The Arithmetic Pill: ADHD, ADD, and the Evidence

An Essay

In 1994, the American Psychiatric Association’s Textbook of Psychiatry made a quiet admission. After sixty years of prescribing stimulants to difficult children, the profession acknowledged that these drugs “do not produce lasting improvements in aggressivity, conduct disorder, criminality, educational achievement, job functioning, marital relationships, or long-term adjustment.” The statement appeared without fanfare, buried in a chapter that nonetheless recommended stimulant treatment.

The following year, a team of prominent ADHD researchers selected to lead a major National Institute of Mental Health study acknowledged the same thing. “The long-term efficacy of stimulant medication has not been demonstrated for any domain of child functioning,” they wrote in the study’s planning documents.

The NIMH then funded them to conduct the largest and longest trial of ADHD treatment ever attempted—579 children followed across multiple sites. But the investigators did not include a placebo control. Withholding “treatment of known efficacy,” they reasoned, would be unethical.

This circular logic—the drugs work, therefore we cannot test whether they work—structured everything that followed.

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Inventing a Disease

The condition now called ADHD has been renamed five times since 1952, each revision a strategic retreat from claims that research failed to support.

Psychiatry’s first Diagnostic and Statistical Manual described children with severe behavioral problems as suffering from “organic brain syndrome”—the assumption being that actual brain damage, perhaps from birth trauma or childhood illness, explained their difficulties. When no brain damage could be identified in most cases, the diagnosis became “minimal brain disease.” When no minimal brain disease could be demonstrated, it became “minimal brain dysfunction.” When no dysfunction could be reliably measured, DSM-III in 1980 abandoned biological language entirely and renamed it “attention deficit disorder,” a description of behavior rather than pathology.

The 1987 revision loosened the boundaries further, creating “attention deficit/hyperactivity disorder” and allowing diagnosis based on either inattention or hyperactivity or both. The population of potentially diagnosable children expanded dramatically. Fidgeting, difficulty waiting one’s turn, talking excessively, losing things—these became symptoms of a medical condition.

Peter Gøtzsche, the Danish physician and researcher, observes the logical endpoint of this framework. Those more energetic than average receive ADHD diagnoses. Those quieter than average receive ADD diagnoses. Perhaps, he suggests, we will eventually see a diagnosis for those in the middle: Activity Normal Disorder. These people too will surely need treatment.

The diagnostic category’s instability reflects not progressive scientific refinement but the absence of anything stable to refine. “Attempts to define a biological basis for ADHD have been consistently unsuccessful,” pediatric neurologist Gerald Golden wrote in 1991. “The neuroanatomy of the brain, as demonstrated by imaging studies, is normal. No neuropathologic substrate has been demonstrated.” Seven years later, a panel convened by the National Institutes of Health reached the same conclusion: “After years of clinical research and experience with ADHD, our knowledge about the cause or causes of ADHD remains largely speculative.”

During the 1990s, the parent advocacy group CHADD—funded in part by Ciba-Geigy, the manufacturer of Ritalin—advised the public that children with ADHD suffered from a chemical imbalance characterized by an underactive dopamine system. This was a marketing claim, not a scientific finding. The diagnosis today encompasses perhaps 3.5 million American children on stimulants. The United States consumes three times the quantity of these drugs consumed by the rest of the world’s children combined.

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What the Drugs Actually Do

The therapeutic story told about stimulants is that they correct an underlying deficit, allowing the child to function normally. The research literature tells a different story.

In 1978, Ohio State University psychologist Herbert Rie conducted a double-blind study of twenty-eight hyperactive children over three months. Half received methylphenidate. Here is what he observed:

Children who were retrospectively confirmed to have been on active drug treatment appeared, at the times of evaluation, distinctly more bland or “flat” emotionally, lacking both the age-typical variety and frequency of emotional expression. They responded less, exhibited little or no initiative or spontaneity, offered little indication of either interest or aversion, showed virtually no curiosity, surprise, or pleasure, and seemed devoid of humor. Jocular comments and humorous situations passed unnoticed. In short, while on active drug treatment, the children were relatively but unmistakably affectless, humorless, and apathetic.

