Anatomy of an Epidemic Chapter 11 The Epidemic Spreads to Children

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Anatomy of an Epidemic Chapter 11. The Epidemic Spreads to Children

Author: Robert Whitaker Publisher: New York , NY: Crown Publishing. Publish Date: 2010-3-31 Review Date: Status:💥

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The notion that stimulants might be beneficial for such children arose in 1937, when Charles Bradley gave a newly synthesized amphetamine, Benzedrine, to hyperactive children who complained of headaches. Although the drug didn’t cure their head pain, Bradley reported that it “subdued” the children and helped them concentrate better on their schoolwork. The children dubbed Benzedrine the “arithmetic pill.”6

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Although his report was mostly forgotten for the next twenty years, in 1956 Ciba-Geigy brought Ritalin (methylphenidate) to market as a treatment for narcolepsy, touting it as a “safe” alternative to amphetamines, and physicians at Johns Hopkins University School of Medicine, who were aware of Bradley’s findings, soon deemed this new drug useful for quieting “disturbed” children who were thought to be suffering from a “brain damage syndrome.”7

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There was no great rush by psychiatrists during the 1960s to prescribe Ritalin to fidgety children who went to regular schools. At that time, there was a sense that psychoactive drugs, because of their many risks, should be administered only to hospitalized children, or children in residential facilities. The population of children so hyperactive that they might be diagnosed with “organic brain dysfunction” was small. However, psychiatry’s use of Ritalin slowly began to climb during the 1970s, such that by the end of the decade perhaps 150,000 children in the United States were taking the drug. Then, in 1980, the field published a third edition of its Diagnostic and Statistical Manual (DSM-III), and it identified “attention-deficit disorder” as a disease for the first time. The cardinal symptoms were “hyperactivity,” “inattention,” and “impulsivity,” and given that many children fidget in their seats and have trouble paying attention in school, the diagnosis of ADD began to take off. In 1987, psychiatry further loosened the diagnostic boundaries, renaming it attention-deficit/hyperactivity disorder in a revised edition of DSM-III. Next, Ciba-Geigy helped fund Children and Adults with Attention Deficit Hyperactivity Disorder (CHADD), a “patient-support group” that immediately began promoting public awareness of this “disease.”

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Finally, in 1991, CHADD successfully lobbied Congress to include ADHD as a disability that would be covered by the Individuals with Disabilities Education Act. Children diagnosed with ADHD were now eligible for special services, which were to be funded with federal money, and schools regularly began identifying children who seemed to have this condition. As the Harvard Review of Psychiatry noted in 2009, even today the diagnosis of ADHD arises primarily from teacher complaints, as “only a minority of children with the disorder exhibit symptoms during a physician’s office visit.”8

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Suddenly, ADHD children could be found in every classroom. The number of children so diagnosed rose to nearly 1 million in 1990, and more than doubled over the next five years. Today, perhaps 3.5 million American children take a stimulant for ADHD, with the Centers for Disease Control reporting in 2007 that one in every twenty-three American children four to seventeen years old is so medicated. This prescribing practice is mostly a U.S. phenomenon—children here consume three times the quantity of stimulants consumed by the rest of the world’s children combined.

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Although the public often hears that research has shown that ADHD is a “brain disease,” the truth is that its etiology remains unknown. “Attempts to define a biological basis for ADHD have been consistently unsuccessful,” wrote pediatric neurologist Gerald Golden in 1991. “The neuroanatomy of the brain, as demonstrated by imaging studies, is normal. No neuropathologic substrate has been demonstrated.”9 Seven years later, a panel of experts convened by the National Institutes of Health reiterated this same point: “After years of clinical research and experience with ADHD, our knowledge about the cause or causes of ADHD remains largely speculative.”10

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G. Golden, “Role of attention deficit hyperactivity disorder in learning disabilities,” Seminars in Neurology 11 (1991): 35–41.

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NIH Consensus Development Conference statement, “Diagnosis and treatment of attention deficit hyperactivity disorder,” November 16–18, 1998.

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During the 1990s, CHADD advised the public that children with ADHD suffered from a chemical imbalance, characterized by an underactive dopamine system, but that was simply a drug-marketing claim. Ritalin and other stimulants increase dopamine levels in the synaptic cleft, and thus CHADD was attempting to make it seem that such drugs “normalized” brain chemistry, but, as the American Psychiatric Press’s 1997 Textbook of Neuropsychiatry confessed, “efforts to identify a selective neurochemical imbalance [in ADHD children] have been disappointing.”11

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Given that the biology of ADHD remains unknown, it is fair to say that Ritalin and other ADHD drugs “work” by perturbing neurotransmitter systems. Ritalin could best be described as a dopamine reuptake inhibitor. At a therapeutic dose, it blocks 70 percent of the “transporters” that remove dopamine from the synaptic cleft and bring it back into the presynaptic neuron. Cocaine acts on the brain in the same way. However, methylphenidate clears much more slowly from the brain than cocaine does, and thus it blocks dopamine reuptake for hours, as opposed to cocaine’s relatively brief disruption of this function.*

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In response to methylphenidate, the child’s brain goes through a series of compensatory adaptations. Dopamine is now remaining in the synaptic cleft too long, and so the child’s brain dials down its dopamine machinery. The density of dopamine receptors on the postsynaptic neurons declines. At the same time, the amount of dopamine metabolites in the cerebrospinal fluid drops, evidence that the presynaptic neurons are releasing less of it.

