, which has gone from 100,000 children in the 1970s to millions today.

The second questionable move comes when Hinshaw suggests that, when all that is excessive to “ADHD” is removed, a core medical problem remains. This assumption is implicit throughout Hinshaw’s statement. But he offers not a single concrete piece of evidence to support it. He lays a trap for the reader by saying that, because the symptoms upon which the “ADHD” diagnosis is based are real, “ADHD” is therefore a medical disorder. I agree that millions of children are having behavioral and cognitive difficulties that impair them, and I agree that these problems have underlying physiological correlates. What I disagree with is the con­clusion that, because those two points are true, “ADHD” is therefore a medical problem. Hinshaw does not acknowledge that certain developmental experiences can by themselves lead to an out-of-control or emotionally disturbed child, nor that impairment can exist without the problem being in any way a medical one. 

MISMEASURE OF MIND

Hinshaw says that neurobiological research into the “underpinnings” of ADHD is a “growth industry.” To be sure, it has long been a growth industry—to the persistent exclusion of research into child development and family systems. Again, this raises several concerns. First is the mistake of treating nature and nurture as opposing explanations.

Second is the mistake of confusing correla­tion with causation—concluding that because two things occur together, one must cause the other. Third is the mistake of treating statistical differences between groups of children (that fall within a normal range) as if they were not averages but discrete differences that could be used to distinguish individual children—as though the differences reflected true neuropathology.

When Hinshaw talks of the biological “underpinnings” of ADHD, for example, it is not at all clear what he even means by this word. To the extent that it means physiological differences between those who are and are not diagnosed as “ADHD,” we must ask whether these differences are just the underlying physiological expression of the behavior already in full view, thus proving only that the child has a brain. To the extent that it means physiological differences of an anatomical sort, we must consider the possibility that this may be the result of chronic stimulant use.

“MY GENES MADE ME DO IT”

Hinshaw also raises the specter of genetics, abusing the notion of heritability and ignoring the fact that “ADHD” runs in families in much the same way as being Catholic runs in families. He suggests that “a child’s environment may powerfully influence even strongly heritable traits.” This is misleading, since readers have been primed by his earlier statements to interpret “herita­ble” as meaning genetically determined. What “heritable” really means is that genes may play a role in a trait under some conditions, and thus a more accurate statement is this:

Genetic influence is always mediated by environment, and thus heritability is itself highly influenced by the environment. For example, a diverse environment and a uniform gene pool produce a much lower heritability for “IQ” or “ADHD” than do a uniform environment and a diverse gene pool. As such, Hinshaw’s conclusion that “ADHD” prob­lems are “largely the products of genes” is simply false. Hinshaw and I offer the reader two very different statements about how to understand genes and human behavior— one pulls nature and nurture apart, the other puts them back together.

Hinshaw also joins the ranks of “ADHD” experts like Russell Barkley in ignoring studies with lower heritability scores. There are studies showing that only half of identical twins and one-third of non­identical twins were diagnosed with ADHD if their twin had been so diagnosed, but they emphasize instead only those showing a high heritability.*  I wonder why?

Finally, Hinshaw dazzles us with fancy genetic codes like “DR4R.” In doing so, he fails to consider the full story. If some mix of genes correlates with some subset of children diagnosed with “ADHD,” one would still have to consider that these same genes might give children a push in different directions in different environments. If so, this would explain the vast cross-cultural differences in these problems: Children with more or less the same genetic mixtures elsewhere do not suffer these problems because they have very different developmental experiences. (After all, do we really believe that 5 percent of Amish sixth-graders today are “ADHD”?) Ignoring this, Hinshaw suggests that 3 percent to 7 percent of children are “ADHD,” and argues, without any evidence, that these problems are a“serious concern” in other nations. Maybe he is confused: The International Narcotics Control Board of the UN did suggest a serious concern, but the concern was that other nations were following the American trend toward medicalizing childhood. Citing Eric Taylor of the United Kingdom as “international attention” is no help, either, as Taylor’s Americanized views are not widely held in the United Kingdom. Ultimately, one has to explain certain reali­ties, such as when one visits a museum and finds 10 American teachers struggling to manage 100 American children, and one Japanese teacher easily managing 100 Japanese children.