Rie was not an outlier. Researchers reported in 1978 that children on Ritalin showed “a marked drug-related increase in solitary play and a corresponding reduction in their initiation of social interactions.” Nancy Fiedler at Bowling Green State University found the drug reduced children’s “curiosity about the environment.” Canadian pediatrician Till Davy noted that medicated children sometimes “lose their sparkle.” UCLA psychologists concluded in 1993 that stimulant-treated children often become “passive, submissive” and “socially withdrawn.” James Swanson, director of an ADHD center at the University of California, Irvine, observed that some children on the drugs “seem zombie-like.”

The Oxford Textbook of Clinical Psychopharmacology and Drug Therapy explains the mechanism straightforwardly: stimulants curb hyperactivity by “reducing the number of behavioral responses.”

These observations clarify what the drugs accomplish. A child who previously annoyed teachers by fidgeting or talking to classmates becomes still. Given a repetitive task like arithmetic problems, the child may focus intently. Charles Bradley, who first administered amphetamines to children in 1937, called this change “an improvement from the social viewpoint.” The children dubbed Benzedrine the “arithmetic pill.”

The social viewpoint is the teacher’s viewpoint. Rating instruments filled out by teachers and observers treat a reduction in the child’s movements and social engagement as positive outcomes. When results are tabulated, 70 to 90 percent of children register as “good responders.” NIMH investigators wrote in 1995 that stimulants dramatically reduce “task-irrelevant activity (e.g., finger tapping, fidgetiness, fine motor movement, off-task behavior during direct observation) and classroom disturbance.”

None of this tells of treatment that benefits the child.

When researchers asked the children themselves what they thought of Ritalin, they found something different. “Above all else,” wrote Esther Sleator, a physician at the University of Illinois who interviewed fifty-two children, “we found a pervasive dislike among hyperactive children for taking stimulants.” University of Texas psychologist Deborah Jacobvitz reported in 1990 that children on Ritalin rated themselves as “less happy and less pleased with themselves and more dysphoric.” When it came to making and keeping friends, stimulants produced “few significant positive effects and a high incidence of negative effects.”

Other researchers documented how the drugs damaged children’s self-conception. The child comes to believe, as University of Minnesota psychologist Alan Sroufe wrote in 1973, “not in the soundness of his own brain and body, not in his own growing ability to learn and to control his behavior, but in ‘my magic pills that make me into a good boy.’”

The question of whether stimulants at least helped children succeed academically—to get good grades and thrive as students—met the same wall. Being able to focus intently on a math test did not translate into long-term academic achievement. Sroufe explained that the drugs enhance performance on “repetitive, routinized tasks that require sustained attention,” but “reasoning, problem solving and learning do not seem to be positively affected.” Rie found no benefit on “vocabulary, reading, spelling, or math,” and noted that the drugs hindered problem-solving ability. “The reactions of the children strongly suggest a reduction in commitment of the sort that would seem critical for learning.”

Barkley concluded in 1978 that “the major effect of stimulants appears to be an improvement in classroom manageability rather than academic performance.” Carol Whalen, a psychologist at UC Irvine, warned in 1997 that “especially worrisome has been the suggestion that the unsalutary effects occur in the realm of complex, high-order cognitive functions such as flexible problem-solving or divergent thinking.” A 2002 Canadian meta-analysis of fourteen studies involving 1,379 youths found “little evidence for improved academic performance.”

Nor did staying on stimulants produce sustained behavioral improvement. When children stopped taking Ritalin, ADHD behaviors regularly flared up worse than before. “It is often disheartening to observe how rapidly behavior deteriorates when medication is discontinued,” Whalen acknowledged. Swanson advised in 1993 that “teachers and parents should not expect long-term improvement in academic achievement or reduced antisocial behavior.”

This was the state of knowledge when the NIMH launched its landmark study.