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Ritalin also acts on serotonin and norepinephrine neurons, and that causes similar compensatory changes in those two pathways. Receptor densities for serotonin and norepinephrine decline, and the output of those two chemicals by presynaptic neurons is altered as well. The child’s brain is now operating, as Steven Hyman said, in a manner that is “qualitatively as well as quantitatively different from the normal state.”12

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Ritalin and other ADHD drugs do reliably change a child’s behavior, and in his 1937 report, Charles Bradley set the stage for the efficacy story that eventually emerged: “Fifteen of the thirty children responded to Benzedrine by becoming distinctly subdued in their emotional responses. Clinically in all cases this was an improvement from the social viewpoint.”13 Ritalin, which the FDA approved for use in children in 1961, was found to have a similar subduing effect. In a 1978 double-blind study, Ohio State University psychologist Herbert Rie studied twenty-eight “hyperactive” children for three months, half of whom were prescribed methylphenidate. Here is what he wrote:

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.14

Numerous investigators reported similar observations. Children on Ritalin show “a marked drug-related increase in solitary play and a corresponding reduction in their initiation of social interactions,” announced Russell Barkley, a psychologist at the Medical College of Wisconsin, in 1978.15 This drug, observed Bowling Green State University psychologist Nancy Fiedler, reduced a child’s “curiosity about the environment.”16 At times, the medicated child “loses his sparkle,” wrote Canadian pediatrician Till Davy in 1989.17 Children treated with a stimulant, concluded a team of UCLA psychologists in 1993, often become “passive, submissive” and “socially withdrawn.”18 Some children on the drug “seem zombie-like,” noted psychologist James Swanson, director of an ADHD center at the University of California, Irvine.19 Stimulants, explained the editors of the Oxford Textbook of Clinical Psychophamacology and Drug Therapy, curb hyperactivity by “reducing the number of behavioral responses.”20

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Breggin, Talking Back to Ritalin, 83.

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H. Rie, “Effects of methylphenidate on underachieving children,” Journal of Consulting and Clinical Psychology 44 (1976): 250–60.

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C. Cunningham, “The effects of methylphenidate on the mother-child interactions of hyperactive identical twins,” Developmental Medicine & Child Neurology 20 (1978): 634–42.

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N. Fiedler, “The effects of stimulant drugs on curiosity behaviors of hyperactive boys,” Journal of Abnormal Child Psychology 11 (1983): 193–206.

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T. Davy, “Stimulant medication and short attention span,” Journal of Developmental & Behavioral Pediatrics 10 (1989): 313–18.

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D. Granger, “Perceptions of methylphenidate effects on hyperactive children’s peer interactions,” Journal of Abnormal Child Psychology 21 (1993): 535–49.

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J. Swanson, “Effects of stimulant medication on learning in children with ADHD,” Journal of Learning Disabilities 24 (1991): 219–30.

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Breggin, Talking Back to Ritalin, 92.

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All of these reports told the same story. On Ritalin, a student who previously had been an annoyance in the classroom, fidgeting too much in his or her chair or talking to a nearby classmate while the teacher scribbled on the blackboard, would be stilled. The student wouldn’t move around as much and wouldn’t engage as much socially with his or her peers. If given a task like answering arithmetic problems, the student might focus intently on it. Charles Bradley thought this change in behavior was “an improvement from the social viewpoint,” and it is that perspective that shows up in efficacy trials of Ritalin and other ADHD drugs. Teachers and other observers fill out rating instruments that view a reduction in the child’s movements and engagement with others as positive, and when the results are tabulated, 70 to 90 percent of the children are reported to be “good responders” to ADHD medications. These drugs, NIMH investigators wrote in 1995, are highly effective in “dramatically reducing a range of core ADHD symptoms such as task-irrelevant activity (e.g., finger tapping, fidgetiness, fine motor movement, off-task [behavior] during direct observation) and classroom disturbance.”21 ADHD experts at Massachusetts General Hospital summed up the scientific literature in a similar way: “The extant literature clearly documents that stimulants diminish behaviors prototypical of ADHD, including motoric overactivity, impulsivity, and inattentiveness.”22

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J. Richters, “NIMH Collaborative Multisite Multimodal Treatment Study of Children with ADHD,” Journal of the American Academy of Child & Adolescent Psychiatry 34 (1995): 987–1000.

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T. Spencer, “Pharmacotherapy of attention-deficit hyperactivity disorder across the life cycle,” Journal of the American Academy of Child & Adolescent Psychiatry 35 (1996): 409–32.

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However, none of this tells of drug treatment that benefits the child. Stimulants work for the teacher, but do they help the child? Here, right from the start, researchers ran into a wall. “Above all else,” wrote Esther Sleator, a physician at the University of Illinois who asked fifty-two children what they thought of Ritalin, “we found a pervasive dislike among hyperactive children for taking stimulants.”23 Children on Ritalin, University of Texas psychologist Deborah Jacobvitz reported in 1990, rated themselves as “less happy and [less] pleased with themselves and more dysphoric.” When it came to helping a child make friends and sustain friendships, stimulants produced “few significant positive effects and a high incidence of negative effects,” Jacobvitz said.24 Other researchers detailed how Ritalin harmed a child’s self-esteem, as the children felt they must be “bad” or “dumb” if they had to take such a pill. “The child comes to believe 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,’” said University of Minnesota psychologist Alan Sroufe.25

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E. Sleator, “How do hyperactive children feel about taking stimulants and will they tell the doctor?” Clinical Pediatrics 21 (1982): 474–79.

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D. Jacobvitz, “Treatment of attentional and hyperactivity problems in children with sympathomimetic drugs,” Journal of the American Academy of Child & Adolescent Psychiatry 29 (1990): 677–88.

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A. Sroufe, “Treating problem children with stimulant drugs,” New England Journal of Medicine 289 (1973): 407–13.