As more parents are pushed away from the real task of parenting and more kids are raised by TV, video games, and total strangers, the  “ADHD” family will become the norm of American society.

ENSURING A POOR PROGNOSIS

As I noted in my opening statement, there is indeed a body of careful prospective research that shows family determinants of ADHD-type problems, even when the influence of the hyperactive child on thefamily is taken into account. Like Russell Barkley, Hinshaw denies this. Furthermore, and contrary to Hinshaw’s inflammatory rhetoric of “deficient parenting,” it is well established that dynamic family systems can create severe problems in children even when the family is essentially “doing its best.” Indeed, as more parents are pushed away from the real task of parenting and more kids are raised by TV, video games, and total strangers, the “ADHD” family will become the norm of American society, no longer the exception it once was. For this reason, Hinshaw’s idea of “develop­mental norms” for diagnosing “ADHD” makes no sense and reveals an assumption that no family scholar would ever touch: namely, that the developmental context of childhood in America is unchanging.

Hinshaw joins his colleagues in hailing the virtues of Ritalin, and points to the recent MTA Cooperative Group multimodal treatment study of children with ADHD, in which he played some part. Readers should be warned, however, that the “best-delivered behavioral/psycho-social treatments” used in the MTA study were anything but. Not only did the study fail miserably to uphold good standards of methodology for this type of research, but the very research itself was biased toward pro-drug results— and with more than a hint of drug-company money greasing the gears (most if not all of the principal investigators of the MTA study, and its main architect, have long-standing ties to the pharmaceutical industry). The only real effect of the study was on adults, who were all too pleased to be able to control children’s behaviors through medication. That stimulants do not work for the children wandering the halls of medicine is a fact established in the literature, not a theory of two-headed critics, and no amount of junk science will cover it up.

Thankfully, there are hopeful inter­ventions being developed elsewhere that escape the poor prognosis of medicine. The following example is just one of many, provided by Eileen Tracy, writing for The Guardian (Tuesday, April 12, 2000):

Professor Steve Baldwin, director of Clin­ical and Counseling Training Units at the University of Teesside, uses behavioural self-control training to cure ADHD-style behaviour…When a child bullies other children, or disrupts classes, parents can feel tremendous pressure to medicate. But a behavioural therapist like Baldwin can teach the child self-control, by work­ing closely with the parents to encourage appropriate behaviour whilst discourag­ing disruptive outbursts. After a few weeks, the child learns to behave, and the effect is usually long-lasting.

In the end, the poor prognosis Hinshaw predicts for these children does not reflect on their true capacities. It reflects on America as an individualistic and hurried society hooked on quick-fix pseudo-solutions. An outspoken defender of children’s welfare, Peter Breggin, once said to a child, “Your doctor should have loved you more and drugged you less.” To this, I would only add, “so should have your society.”

*These concordance rates refer to the likelihood of one twin being diagnosed when the other twin has been diagnosed. A rate of 1.0 would mean 100 percent concordance: when one twin is diagnosed, so is the other, without exception.

HINSHAW

REJOINDER

The exchange in our opening statements epitomizes the current controversy sur­rounding ADHD. DeGrandpre contends that ADHD is an inappropriate diagnosis that has led society away from understanding the true nature of children’s emotional and behavioral difficulties. He lambastes the medicalization of social problems and the treatment of millions of children with potentially dangerous stimulants. Some of his ideas are thoughtful; others are not based in fact. I address errors first, then turn to discussion of several important questions raised by the current debate.