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The MTA Study

The Multisite Multimodal Treatment Study of Children with ADHD enrolled 579 children and randomized them to four groups: medication management, behavioral therapy, combined treatment, or routine community care. It was the first major clinical trial the NIMH had ever conducted of a childhood mental disorder.

At fourteen months, the investigators declared victory for medication. “Carefully crafted medication management” had proven “superior” to behavioral treatment in reducing core ADHD symptoms. There was also a hint that medicated children fared better on reading tests. The researchers concluded that “since ADHD is now regarded by most experts as a chronic disorder, ongoing treatment often seems necessary.”

The study then shifted to naturalistic follow-up. Children were no longer randomized; investigators simply tracked who was taking medication and how everyone fared over time.

At three years, the results reversed. Medication use was now “a significant marker not of beneficial outcome, but of deterioration.” Children using medication showed increased symptomatology compared to those not taking drugs. They also had higher delinquency scores, meaning they were more likely to get into trouble at school and with police. They were shorter and weighed less than their off-medication counterparts.

It took seven years from the original fourteen-month results for the investigators to publish this three-year data. A companion paper reported higher rates of substance abuse in the methylphenidate group than in the behavioral therapy group, though this finding was difficult to locate amid complicated statistics. The authors disclosed their financial conflicts of interest: on average, thirteen drug companies per author.

At six and eight years, the findings held. Medication use remained associated with worse hyperactivity-impulsivity and oppositional symptoms, with greater overall functional impairment. There were no differences between groups for school grades, arrests, or psychiatric hospitalizations. By this point, 62 percent of participants had stopped taking the study medications—a natural experiment that should have influenced prescribing practices but did not.

William Pelham, one of the principal investigators, eventually said publicly what the data showed: “We had thought that children medicated longer would have better outcomes. That didn’t happen to be the case. There were no beneficial effects, none. In the short term, medication will help the child behave better, in the long run it won’t. And that information should be made very clear to parents.”

The NIMH did not make it clear. When announcing the three-year results, the press release carried this headline: IMPROVEMENT FOLLOWING ADHD TREATMENT SUSTAINED FOR MOST CHILDREN. The text acknowledged that “continuing medication was no longer associated with better outcomes by the third year,” but lead author Peter Jensen provided a quote suggesting continued reason for optimism: “Our results suggest that medication can make a long-term difference for some children if it’s continued with optimal intensity, and not started or added too late in a child’s clinical course.”

The agency issued eighty-nine press releases in 2007. None announced the findings of Martin Harrow’s long-term study of schizophrenia outcomes showing superior results for unmedicated patients—arguably the best such study ever conducted in the United States. The pattern is consistent: when findings support medication, the press release gong sounds; when findings undermine medication, silence.

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The Study That Never Was

Nadine Lambert, a professor at UC Berkeley, conducted a 26-year follow-up of 492 children, half of whom had received an ADHD diagnosis. Her findings, presented at a 1998 conference, were stark.

Among those who had never smoked and never taken stimulants, 2 percent became cocaine-dependent as adults. Among those who both smoked and were treated with stimulants: 40 percent.

The study was not a randomized trial. But the magnitude of the finding—a twentyfold increase in cocaine dependence—warranted attention, replication, investigation. Instead, after Lambert presented her results, the National Institute on Drug Abuse stopped funding her work.

Lambert died in a car accident in 2006. Her study was never published. Her colleagues, perhaps, did not favor her conclusions.

The MTA study’s companion paper on substance abuse had already pointed in the same direction, showing higher rates in the methylphenidate group. This outcome should not surprise. The drugs are, after all, narcotics.

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The Controlled Substance Paradox

Methylphenidate is classified by the Drug Enforcement Administration as Schedule II—the most restrictive category for drugs with accepted medical use, reserved for substances with high potential for abuse that may lead to severe psychological or physical dependence. It shares this classification with morphine, oxycodone, and cocaine.

Goodman and Gilman’s The Pharmacological Basis of Therapeutics, the standard pharmacology reference, states that Ritalin is “structurally related to amphetamine” and that “its pharmacological properties are essentially the same as those of the amphetamines.”