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All of this told of harm done, of a drug that made a child depressed, lonely, and filled with a sense of inadequacy, and when researchers looked at whether Ritalin at least helped hyperactive children fare well academically, to get good grades and thus succeed as students, they found that it wasn’t so. Being able to focus intently on a math test, it turned out, didn’t translate into long-term academic achievement. This drug, Sroufe explained in 1973, enhances performance on “repetitive, routinized tasks that require sustained attention,” but “reasoning, problem solving and learning do not seem to be [positively] affected.”26 Five years later, Herbert Rie was much more negative. He reported that Ritalin did not produce any benefit on the students’ “vocabulary, reading, spelling, or math,” and hindered their ability to solve problems. “The reactions of the children strongly suggest a reduction in commitment of the sort that would seem critical for learning.”27 That same year, Russell Barkley at the Medical College of Wisconsin reviewed the relevant scientific literature and concluded “the major effect of stimulants appears to be an improvement in classroom manageability rather than academic performance.”28 Next it was James Swanson’s turn to weigh in. The fact that the drugs often left children “isolated, withdrawn and overfocused” could “impair rather than improve learning,” he said.29 Carol Whalen, a psychologist from the University of California at Irvine, noted in 1997 that “especially worrisome has been the suggestion that the unsalutary effects [of Ritalin] occur in the realm of complex, high-order cognitive functions such as flexible problem-solving or divergent thinking.”30 Finally, in 2002, Canadian investigators conducted a meta-analysis of the literature, reviewing fourteen studies involving 1,379 youths that had lasted at least three months, and they determined that there was “little evidence for improved academic performance.”31

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Ibid.

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Rie, “Effects of methylphenidate.”

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R. Barkley, “Do stimulant drugs improve the academic performance of hyperkinetic children?” Clinical Pediatrics 8 (1978): 137–46.

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Swanson, “Effects of stimulant medication.”

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C. Whalen, “Stimulant pharmacotherapy for attention-deficit hyperactivity disorders,” in S. Fishberg and R. Greenberg, eds., From Placebo to Panacea (New York: John Wiley & Sons, 1997), 329.

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R. Schachar, “Attention-deficit hyperactivity disorder,” Canadian Journal of Psychiatry 47 (2002): 337–48.

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There was one other disappointment with Ritalin. When researchers looked at whether stimulants improved a child’s behavior over the long term, they couldn’t find any benefit. When a child stopped taking Ritalin, ADHD behaviors regularly flared up, the “excitability, impulsivity, or talkativeness” worse than ever. “It is often disheartening to observe how rapidly behavior deteriorates when medication is discontinued,” Whalen confessed.32 Nor was there evidence that staying on a stimulant led to a sustained improvement in behavior. “Teachers and parents should not expect long-term improvement in academic achievement or reduced antisocial behavior,” Swanson wrote in 1993.33 The 1994 edition of the APA’s Textbook of Psychiatry admitted to the same bottom-line conclusion: “Stimulants do not produce lasting improvements in aggressivity, conduct disorder, criminality, education achievement, job functioning, marital relationships, or long-term adjustment.”34 Thirty years of research had failed to provide any good-quality evidence that stimulants helped “hyperactive” children thrive, and in the early 1990s, a team of prominent ADHD experts picked to lead a long-term NIMH study, known as the Multisite Multimodal Treatment Study of Children with ADHD, acknowledged that this was so. “The long-term efficacy of stimulant medication has not been demonstrated for any domain of child functioning,” they wrote.35

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Whalen, “Stimulant pharmacotherapy,” 327.

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P. Breggin, “Psychostimulants in the treatment of children diagnosed with ADHD,” International Journal of Risk & Safety in Medicine 12 (1993): 3–35.

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Ibid.

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Richters, “NIMH Collaborative Multisite.”

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The NIMH touted its ADHD study as “the first major clinical trial” the institute had ever conducted of “a childhood mental disorder.” However, it was a rather flawed intellectual exercise right from the start. Although the investigators, led by Peter Jensen, associate director of child and adolescent research at the NIMH, acknowledged during the planning stages that there was no evidence in the scientific literature that stimulants improved long-term outcomes, they did not include a placebo control in the study, reasoning that it would have been “unethical” to withhold “treatment of known efficacy” for an extended period. The study basically compared drug treatment to behavioral therapy, but in that latter group, 20 percent were on a stimulant at the start of the trial, and there never was a time during the fourteen months that all of the children in that group were off such medication.36

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P. Jensen, “3-year follow-up of the NIMH MTA study,” Journal of the American Academy of Child & Adolescent Psychiatry 46 (2007): 989–1002. See chart on page 997 for medication use.

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Despite this obvious design flaw, the NIMH-funded investigators declared victory for the stimulants at the end of fourteen months. “Carefully crafted medication management” had proven to be “superior” to behavioral treatment in terms of reducing core ADHD symptoms. There was also a hint that the medicated children had fared better on reading tests (although not in other academic subjects), and as a result, psychiatry now had a long-term study that documented the continuing benefits of stimulants. “Since ADHD is now regarded by most experts as a chronic disorder, ongoing treatment often seems necessary,” the researchers concluded.37

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The MTA Cooperative Group, “A 14-month randomized clinical trial of treatment strategies for attention-deficit/hyperactivity disorder,” Archives of General Psychiatry 56 (1999): 1073–86.

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After that initial fourteen-month period of treatment, the investigators followed up periodically with the students, assessing how they were doing and whether they were taking an ADHD medication.

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At the end of three years, Jensen and the others discovered that “medication use was a significant marker not of beneficial outcome, but of deterioration. That is, participants using medication in the 24-to-36 month period actually showed increased symptomatology during that interval relative to those not taking medication.”38

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Jensen, “3-year follow-up.”