CLARIFICATIONS

DeGrandpre cites the NIH Consensus Statement3 to the effect that ADHD is not reliably diagnosed and has no known psycho-biologic underpinnings or risk factors. The official statement contends, however, that “the diagnosis of ADHD can be made reliably using well-tested diagnostic interview methods.” It also emphasizes that ADHD has been validated in terms of developmental course or progression, cross-national studies of risk factors, clear familial aggregation, and strong heritability. I do note in passing DeGrandpre’s point that psycho-biologic investigations could well be contaminated by attributing the effects of stimulant treatment to ADHD itself; but untreated children, in fact, show the same risk patterns. As I emphasized earlier, careful assessment is essential for accurate diagnosis; a brief examination and shotgun prescribing are not at all adequate. Yet claiming that there is no reliability or validity ignores several decades of carefully controlled, illuminating research efforts.

DeGrandpre questions Russell Barkley’s citation of .80 for the heritability of ADHD, claiming (among other things) that it does not take into account cross-cultural investigations. One must simply read the relevant literature. A spate of investigations in the last decade, spanning Australia, Scandinavia, the United States, and the United Kingdom, all converge on similarly high estimates of the heritability of the constituent symptoms of ADHD.1 The meaning is not (as emphasized earlier) that environments are unimportant for the expression of ADHD—or particularly for its frequent companion, aggression. Rather, heritabilities as high as .80 signify that indi­vidual differences in levels of hyperactivity, inattention, and impulsivity are strongly influenced by genes—more so than in schizophrenia or unipolar depression. What appears to be inherited is not a yes/no diagnosis of ADHD but a likelihood of having many of its constituent symptoms. How the environment “deals with” this likelihood is crucial for each individual case. 

DeGrandpre also contends that far higher rates of ADHD in the United States than in other countries (particularly the United Kingdom) mean that America is clearly wrong headed. This notion was care­fully investigated over a decade ago. When the former British definition of “hyperkinesis” (applying to a small group of mentally impaired children with wildly high activity levels) was supplanted by an internationally agreed-upon definition, rates of diagnosis between the United States and United Kingdom became nearly equivalent. An example from history may be instructive here. In the early 1960s, adult schizophrenia was eight times more likely to be diagnosed in New York City than in London, because of a different set of diagnostic standards in the two countries. Nearly all psychosis in America was viewed as the product of underlying schizophrenia, whereas Europe held to a model recognizing multiple sources of psychotic functioning, including bipolar disorder. The application of a uniform international diagnostic standard made rates of diagnosis equivalent.

OPEN QUESTIONS

Turning from actual misstatements to matters for discussion, I now look at four major questions raised by the debate.

Dimensions versus categories.

DeGrandpre is critical of diagnostic systems, like the DSM, that categorize ADHD as present versus absent, when in fact the underlying symptoms can exist in varying mixes and degrees of severity. (Or, as we say, the symptoms are “distributed” along a con­tinuum.) The criticism is directed mainly at medication treatments for ADHD, which he claims are fostered by an arbitrary yes/no diagnosis. Just because underlying problems lie along a continuum, however, does not mean that categorical diagnosis is unneces­sary or wrong.

Consider the analogy to hypertension. Although there is no clear “break” in the underlying distribution of blood pressure levels, it is clinically defensible to indicate certain cutoff scores (selected on the basis of sound research) that designate hyperten­sion needing treatment. Indeed, doing so saves lives. Except for relatively rare “true categories” (for example, Huntington’s disease, caused by the presence of a single gene), all of medicine and psychiatry must contend with decisions regarding where to draw lines indicating that symptoms and problems are of a degree that warrant a medical diagnosis.

Greater understanding of causal mechanisms may someday clarify meaningful subgroups of ADHD, which appear similar on dimensional scales but which require different treatments.