The DSM itself, in its 1987 revision, described the pattern of Ritalin abuse as “very similar to those of Cocaine Dependence and Abuse” and noted that “controlled studies have shown that experienced users are unable to distinguish amphetamine from cocaine.”

That same DSM described the typical pattern of amphetamine dependence: “Chronic daily, or almost daily, use may be at high or low doses. Use may be throughout the course of the day or be restricted to certain hours, e.g., only during the working hours or only during the evening. In this pattern there are usually no wide fluctuations in the amount of amphetamine used on successive occasions, but there is often a general increase in doses over time.”

This description matches precisely the regimen physicians impose on children diagnosed with ADHD—daily use, often restricted to school hours, frequently with dose increases over time.

Peter Breggin poses the question the profession has never adequately answered: When an adult uses stimulants daily in a compulsive pattern, this constitutes a serious epidemic disease requiring intervention. When the same pattern is imposed on children by physicians, it constitutes treatment. On what basis is the distinction made?

The drugs also cause the very problems they purportedly treat. Long-term use tends to create “attentional disturbances” and “memory problems” as well as irritability and hyperactivity. When children continue to have focusing difficulties after years on Ritalin, the disorder itself may be drug-induced—a vicious circle in which drug-caused inattention leads to increased dosing, all while the problem is blamed on the child’s defective brain.

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What Animal Studies Show

Rats and monkeys cannot tell us what the drugs feel like. They can show what the drugs do to developing brains.

Yale School of Medicine researchers reported in 1999 that repeated amphetamine exposure caused monkeys to exhibit aberrant behaviors that persisted long after drug exposure stopped. Scientists at Texas Southwestern Medical Center found that preadolescent rats exposed to methylphenidate for fifteen days became anxious, depressed adult rats. They moved around less, responded less to novel environments, and showed deficits in sexual behavior. The researchers concluded that methylphenidate administration during brain development “results in aberrant behavioral adaptations during adulthood.”

Other rat studies suggested that lengthy methylphenidate exposure might permanently desensitize dopaminergic pathways. Since dopamine constitutes the brain’s reward system, medicating children may produce adults with a reduced physiological capacity to experience pleasure—a finding consistent with Lambert’s observation of elevated cocaine dependence among the stimulant-treated.

Henry Nasrallah’s 1986 study found cortical atrophy in more than half of young adults with a history of stimulant treatment—the same kind of brain shrinkage associated with antipsychotic drugs. “This finding,” the authors wrote, “may be a long-term adverse effect of this treatment.” One study, never replicated, never refuted. The profession moved on.

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The Harm Ledger

With any medication, physicians weigh benefits against risks. In this case, the NIMH’s own flagship study found no long-term benefits to enter on the ledger. That leaves only risks.

The physical effects: drowsiness, appetite loss, lethargy, insomnia, headaches, abdominal pain, motor abnormalities, facial and vocal tics, jaw clenching, skin problems, liver disorders, weight loss, growth suppression, hypertension, cardiac arrhythmias, and sudden death. The emotional effects: depression, apathy, general dullness, mood swings, crying jags, irritability, anxiety, and hostility. The psychiatric effects: obsessive-compulsive symptoms, mania, paranoia, psychotic episodes, and hallucinations. FDA package inserts list cardiovascular events including myocardial infarction and stroke. Children have dropped dead.

Stimulants double the risk of cardiovascular events. The FDA warned in 2023 that these drugs can lead to substance use disorder and addiction even when prescribed for an indicated disorder, and that this can result in overdose and death. In 2017, there were 10,333 stimulant-involved drug overdose deaths in the United States, compared to 1,378 in 2007.

Adderall—a mixture of amphetamine salts—was originally marketed as Obetrol, a weight-loss drug withdrawn due to its addictive properties. It was reformulated and rebranded for ADHD. Canada withdrew it in 2005 after 14 children suddenly died and two had strokes. The FDA took no action except to lobby Canadian regulators to reverse their decision.