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In other words, those on medications saw their core ADHD symptoms—the impulsiveness, the inattentiveness, the hyperactivity—worsen, at least in comparison to those not on drugs. In addition, those on meds had higher “delinquency scores” at the end of three years, which meant they were more likely to get into trouble in school and with the police.39 They were also now shorter and weighed less than their off-med counterparts, evidence that the drugs suppressed growth. These results told of a drug therapy causing long-term harm, and when the NIMH-funded investigators reported on six-year outcomes, the findings remained the same. Medication use was “associated with worse hyperactivity-impulsivity and oppositional defiant disorder symptoms” and with greater “overall functional impairment.”40

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B. Molina, “Delinquent behavior and emerging substance use in the MTA at 36 months,” Journal of the American Academy of Child & Adolescent Psychiatry 46 (2007): 1028–39.

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B. Molina, “MTA at 8 years,” Journal of the American Academy of Child & Adolescent Psychiatry 48 (2009): 484–500.

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Ritalin and the other ADHD medications cause a long list of physical, emotional, and psychiatric adverse effects. The physical problems include 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, and sudden cardiac death. The emotional difficulties include depression, apathy, a general dullness, mood swings, crying jags, irritability, anxiety, and a sense of hostility toward the world. The psychiatric problems include obsessive-compulsive symptoms, mania, paranoia, psychotic episodes, and hallucinations. Methylphenidate also reduces blood flow and glucose metabolism in the brain, changes that usually are associated with “neuropathologic states.”42

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Animal studies of stimulants are also cause for alarm. Repeated exposure to amphetamines, scientists at the Yale School of Medicine reported in 1999, caused monkeys to exhibit “aberrant behaviors” that remained long after the drug exposure had stopped.43 Various rat studies suggested that lengthy exposure to methylphenidate might cause dopaminergic pathways to become permanently desensitized, and since dopamine is the brain’s “reward system,” medicating the child may produce an adult with a “reduced ability to experience pleasure.”44 Scientists at Texas Southwestern Medical Center in Dallas found that “preadolescent” rats exposed to methylphenidate for fifteen days turned into anxious, depressed “adult” rats. The adult rats moved around less, were less responsive to novel environments, and showed a “deficit in sexual behavior.” They concluded that “administration of methylphenidate” while the brain is still developing “results in aberrant behavioral adaptations during adulthood.”45

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S. Castner, “Long-lasting psychotomimetic consequences of repeated low-dose amphetamine exposure in rhesus monkeys,” Neuropsychopharmacology 20 (1999): 10–28.

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Breggin, Talking Back to Ritalin; K. Bolla, “The neuropsychiatry of chronic cocaine abuse,” Journal of Neuropsychiatry and Clinical Neurosciences 10 (1998): 280–89.

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W. Carlezon, “Enduring behavioral effects of early exposure to methylphenidate in rats,” Biological Psychiatry 54 (2003): 1330–37.

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C. Bolanos, “Methylphenidate treatment during pre- and periadolescence alters behavioral responses to emotional stimuli at adulthood,” Biological Psychiatry 54 (2003): 1317–29.

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The FDA did approve Prozac for use in children, as two of the three positive studies reviewed by Laughren had come from trials of this drug. But, as many critics have pointed out, from a scientific perspective, there is no reason to think that Prozac is any better than the other SSRIs. The percentage of children who responded to Prozac in the two positive trials was similar to the drug response rate in the twelve failed trials; Eli Lilly simply had been better at using biased trial designs to make it appear that its drug worked. For example, in one of the two Prozac trials, all of the children were initially put on placebo for one week, and if they got better during that period, they were excluded from the study. This helped knock down the placebo response rate. Next, the children who were randomized onto Prozac were evaluated for a week, and only those “who adapted well” to the drug were then enrolled in the study. This helped increase the drug response rate. “Before the study even started,” explained Jonathan Leo, editor in chief of the journal Ethical Human Psychology and Psychiatry, “there was a mechanism in place to maximize any difference between the drug and placebo groups—the placebo group was preselected for nonresponders, while the drug group was preselected for

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J. Leo, “The SSRI trials in children,” Ethical Human Psychology and Psychiatry 8 (2006): 29–41.

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Yet, even with this extremely biased trial design, the Prozac-treated children still fared no better than the placebo group on self-rating scales or ratings by their parents. In addition, the trial failed to show efficacy for fluoxetine on its “primary endpoint,” and thus efficacy arose entirely from a secondary “improvement” scale filled out by the psychiatrists paid by Eli Lilly to run the trial.

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In the absence of any efficacy benefit, we are now left with the unhappy task of tallying up the harm done by the prescribing of antidepressants to children and teenagers. We can start with the physical problems. SSRIs may cause insomnia, sexual dysfunction, headaches, gastrointestinal problems, dizziness, tremors, nervousness, muscle cramps, muscle weakness, seizures, and a severe inner agitation known as akathisia, which is associated with an increased risk of violence and suicide.

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The psychiatric problems they can trigger are even more problematic. Timothy Wilens and Joseph Biederman at Massachusetts General Hospital conducted a chart review of eighty-two children treated with SSRIs, and determined that 22 percent of the children had suffered an adverse psychiatric event. Ten percent had become psychotic, and another 6 percent manic. “One of the most disturbing adverse outcomes is a worsening of emotional, cognitive or behavioral symptoms,” they wrote. “These psychiatric adverse events to medication can be significantly impairing.”55 North Carolina psychiatrist Thomas Gualtieri determined that 28 percent of the 128 children and adolescents he treated with SSRIs developed some type of “behavioral toxicity.”56 Other physicians have told of their SSRI-treated younger patients suffering panic attacks, anxiety, nervousness, and hallucinations.