Family socialization versus biological causes. DeGrandpre cites the interesting research of Deborah Jacobvitz and Alan Sroufe, who found in a sample of low-income, high-risk young mothers in Minneapolis that aspects of early mother-child interaction, and not early psycho-biologic measures, were predictive of subsequent ADHD symptoms. Although provocative, this study requires replication. For instance, other investigations have clearly linked ADHD with such prenatal and perinatal factors as low birth weight. Also, it is not known from research like that in the Minneapolis study whether the link between parenting and outcomes for children actually depends on a third variable (for example, genetically impulsivity) that could explain both the mothers’ insensitive parenting and the children’s behavioral tendencies. The strongly heritable nature of ADHD renders insufficient the usual family socialization research designs, which assume that influences from parent to child are entirely psycho-social. Complex interactions of genetic and environmental influences are the rule.

Treatment of symptoms versus underlying causes. DeGrandpre raises the specter that stimulant medications suppress symptoms but do not deal with underlying causes.

This is a provocative and complex matter. First, let me point out that there is no single, underlying “cause” for most medical and psychological disorders (for example, rheumatoid arthritis, coronary artery disease, schizophrenia, depression, and ADHD). For such conditions, treatments affect some portion of complex bio-psycho-social pathways, the ultimate nature of which is not yet understood. Again, the example of hypertension shows several interacting risk factors (ethnicity, genetic vulnerability, diet, stress levels) to be prominent. Antihyper­tensive medication may act on some part of the chain (for example, alpha adrenergic transmitted receptors, artery walls) to treat the symptom of high blood pressure. The value to the patient is significant, even though the “underlying cause” (if there even is one such cause) may not be altered.

The brain both shapes and is shaped by the environment; under-lying psychbiologic risk factorscan be treated environmentally; and some conditions resulting from stressful life events could be dealt with by biological intervention.

Once specific etiologic influences are better understood, the different causal pathways that lead to ADHD may be treatable more specifically and powerfully. Among the possible causal influences are underlying susceptibility genes, dopamine receptor subtypes, effects of anoxia at birth, and ramifications of certain parenting styles in combination with difficult temperament. Also crucial will be interventions that can enhance personal, family, or community-level protective factors to help offset certain types of risks. We must transcend either/or, biological/environmental, thinking. The brain both shapes and is shaped by the environment; underlying psycho-biologic risk factors can be treated environmentally; and some conditions resulting from stressful life events could be dealt with by biological intervention. As for prevention, increased knowledge of just how such influences as preschool classrooms, television-based “socialization,” and family expectations shape patterns of brain development, which in turn mediate impulse control and attention span, should lead to the design of healthier environments and reduce the propensity for impairing inattention and disinhibition.

Again, if ADHD is misdiagnosed or poorly evaluated (for example, if abused children or youth in chaotic environments who merely look as though they display ADHD are being treated inappropriately with medication), no one wins, least of all the children. But if careful assessments are made (particularly in the future, when genetic analysis may spur the development of rational, selective medications for specific problems in neurotransmission), then such treatments, integrated with better educa­tional practices and authoritative parenting strategies, may fuel a “virtuous cycle” of improved learning, enhanced family interac­tions, better opportunities for friendship, and increased self-esteem. Medication alone is not likely to lead to such long-term, clini­cally significant improvement.

Cyclic nature of social issues. Certainly prescriptions for stimulant treatment of ADHD have made a steep climb in the United States. Is this a sign of long-awaited acceptance and treatment of a valid diagnosis? Or is it a harbinger of dangerous social control? The answer probably lies some­where between those endpoints. History reveals that there are cycles in how society conceives a disorder. Extreme biological perspectives give way to extreme environ­mental and social perspectives; then perspectives change, and the cycle is repeated.

After years of ignorance, misunder­standing, and neglect, ADHD has “come out of the closet” as a result of sound scientific groundwork. Yet, in some quarters, it has been invoked as a catchall diagnosis, perhaps due to the enormous pressures for conformity and school achievement in our postindustrial society. This current zeitgeist should and will attenuate; critics like DeGrandpre are important in sounding the alarm at the impli­cations of wholesale espousing of a given diagnosis. The critics, however, tend to ignore the complexities and realities in the field, leading them to negate the clear scientific and clinical progress that has been achieved. Denying the reality of ADHD is to swing back to a time when understanding was limited, running the grave risk of depriv­ing 3 to 7 percent of our youth of the critical opportunities they need for compassion, remedial help, and sound treatment planning. 