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Where the Children Go Next

There is one additional pathway that the stimulant-treated child may travel, and it leads somewhere darker.

Stimulants induce both arousal and dysphoric symptoms. These drug-induced effects overlap remarkably with the symptoms psychiatry uses to diagnose juvenile bipolar disorder. Every child on a stimulant turns, in effect, a bit bipolar.

Joseph Biederman, the Harvard psychiatrist who promoted ADHD as a chronic disorder requiring lifelong treatment, reported in 1996 that 11 percent of children diagnosed with ADHD developed bipolar symptoms—symptoms not present at initial diagnosis—within four years of starting stimulant treatment. If 3.5 million American children take stimulants, this rate would generate approximately 400,000 new bipolar cases.

SSRIs prescribed to children compound the effect. University of Pittsburgh researchers found in 1992 that 23 percent of boys treated with Prozac developed mania or manic-like symptoms. Yale researchers determined in 2004 that the risk of antidepressant-induced mania is highest in children under thirteen. Harvard psychiatrists found that 25 percent of children diagnosed with depression convert to bipolar within two to four years, with antidepressants likely inducing the switching. Barbara Geller at Washington University extended follow-up to ten years: nearly half of prepubertal children treated for depression became bipolar.

The childhood bipolar diagnosis was virtually unknown before the 1990s. By 2003, prevalence had increased fortyfold. By 2007, half a million children—twenty thousand of them under age six—were prescribed antipsychotic medications that a decade earlier would have been reserved for the most severe adult cases. American doctors now diagnose childhood bipolar 100 times more often than their British counterparts.

The antipsychotics prescribed to bipolar children carry their own devastation: sedation so heavy it becomes impossible to determine whether the drugs treat the condition or simply tranquilize the child; cataracts, obesity, diabetes, tardive dyskinesia; a twelve-to-twenty-year decrease in life expectancy for treated versus untreated patients.

Biederman received $1.6 million from pharmaceutical companies between 2000 and 2007, much of it from Janssen, which manufactures Risperdal. He established the Johnson & Johnson Center for Pediatric Psychopathology, which he described in internal documents as a “strategic collaboration” designed to “move forward the commercial goals of J&J.” The center would train physicians to diagnose juvenile bipolar and promote understanding that these children would need Risperdal “from childhood through adulthood.”

Asked in a 2009 deposition how he determined that children previously labeled with conduct disorder or oppositional-defiant disorder should instead receive bipolar diagnoses, Biederman explained: “The conditions that we see in front of us are reconceptualized.” He had previously, he noted, “successfully led the medical profession to conceive of ADHD as a chronic illness,” and now he would do the same for bipolar disorder.

The child diagnosed with ADHD receives stimulants. The stimulants induce mood instability. The mood instability generates a bipolar diagnosis. The bipolar diagnosis leads to antipsychotics. The antipsychotics cause metabolic syndrome and shortened lifespan. At each stage, the drugs create the symptoms that justify the next diagnosis and the next prescription.

Every child who enters this sequence is, from a business perspective, a reliable long-term customer.

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What Should Be Made Clear

William Pelham said the MTA data should be made very clear to parents. It has not been.

The profession continues to prescribe stimulants to millions of children while acknowledging in its own literature that these drugs produce no lasting benefits in any domain of functioning. It classifies these drugs alongside morphine and cocaine while assuring parents they are safe and effective. It publishes studies showing that medication use predicts worse long-term outcomes, then issues press releases claiming sustained improvement. It watches one in nine medicated children develop bipolar symptoms and responds by prescribing additional drugs.

The children who take these medications experience themselves as less happy and more dysphoric. They lose curiosity, spontaneity, the capacity for surprise and pleasure. They become, in the clinical language, affectless and apathetic. They sit still.

Their teachers are satisfied. The rating scales show improvement. The drugs, by every measure that matters to the adults who administer them, work.

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References

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Whitaker, Robert. Anatomy of an Epidemic, 2nd ed. New York: Broadway Paperbacks, 2015.

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