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T. Wilens, “A systematic chart review of the nature of psychiatric adverse events in children and adolescents treated with selective serotonin reuptake inhibitors,” Journal of Child and Adolescent Psychopharmacology 13 (2003): 143–52.

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T. Gualtieri, “Antidepressant side effects in children and adolescents,” Journal of Child and Adolescent Psychopharmacology 16 (2006): 147–57.

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If the children go off the medication, they can expect to suffer withdrawal symptoms, both physical and mental. Should they remain on the drugs for years, they are at high risk of becoming chronically depressed. They may also develop—as the American Psychiatric Association warns in one of its textbooks—an “apathy syndrome,” which “is characterized by a loss of motivation, increased passivity, and often feelings of lethargy and ‘flatness.’”57 There is also memory loss and cognitive decline to worry about, and, as we saw earlier, animal studies suggest that the drugs may cause serotonergic neurons to become swollen and misshapen.

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P. Breggin, Brain-Disabling Treatments in Psychiatry (New York: Springer Publishing Company, 2008), 153.

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First there was the ADHD explosion, and then came the news that childhood depression was rampant, and not long after that, in the late 1990s, juvenile bipolar disorder burst into public view. Newspapers and magazines ran features on this phenomenon, and once more psychiatry explained its appearance with a story of scientific discovery. “It has long been thought in the psychiatric community that children could not be given a diagnosis of bipolar disorder until the mid-to-late teens, and that mania in children was extremely rare,” wrote psychiatrist Demitri Papolos, in his bestselling book The Bipolar Child. “But scientists in the research vanguard are beginning to prove that the disorder can begin very early in life and that it is far more common than was previously supposed.”58 Yet the rise in the number of children and adolescents with this diagnosis was so astonishing—a fortyfold increase from 1995 to 2003—that Time, in an article titled “Young and Bipolar,” wondered if something else might be going on.59

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D. Papolos, The Bipolar Child (New York: Broadway Books, 2000), xiv.

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C. Moreno, “National trends in the outpatient diagnosis and treatment of bipolar disorder in youth,” Archives of General Psychiatry 64 (2007): 1032–39.

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But then, slowly but surely, such case reports began to appear. In the late 1960s and early 1970s, psychiatrists began prescribing Ritalin to hyperactive children, and suddenly, in 1976, Washington University’s Warren Weinberg, a pediatric neurologist, was writing in the American Journal of Diseases of Childhood that it was time for the field to realize that children could go manic. “Acceptance of the concept that mania occurs in children is important in order that affected children can be identified, the natural history defined, and appropriate treatment established and offered to these children,” he wrote.65

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This was the moment in the medical literature that pediatric bipolar disorder was, in essence, “discovered.” In his article, Weinberg reviewed the case histories of five children suffering from this previously unrecognized illness, but he rushed past the fact that at least three of the five children had been treated with a tricyclic or Ritalin prior to becoming manic. Two years later, doctors at Massachusetts General Hospital announced that they had identified nine children with manic-depressive illness, and they, too, skipped over the fact that seven of the nine had been previously treated with amphetamines, methylphenidate, or “other medications to affect behavior.”66

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J. Kluger, “Young and Bipolar,” Time, August 19, 2002.

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Then, in 1982, Michael Strober and Gabrielle Carlson at the UCLA Neuropsychiatric Institute put a new twist into the juvenile bipolar story. Twelve of the sixty adolescents they had treated with antidepressants had turned “bipolar” over the course of three years, which—one might think—suggested that the drugs had caused the mania. Instead, Strober and Carlson reasoned that their study had shown that antidepressants could be used as a diagnostic tool. It wasn’t that antidepressants were causing some children to go manic, but rather the drugs were unmasking bipolar illness, as only children with the disease would suffer this reaction to an anti-depressant. “Our data imply that biologic differences between latent depressive subtypes are already present and detectable during the period of early adolescence, and that pharmacologic challenge can serve as one reliable aid in delimiting specific affective syndromes in juveniles,” they said.67

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M. Strober, “Bipolar illness in adolescents with major depression,” Archives of General Psychiatry 39 (1982): 549–55.

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R. DeLong, “Lithium carbonate treatment of select behavior disorders in children suggesting manic-depressive illness,” Journal of Pediatrics 93 (1978): 689–94.

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W. Weinberg, “Mania in childhood,” American Journal of Diseases of Childhood 130 (1976): 380–85.

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The “unmasking” of bipolar illness in children soon speeded up. The prescribing of Ritalin and antidepressants took off in the late 1980s and early 1990s, and as this occurred, the bipolar epidemic erupted. The number of hostile, aggressive, and out-of-control children admitted to psychiatric wards soared, and in 1995 Peter Lewinsohn from the Oregon Research Institute concluded that 1 percent of all American adolescents were now bipolar.68 Three years later, Carlson reported that 63 percent of the pediatric patients treated at her university hospital suffered from mania, the very symptom that doctors in the pre-psychopharmacologic era almost never saw in children. “Manic symptoms are the rule, rather than the exception,” she noted.69 Indeed, Lewinsohn’s epidemiological data was now already out of date. The number of children discharged from hospitals with a bipolar diagnosis rose fivefold between 1996 and 2004, such that this “ferocious mental illness” was now said to strike one in every fifty prepubertal children in America. “We don’t have the exact numbers yet,” University of Texas psychiatrist Robert Hirschfeld told Time in 2002, “except we know it’s there, and it’s underdiagnosed.”70

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P. Lewinsohn, “Bipolar disorders in a community sample of older adolescents,” Journal of the American Academy of Child & Adolescent Psychiatry 34 (1995): 454–63.