DEGRANDPRE

CLOSING STATEMENT

Readers of this exchange are likely to be convinced of at least one thing: It is difficult to know what to believe about the “ADHD” epidemic. Realizing this, I focus my final remarks on the salient facts.

First, it may be a matter of opinion whether or not “ADHD” is a pseudo-scientific disorder. But it is a fact that “ADHD” simply does not exist to any notable degree in many parts of the world. When Hinshaw implies that other countries have comparable rates of “ADHD,” he is flatly wrong. Although “ADHD” problems are growing elsewhere, some 98 percent of the world’s Ritalin is consumed in North America. In places such as France, Japan, and Hong Kong, “ADHD” is essentially unknown. Ritalin advocates argue that some cultures interpret the same problems in a different way, but this is no explanation. If “ADHD” problems are highly distinguishable, as they must be in order to be diagnosed, then why, when you visit classrooms in France and many other places around the world, can you not find them?

It may also be a matter of opinion whether or not Ritalin—a drug with the same pharmacological actions as cocaine —is a quick-fix solution to a complex array of socio-developmental problems. But it is a fact that Ritalin has been shown conclusively to be ineffective.11,12 Yes, more adults are becoming hooked on Ritalin’s effects on child manageability, but this does not mean that stimulants are effective for the child. A physician writes in Newsweek (April 24, 2000) that “stimulants such as Ritalin...are highly effective...and parents shouldn’t feel guilty about employing them.” Could the role of physician as legal drug pusher for our quick-fix society be any clearer?

Whether or not behavioral genetics is a pseudo-science that bolsters the prevailing cultural predilection to blame our problems on biology may be a further matter of opinion. But it is a fact that our genes do not, and cannot, determine how we behave.

Whether or not behavioral genetics is a pseudo-science that bolsters the prevailing cultural predilection to blame our problems on biology may be a further matter of opinion. But it is a fact that our genes do not, and cannot, determine how we behave. Hinshaw says we must “transcend either/ or, biological/environmental thinking,” yet he repeatedly privileges genes over development. He also relies on the big myth of behavioral genetics, that by using twin studies one can separate the influence of nature from nurture. In truth, when researchers compare identical and fraternal twins, they are still comparing nature-nurture interactions (in one group) with nature-nurture interactions (in another group). The real discovery of ­behavioral genetics is that genes are tangled up in almost everything we do. But so what?

We can change the lives of children, and profoundly, but we cannot change their genes.

Finally, it may be a matter of opinion whether or not studies of family influence on “ADHD” are systematically ignored by the medical establishment because that establishment is in the business of turning all psycho-social problems into medical ones. But it is a fact that these studies exist in growing numbers, and consistently show the powerful effects of parenting on children. (Even a study by Russell Barkley showed that one of the best predictors of “ADHD” was how much time Dad spent at home.) Hinshaw says the work by Jacobvitz and others needs replication, but replication has long existed. For example, Sheryl Olson and others conducted a six-year longitudinal study, reporting that parenting during the child’s first two years had clear effects on later development of impulse control.3 Hinshaw blames parenting problems on the child, but longitudinal studies measure the effects of parenting prior to the onset of the child’s behavioral problems.

In the end, Hinshaw counsels us not to worry. Yet he concedes that “ADHD” is widely overdiagnosed, that Ritalin may indeed cause brain damage, that Ritalin does not cure a child’s problems, and that psycho-social interventions can have powerful effects. Where, in all this, are we to find the basis for Hinshaw’s optimism? Nothing in the current medicalized approach acts as a brake on the rush to diagnose and drug children, and there are absolutely no safeguards within that approach to begin to slow the observed trends. Moreover, the manner in which one may diagnose “ADHD”—and the nonspecific but easily observed effects of stimulants on children with any of a variety of developmental problems—is such that the medicalized approach knows no bounds.