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G. Carlson, “Manic symptoms in psychiatrically hospitalized children—what do they mean?” Journal of Affective Disorders 51 (1998): 123–35.

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J. Kluger, “Young and Bipolar.”

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Even before the prescribing of Ritalin took hold, it was well known that amphetamines could stir psychotic and manic episodes. Indeed, amphetamines did this with such regularity that psychiatric researchers pointed to this effect as evidence supporting the dopamine hypothesis of schizophrenia. Amphetamines upped dopamine levels in the brain, suggesting that psychosis was caused by too much of this neurotransmitter. In 1974, David Janowsky, a physician at the University of California at San Diego School of Medicine, tested this hypothesis by giving three dopamine-elevating agents—d-amphetamine, l-amphetamine, and methylphenidate—to his schizophrenia patients. While all three drugs made them more psychotic, methylphenidate turned out to be tops in this regard, doubling the severity of their symptoms.71

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D. Janowsky, “Proceedings: effect of intravenous d-amphetamine, l-amphetamine and methylphenidate in schizophrenics,” Psychopharmacology Bulletin 19 (1974): 15–24.

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Given this understanding of methylphenidate, psychiatry could expect that giving Ritalin to young children would cause many to suffer a manic or psychotic episode. Although this risk isn’t well quantified, Canadian psychiatrists reported in 1999 that nine of ninety-six ADHD children they treated with stimulants for an average of twenty-one months developed “psychotic symptoms.”72 In 2006, the FDA issued a report on this risk. From 2000 to 2005, the agency had received nearly one thousand reports of stimulant-induced psychosis and mania in children and adolescents, and given that these MedWatch reports are thought to represent only 1 percent of the actual number of adverse events, this suggests that 100,000 youths diagnosed with ADHD suffered psychotic and or manic episodes during that five-year period. The FDA determined that these episodes regularly occurred in “patients with no identifiable risk factors” for psychosis, meaning that they were clearly drug-induced, and that a “substantial portion” of the cases occurred in children ten years or less. “The predominance in young children of hallucinations, both visual and tactile, involving insects, snakes and worms is striking,” the FDA wrote.73

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E. Cherland, “Psychotic side effects of psychostimulants,” Canadian Journal of Psychiatry 44 (1999): 811–13.

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K. Gelperin, “Psychiatric adverse events associated with drug treatment of ADHD,” FDA, Center for Drug Evaluation and Research, March 3, 2006.

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Once this drug-induced psychosis occurs, the children are usually diagnosed with bipolar disorder. Moreover, this diagnostic progression, from medicated ADHD to bipolar illness, is well recognized by experts in the field. In a study of 195 bipolar children and adolescents, Demitri Papolos found that 65 percent “had hypomanic, manic and aggressive reactions to stimulant medications.”74 In 2001, Melissa DelBello, at the University of Cincinnati Medical Center, reported that twenty-one of thirty-four adolescent patients hospitalized for mania had been on stimulants “prior to the onset of an affective episode.” These drugs, she confessed, may “precipitate depression and/or mania in children who would not have otherwise developed bipolar disorder.”75

516

D. Papolos, “Bipolar disorder, co-occuring conditions, and the need for extreme caution before initiating drug treatment,” Bipolar Child Newsletter 1 (November 1999).

516

M. DelBello, “Prior stimulant treatment in adolescents with bipolar disorder,” Bipolar Disorders 3 (2001): 53–57.

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Yet there is an even bigger problem with stimulants. They cause children to cycle through arousal and dysphoric states on a daily basis. When a child takes the drug, dopamine levels in the synapse increase, and this produces an aroused state. The child may show increased energy, an intensified focus, and hyperalertness. The child may become anxious, irritable, aggressive, hostile, and unable to sleep. More extreme arousal symptoms include obsessive-compulsive and hypomanic behaviors. But when the drug exits the brain, dopamine levels in the synapse sharply drop, and this may lead to such dysphoric symptoms as fatigue, lethargy, apathy, social withdrawal, and depression.

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Parents regularly talk of this daily “crash.” But—and this is the key—such arousal and dysphoric symptoms are the very symptoms that the National Institute of Mental Health identifies as characteristic of a bipolar child. Symptoms of mania in children, the NIMH says, include increased energy, intensified goal-directed activity, insomnia, irritability, agitation, and destructive out bursts. Symptoms of depression in children include loss of energy, social isolation, a loss of interest in activities (apathy), and a sad mood.

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The ADHD to Bipolar Pathway

Image

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Stimulants used to treat ADHD induce both arousal and dysphoric symptoms. These drug-induced symptoms overlap to a remarkable degree the symptoms said to be characteristic of juvenile bipolar disorder.

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In short, every child on a stimulant turns a bit bipolar, and the risk that a child diagnosed with ADHD will move on to a bipolar diagnosis after being treated with a stimulant has even been quantified. Joseph Biederman and his colleagues at Massachusetts General Hospital reported in 1996 that 15 of 140 children (11 percent) diagnosed with ADHD developed bipolar symptoms—which were not present at initial diagnosis—within four years.76

516

J. Biederman, “Attention-deficit hyperactivity disorder and juvenile mania,” Journal of the American Academy of Child & Adolescent Psychiatry 35 (1996): 997–1008.

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This gives us our first mathematical equation for solving the juvenile bipolar epidemic: If a society prescribes stimulants to 3.5 million children and adolescents, as is the case in the United States today, it should expect that this practice will create 400,000 bipolar youth. As Time noted, most children with bipolar illness are diagnosed with a different psychiatric disorder first, with “ADHD the likeliest first call.”

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Now let’s look at the SSRIs.

It is well established that antidepressants can induce manic episodes in adults, and naturally they have this effect on children, too. As early as 1992, when the prescribing of SSRIs to children was just getting started, University of Pittsburgh researchers reported that 23 percent of boys eight to nineteen years old treated with Prozac developed mania or maniclike symptoms, and another 19 percent developed “drug-induced” hostility.77 In Eli Lilly’s first study of Prozac for pediatric depression, 6 percent of the children treated with the drug suffered a manic episode; none in the placebo group did.78 Luvox, meanwhile, was reported to cause a 4 percent rate of mania in children under 18.79 In 2004, Yale University researchers assessed this risk of antidepressant-induced mania in young and old, and they found that it is highest in those under thirteen years of age.80

516

J. Jain, “Fluoxetine in children and adolescents with mood disorders,” Journal of Child & Adolescent Psychopharmacology 2 (1992): 259–65.

516

G. Emslie, “A double-blind, randomized, placebo-controlled trial of fluoxetine in children and adolescents with depression,” Archives of General Psychiatry 54 (1997): 1031–37.

516

P. Breggin, The Anti-Depressant Fact Book (Cambridge, MA: Perseus Publishing, 2001), 116.

516

A. Martin, “Age effects on antidepressant-induced manic conversion,” Archives of Pediatrics & Adolescent Medicine 158 (2004): 773–80.

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The incidence rates cited above are from short-term trials; the risk rises when children and teenagers stay on antidepressants for extended periods. In 1995, Harvard psychiatrists determined that 25 percent of children and adolescents diagnosed with depression convert to bipolar illness within two to four years. “Antidepressant treatment may well induce switching into mania, rapid cycling or affective instability in the young, as it almost certainly does in adults,” they explained.81 Washington University’s Barbara Geller extended the follow-up period to ten years, and in her study, nearly half of prepubertal children treated for depression ended up bipolar.82

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These findings give us our second mathematical equation for solving the bipolar epidemic: If 2 million children and adolescents are treated with SSRIs for depression, this practice will create 500,000 to 1 million bipolar youth.

516

G. Faedda, “Pediatric onset bipolar disorder,” Harvard Review of Psychiatry 3 (1995): 171–95.

516

B. Geller, “Bipolar disorder at prospective follow-up of adults who had prepubertal major depressive disorder,” American Journal of Psychiatry 158 (2001): 125–27.

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We now have numbers that tell of an iatrogenic epidemic: 400,000 bipolar children arriving via the ADHD doorway, and at least another half million through the antidepressant doorway.

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Here are the results. In a 2003 study of seventy-nine juvenile bipolar patients, University of Louisville psychiatrist Rif El-Mallakh determined that forty-nine (62 percent) had been treated with a stimulant or an antidepressant prior to their becoming manic.83 That same year, Papolos reported that 83 percent of the 195 bipolar children he studied had been diagnosed with some other psychiatric illness first, and that two-thirds had been exposed to an antidepressant.84 Finally, Gianni Faedda found that 84 percent of the children treated for bipolar illness at the Luci Bini Mood Disorders Clinic in New York City between 1998 and 2000 had been previously exposed to psychiatric drugs. “Strikingly, in fewer than 10% [of the cases] was diagnosis of bipolar disorder considered initially,” Faedda wrote.85

516

D. Cicero, “Antidepressant exposure in bipolar children,” Psychiatry 66 (2003): 317–22.

516

D. Papolos, “Antidepressant-induced adverse effects in juvenile-onset bipolar disorder,” paper presented at the Fifth International Conference on Bipolar Disorder, June 12–14, 2003, Pittsburgh, PA.

517

G. Faedda, “Pediatric bipolar disorder,” Bipolar Disorders 6 (2004): 305–13.

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As we saw earlier in this book, outcomes for adult bipolar patients have deteriorated dramatically in the past forty years, and the worst outcomes are seen in those with “mixed state” and “rapid cycling” symptoms. That clinical course in adults was virtually never seen prior to the psychopharmacology era, but rather it was one associated with exposure to antidepressants, and, tragically, those are the very symptoms that afflict the overwhelming majority of juvenile bipolar patients. They exhibit symptoms “similar to the clinical picture reported for severely ill, treatment-resistant adults,” explained Barbara Geller in 1997.89

Thus, this is not just a story of children turned bipolar; it’s a story of children afflicted with a particularly severe form of it. Papolos found that 87 percent of his 195 juvenile bipolar patients suffered from “ultra, ultra rapid cycling,” which meant that they were constantly switching between manic and depressed mood states.90 Similarly, Faedda determined that 66 percent of the juvenile bipolar patients treated at the Luci Bini Mood Disorders Clinic were “ultra, ultra rapid-cyclers,” and another 19 percent suffered from rapid cycling only a little bit less extreme. “In contrast to a biphasic, episodic and relatively slow cycling course in some adults with bipolar disorder, pediatric forms usually involve mixed mood states and a sub-chronic, unstable, and unremitting course,” Faedda wrote.91

517

B. Geller, “Child and adolescent bipolar disorder,” Journal of the American Academy of Child & Adolescent Psychiatry 36 (1997): 1168–76.

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Papolos, “Antidepressant-induced adverse effects.”

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G. Faedda, “Treatment-emergent mania in pediatric bipolar disorder,” Journal of Affective Disorders (82): 149–58.