As medical historian David Rothman concluded, writing in the New Republic: “Anyone who expects physicians to save us from ourselves, or from the worst imaginable abuses of twenty-first century medical interventions, whether they involve genetic engineering, pharmacological interventions or surgical procedures, had better start searching for alternatives.” 

HINSHAW

CLOSING STATEMENT

This exchange ranges across science, medi­cine, politics, and policy. Unfortunately, DeGrandpre has resorted to emotional attacks rather than scientific data to bolster his claims. It is fallacious to pretend that serious psychiatric conditions of childhood (or adulthood) are solely social constructions or responses to the environment.

MISCONCEPTIONS AND MISINTERPRETATIONS

I suggest six important misconceptions or misinterpretations in what DeGrandpre writes.

First, counter to DeGrandpre’s accu­sation, I strongly believe that developmental experiences can lead to disturbance; child abuse provides a clear example. But, where­as impairment can exist in the absence of a medical disorder, ADHD is a complex condition in which several psycho-biologic risk factors (genetic, prenatal, perinatal) are influenced from an early age by a child’s relationships with parents and teachers, which in turn influence the child’s subsequent brain development and emerging capacities.

Overly permissive or overly harsh parenting can lead to troublesome outcomes, but alone they do not cause ADHD. Unfortu­nately, DeGrandpre’s critiques of the medical model apply to stereotypic, outmoded views, which have been supplanted by complex bio-psycho-social conceptions of disorder. He is out of date.

He also claims that any physiologic imbalances in children with ADHD may be the result of chronic use of stimulants. As already stated, studies with untreated children directly counter this notion. He says, in addition, that I “concede” that Ritalin causes brain damage. In fact, I stated that, whereas Ritalin and other stimulants can be drugs of abuse if used indiscriminately, no evidence of brain damage exists with appropriate medical use.

Next, DeGrandpre has trouble distinguishing between concordance and heritability: The former is a measure of twin similarity; the latter, a proportion of trait variance attributable to genetic influence. The key point is that although genetic influences for ADHD are strong, they are not final determinants of outcome for any individual child. In terms of culture, DeGrandpre claims that ADHD simply does not exist in other countries, a con­tention without empirical support

DeGrandpre contends that mine is a static conception of the context in which children are developing, but he ignores my earlier words: Increased demands for sustained attention, influences of media and video games, and faster pacing of society may have profound influences on the development of attentional and inhibitory capacities. Further, my own research with carefully diagnosed children with ADHD has shown that negative parenting predicts noncompliance and covert antisocial behavior, such as stealing, in such children, even when we control statistically for the child’s difficult behavior with the parent. That is, harsh, critical parenting contributes to ADHD children’s antisocial outcomes outside the home. I have also demonstrated that authoritative parenting beliefs—such as parental warmth, limit setting, and encour­agement of autonomy—predict social competence in boys with ADHD, specifically acceptance from peers. Such parenting beliefs are difficult to maintain when raising a child with ADHD, but they make a difference in terms of social competence. In sum, both impairments and competencies in children with ADHD are clearly subject to environmental influence.

Regarding treatment, DeGrandpre contends that pharmaceutical companies underwrote the MTA study (untrue: it was funded completely by the National Institute of Mental Health and the Office of Educa­tion) and that the psycho-social treatments used were not well delivered or intensive. In fact, the 14-month treatment was state of the art, incorporating the very behavioral management strategies DeGrandpre extols (35 parent-training sessions, biweekly school consultation, eight-week summer treatment program, paraprofessional aide in the classroom for three months). Although I firmly believe in the power of such psycho­social treatments, MTA results echoed those of many previous investigations, showing that medication effects were stronger than effects of these interventions. Again, combination treatment (medication plus psycho-social) yielded the highest percentage of children with meaningful clinical response; such combination treatment appeared optimal for academic, social, and familyrelated outcomes. Concern is justified if medication treatments dissuade families and schools from initiating important social, school, and family treatments that may promote longer-term change. Finally, I caution readers that Peter Breggin, whom DeGrandpre champions as a defender of children, has stated that conditions such as manic-depressive illness are problems in living rather than biologically rooted psychiatric conditions. Such opinions are dangerously ignorant and potentially life-threatening. Serious disorders are not merely social constructions or environmental responses.

Children and society are ill served by extreme positions that overattribute all problems of contemporary youth to ADHD or deny the existence of ADHD as an important syndrome. Light—sound empirical knowledge —rather than heat—polemic— is the antidote.

WHERE ARE WE?

As I sum up, let me call attention to a biologically based, highly heritable childhood condition that also has risen dramatically in prevalence in recent decades and that responds well to aggressive medical intervention. The condition? Asthma. Yet there is little public alarm about asthma’s diagnosis and treatment—largely because its symptoms affect the lungs rather than the brain. There is still strong resistance to the contention that behavioral and emotional disorders are as real, or psycho-biologically based, as physical disorders. At the same time, because the developing brain is quite plastic (that is, subject to enormous environmental influence and capable of self-organization), we must fully consider complex, interacting pathways in the genesis of psychiatric disorders.

Although we have much to learn about ADHD, and although its core symptoms in moderate form are part of normal development, if ADHD is carefully assessed it is a reliable and valid diagnosis, manifest in a range of cultures, and severely impairing. Children and society are ill served by extreme positions that overattribute all problems of contemporary youth to ADHD or deny the existence of ADHD as an important syndrome. Light—sound empirical knowledge—rather than heat—polemic— is the antidote.

References

Richard J. DeGrandpre

  1. These statistics were provided by researcher and author David Cohen.
  2. Tyson, K. Childhood hyperactivity. Smith College Studies in Social Work 1991: 61, 133-160.
  3. Brown, RT, & Pacini, JN. Perceived family function­ing, marital status, and depression in parents of boys with attention deficit disorder. Journal of Learn­ing Disabilities 1989: 22, 581-587; Jacobvitz, D, & Sroufe, LA. The early care giver-child relationship and attention-deficit disorder with hyperactivity in kindergarten: A prospective study. Child Development 1987: 58, 1496-1504; MacDonald, K. Parent-child interactions of ADHD children: Comparisons with children of differing socio metric status. (ERIC Document Reproduction Service No. ED 1989: 307, 999); Olson, SL, Bates, JE, & Bayles, K. Early antecedents of childhood impulsivity: The role of parent-child interaction, cognitive competence, and temperament. Journal of Abnormal Child Psychology 1990: 18, 317-334.
  4. Carlson, EA, Jacobvitz, D., & Sroufe, LA. A develop­mental investigation of inattentiveness and hyperactivity. Child Development 1995: 66, 37-54.
  5. Vaidya, CJ et al. Selective effects of methylphenidate in attention deficit hyperactivity disorder: A functional magnetic resonance study. Proceedings of the National Academy of Sciences 1998: 95, 14494-14499.
  6. DeGrandpre, RJ. Just cause? The Sciences March/April, 1999: 14-18.
  7. Baxter, LR et al. Caudate glucose metabolic rate changes with both drug and behavior therapy for obsessive-compulsive disorder. Archives of General Psychiatry 1992: 49, 681-689; Coleman, M. Serotonin concentrations in whole blood of hyperactive children. Journal of Pediatrics 1971: 78, 985-990.
  8. Nasrallah, HA et al. Cortical atrophy in young adults with a history of hyperactivity in childhood. Psychiatry Research 1986: 17, 241-246.
  9. Barkley, RA. Attention-deficit hyperactivity disorder. Scientific American, September, 1998: 66-71.
  10. DeGrandpre, RJ. Ritalin Nation: Rapid-fire Culture and the Transformation of Human Consciousness 1999. New York: Norton.
  11. Swanson, M et al. Effect of stimulant medication on children with Attention Deficit Disorder: A “Review of Reviews”. Exceptional Children 1993: 60, 154-162.
  12. Barkley, RA & Cunningham, CE. Do stimulant drugs improve the academic performance of hyperkinetic children? Clinical Pediatrics, 1978: 17, 85-92.