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Outcome studies have found that the long-term prognosis for these children is grim. The NIMH, as part of its STEP-BD study, charted the outcomes of 542 children and adolescent bipolar patients, and it reported that pre-adult onset “was associated with greater rates of comorbid anxiety disorders and substance abuse, more recurrences, shorter periods of euthymia [normal mood], and greater likelihood of suicide attempts and violence.”92 Boris Birmaher, at the University of Pittsburgh, determined that “early onset” bipolar patients are symptomatic about 60 percent of the time, and that, on average, they shift “polarity”—from depression to mania or vice versa—an astonishing sixteen times a year. The prepubertal patients were “two times less likely than those with postpubertal onset bipolar to recover,” he said, and it was “expected that children will be poor responders to treatment when they become adults.”93 DelBello followed a group of adolescents hospitalized for a first bipolar episode and concluded that only 41 percent functionally recovered within a year.94 This impairment, Birmaher determined, then worsens after the first year. “Functional impairment in bipolar appears to increase during adolescence regardless of age of onset.”95

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R. Perlis, “Long-term implications of early onset in bipolar disorder,” Biological Psychiatry 55 (2004): 875–81.

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B. Birmaher, “Course and outcome of bipolar spectrum disorder in children and adolescents,” Development and Psychopathology 18 (2006): 1023–35.

517

M. DelBello, “Twelve-month outcome of adolescents with bipolar disorder following first hospitalization for a manic or mixed episode,” American Journal of Psychiatry 164 (2007): 582–90.

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T. Goldstein, “Psychosocial functioning among bipolar youth,” Journal of Affective Disorders 114 (2009): 174–83.

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Youth diagnosed with bipolar illness are typically put on drug cocktails that include an atypical antipsychotic and a mood stabilizer. This means that they now have multiple neurotransmitter pathways in their brains that are being mucked up, and naturally, this treatment does not lead them back to emotional and physical health. In 2002, DelBello reported that lithium, antidepressants, and mood stabilizers all failed to help bipolar youth fare better at the end of two years. Those who were treated with a neuroleptic, she added, “were significantly less likely to recover than those who did not receive a neuroleptic.”96 Six years later, Hayes, Inc., a Pennsylvania consulting firm that conducts “unbiased” assessments of drugs for health-care providers, concluded that there was no good scientific evidence that the mood stabilizers and atypical antipsychotics prescribed for pediatric bipolar were either safe or effective. “Our findings indicate that at this time, anticonvulsants and atypical antipsychotics cannot be recommended for children diagnosed with bipolar disorders,” said Elisabeth Houtsmuller, senior analyst for Hayes.97 These reports attest to a lack of drug efficacy, but as Houtsmuller noted, the side effects from these “pharmacological treatments” are “alarming.” In particular, atypical antipsychotics may cause metabolic dysfunction, hormonal abnormalities, diabetes, obesity, emotional blunting, and tardive dyskinesia.* Eventually, the drugs will induce cognitive decline, and the child who stays on the cocktails into adulthood can expect to die early as well.

517

B. Geller, “Two-year prospective follow-up of children with a prepubertal and early adolescent bipolar disorder phenotype,” American Journal of Psychiatry 159 (2002): 927–33.

517

“Hayes says new treatments for pediatric bipolar disorder not ready for prime time” (December 3, 2008 press release), accessed at hayesinc.com, August 2, 2009.

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There are no good studies yet on the percentage of “early onset” bipolar patients who, when they reach adulthood, end up on the SSI and SSDI disability rolls. However, the astonishing jump in the number of “severely mentally ill” children receiving SSI speaks volumes about the havoc that is being wreaked. There were 16,200 psychiatrically disabled youth under eighteen years old on the SSI rolls in 1987, and they comprised less than 6 percent of the total number of disabled children. Twenty years later, there were 561,569 disabled mentally ill children on the SSI rolls, and they comprised 50 percent of the total.

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This epidemic is even hitting preschool children. The prescribing of psychotropic drugs to two-year-olds and three-year-olds began to become more commonplace about a decade ago, and sure enough, the number of severely mentally ill children under six years of age receiving SSI has tripled since then, rising from 22,453 in 2000 to 65,928 in 2007.98

517

Social Security Administration, annual statistical reports on the SSI program, 1996–2008; Social Security Bulletin, Annual Statistical Supplement, 1988–1992.

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Moreover, the SSI numbers only begin to hint at the scope of the harm being done. Everywhere there is evidence of a worsening of the mental health of children and teenagers. From 1995 to 1999, psychiatric-related emergency room visits by children increased 59 percent.99 The deteriorating mental health of the nation’s children, declared U.S. surgeon general David Satcher in 2001, constituted “a health crisis.”100 Next, colleges were suddenly wondering why so many of their students were suffering manic episodes or behaving in disturbed ways; a 2007 survey discovered that one in six college students had deliberately “cut or burned self” in the prior year.101 All of this led the U.S. Government Accountability Office to investigate what was going on, and it reported in 2008 that one in every fifteen young adults, eighteen to twenty-six years old, is now “seriously mentally ill.” There are 680,000 in that age group with bipolar disorder and another 800,000 ill with major depression, and, the GAO noted, this was in fact an undercount of the problem, as it didn’t include young adults who were homeless, incarcerated, or institutionalized. All of these youth are “functionally impaired” to some degree, the GAO said.102

518

U.S. Government Accountability Office, “Young adults with serious mental illness” (June 2008).

518

B. Whitford, “Depression, eating disorders and other mental illnesses are on the rise,” Newsweek, August 27, 2008.

518

D. Satcher, Report of Surgeon General’s Conference on Children’s Mental Health (U.S. Dept. of Health and Human Services, 2001).

517

Pediatric Academic Societies, “Pediatric psychiatry admissions on the rise,” May 16, 2000, press release.

Notes

Amount: 19

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