Stephen P. Hinshaw

  1. Tannock, R. “Attention deficit hyperactivity disorder: advances in cognitive, Neurobiological, and Genetic Research.” Journal of Child Psychology and Psychiatry 1998; 39: 65-99.
  2. Barkley, RA. ADHD and the Nature of Self-Control. New York. Guilford, 1997.
  3. “Diagnosis and treatment of attention deficit hyper­activity disorder (ADHD).” NIH Consensus Statement 1998 Nov 16-18; 16(2): 1-37.
  4. Hinshaw, SP. “Is ADHD an impairing condition in childhood and adolescence?” In P S Jensen & J R Cooper (Eds.), Diagnosis and Treatment of Attention-deficit Hyperactivity Disorder: An Evidence-Based Approach. Washington, DC. American Psychiatric Press, in press.
  5. Mannuzza, S and Klein, RG. “Adolescent and adult outcomes in attention-deficit hyperactivity disorder.” In HC Quay and AE Hogan (Eds.), Handbook of Disruptive Behavior Disorders. New York: Guilford, 1999: 279-294.
  6. Tannock, R. “Attention deficit hyperactivity disorder: advances in cognitive, neurobiological, and genetic research.” Journal of Child Psychology and Psychiatry 1998; 39:65-99.
  7. Hinshaw, SP, Zupan, BA, Simmel, C, et al. “Peer status in boys with and without attention-deficit hyperactivity disorder: predictions from overt and covert antisocial behavior, social isolation, and authoritative parenting Beliefs.” Child Development 1997; 64: 880-896.
  8. Hinshaw, SP, Owens, EB, Wells, KC, et al. “Family processes and treatment outcome in the MTA: negative/ineffective parenting practices in relation to multimodal treatment.” Journal of Abnormal Child Psychology in Press.
  9. Greenhill, LL. “Childhood Attention Deficit Hyperactivity Disorder: Pharmacological Treatments.” In PE Nathan and JM Gorman (Eds.), A Guide to Treatments that Work. Oxford University Press. New York, 1998: 42-64; Hinshaw, SP. Attention-deficit hyperactivity disorder: The search for viable treatments. In PC Kindall (Ed.), Child and Adult Therapy: Cognitive-Behavioral Procedures (2nd ed). Guilford Press. New York, 2000: 88-128.
  10. MTA Cooperative Group. “Fourteen-month randomized clinical trial of treatment strategies for attention­ deficit hyperactivity disorder.” Archives of General Psychiatry 1999; 56:1073-1086; MTA Cooperative Group. “Moderators and mediators of treatment response for children with ADHD: the MTA study. Archives of General Psychiatry 1999; 56:1088- 1096.
  11. Ibid.
  12. Taylor, E. “Development of clinical services for attention-deficit/hyperactivity disorder.” Archives of General Psychiatry 1999; 56: 1097-1099.
  13. “Diagnosis and treatment of attention deficit hyperactivity disorder (ADHD).” NIH Consensus Statement 1998 Nov 16-18; 16(2): 1-37.
  14. Tannock, R. “Attention deficit hyperactivity disorder: advances in cognitive, neurobiological, and genetic research.” Journal of Child Psychology and Psychiatry 1998; 39: 65-99.



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Scientific Advisory Board
Joseph T. Coyle, M.D., Harvard Medical School
Kay Redfield Jamison, Ph.D., The Johns Hopkins University School of Medicine
Pierre J. Magistretti, M.D., Ph.D., University of Lausanne Medical School and Hospital
Robert Malenka, M.D., Ph.D., Stanford University School of Medicine
Bruce S. McEwen, Ph.D., The Rockefeller University
Donald Price, M.D., The Johns Hopkins University School of Medicine

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