(This review of Robert Whitaker’s latest book is primarily focused upon the long-term mental health outcome studies identified in his book, see Part Three: Outcomes: Chapter 6 (Schizophrenia) A Paradox Revealed, Chapter 7 (Anxiety) The Benzo Trap, Chapter 8 (Depression), An Episode Illness Turns Chronic, Chapter 9 (Bipolar), The Bipolar Boom, Chapter 11, The Epidemic Spreads to Children. Also see Notes: pages 368 – 384.)
Introduction
Welcome to this presentation this morning. Much of what I will share with you today can be found in Robert Whitaker’s latest book, Anatomy of an Epidemic – Magic Bullets, Psychiatric Drugs and the Astonishing Rise of Mental Illness in America.
Whitaker is an investigative medical reporter and has written one other book on this same topic. It’s called Mad in America. Some of the studies contained in Whitaker’s latest book also appear and are discussed in Mad in America. Maybe some of you have heard of both of these books. How many of you are familiar with either of them?
With respect to Anatomy of an Epidemic, I am convinced that Whitaker makes a strong case that indeed there is an epidemic of chronic disabled mental health patients, actually over four million, who have been diagnosed with a mental disability sufficient to be eligible for government assistance. Every day 1,100 adults and children are added to these rolls because they have become newly disabled by mental illness. Of this number 250 of these citizens are children. Using SSI and SSDI and other epidemiological data he argues that this epidemic is now spreading most rapidly among our nation’s children.
I am not here this morning however to try and persuade you to accept Whitaker’s admitally controversial chronic epidemic thesis --- in part because there is not enough time to do so, and because it would seriously detract from and compromise the larger long-term research studies presented in his book. Many readers of this book will argue that perhaps the greatest contribution to the mental health and medical research literature is Whitaker’s systematic documentation and grouping of the scientific long-term outcome studies by the four major mental disorders and for children.
As noted on my bio my expertise and experience includes thirty years as a clinical and program evaluator. I have conducted and have had published several papers on both clinical and program evaluation studies of my own, including an 18 month follow-up study on emotionally disturbed adolescents who were treated in a Wisconsin residential treatment facility.
During these three decades as a professional mental health clinician and evaluator I have tried to keep up on mental health research of all kinds. In fact it was due to such training and experience that my own interest was piqued when Whitaker’s recent book appeared. I just happened to have the good fortune to hear Whitaker interviewed about his book on Wisconsin Public Radio and I was both dismayed and confused when Whitaker began citing several long-term mental health outcome studies which until then I didn’t know even existed. Needless to say I bought the book and here I am.
Before turning to our very first long-term outcome follow-up study I suggest that we begin by comparing what you will hear today with the story presented by the American Psychiatric Association and large pharma. This latter story is one that we all know. It is a story that begins after WW 2 with the experimentation with certain chemical compounds or substances like dyes and their various reactions on caged rats. These various compounds were soon used on humans as an anesthetic in surgery to calm the patient.
Using rats and mice scientists observed that various compounds produced certain effects or behavior in these animals. Some substances produced less hyperactivity, greater calmness and manageability. By 1955 an antipsychotic drug called Thorazine appeared on the market for humans.
American psychiatry and pharmaceutical companies soon began to credit this drug with ending the suffering of the chronically ill and for making deinstitutionalization possible. The APA touted this drug as our first antidote to a mental disorder. One writer haled Thorazine for initiating a revolution in psychiatry, comparable to the introduction of penicillin in general medicine. This was the start of the psychopharmacological revolution. Now all of us are familiar with the story told by big pharma. It is a story that began with the National Institute of Mental Health’s first drug trials what was later called the magic or silver bullet era that now is regularly stoked with ever newer miracle drugs. About this same time the Diagnostic and Statistical Manual also appeared and drew a line as to what is normal and what is not. Also during this early period there was the need to discover and demonstrate an antibiotic-like pill that would “treat the brain by curing chemical imbalances that causes mental disorders.” Slightly before and during the same time period something called “community psychiatry” which was threatening to redefine American psychiatry and vigorously opposed by a more conservative branch of the AMA.
During this same period there was also pressure on the psychiatric profession to adopt a more rigorous research design in order to increase its scientific credibility. They chose a research design that had been recently used and proven in infectious disease: studies which included placebo-controlled, double-blind, randomized clinical trials. Thorazine came on the market over a half century ago in June of 1951 to treat psychotic disorders.
Whitaker asks the reader to compare this idealized and more sexy version of American psychiatric history with a more realistic and candid story told by the numerous long-term mental health outcome studies that his book has just recently brought into public light, and presented to you here today.
Chapter 6: A Paradox Revealed
This story, told in the narrative of long-term scientific studies, really begins when the National Institute of Mental Health was asked to design and conduct the first Thorazine drug trials and evaluate its safety and effectiveness. Here it would be helpful to first consider briefly the difference between Food and Drug Administration’s approved clinical drug trails versus long-term mental health outcome follow-up studies.
As you know, most clinical drug trials are designed to run for as little as four to six weeks, while long term follow-up studies might run for up to one to ten years or more. Unlike clinical trials which target only clinical symptoms typically observed during the intake or initial office visit, such as anxiety, depression, mental confusion, long-term follow-up studies are more likely to use global rating scales and broader and more concrete social functioning indicators such as employment, family relationships, relapses, physical health and medication status.
And, while clinical trials use more narrow industry-driven rating scales often routinely administered by the treating clinician themselves to rate the patient’s progress, long-term outcome studies tend to use several different broad social functioning measures and are rated by more independent and objective verification sources, who are usually, not involved in the treatment or clinical process per se.
Now, what does the long-term scientific mental health evidence tell us with regard to the treatment of schizophrenia with antipsychotic drugs?
In 1961 the Psychopharmacology Service Center using symptom-based rating scales in short term placebo studies researcher found 75 percent of the drug-treated patients to be “much improved” versus 23 percent of the placebo (non-medicated) patients.
Following this study hundreds of smaller studies have since produced similar results. Sixty-six such short-term studies were reviewed and found that 53 percent of the drug withdrawn patients relapsed within ten months versus 16 percent of those maintained on the medications. These results prompted the researcher to conclude that “The efficacy of these medications in reducing the risk of psychotic relapse has been well documented.” 1995 See: NIMH investigators, and Patricia Gilbert, “Neuroleptics withdrawal in schizophrenic patients.”
Later in 1967 the NIMH’s conducted a one year after discharge follow-up study with 299 schizophrenia patients who had been treated with either neuroleptics or placebo upon their admission to a hospital.
In this landmark study the researchers found that patients who received placebo “were less likely to be re-hospitalized than those who received any of the three active phenothiazines.” See: Schooler, N. American Journal of Psychiatry, 123 (1967):986-995.
After this study the researchers described these results as “ so unexpected” but stated that despite these findings, they “were unprepared to recommend placebo as the treatment of choice.”
This study was soon followed by NIMH’s first two relapse studies.
The first such study investigated whether relapse rates increased in direct relation to dosage. The critical finding of this NIMH funded study was that relapse rates rose in direct relation to dosage—the higher the dosage that patients were on before the drugs were withdrawn, the greater the relapse rates.
At the start of this study, 18 patients were on placebo, and only one got worse over the next six months (6%). Sixty-five patients were on 300 mg. of chlorpromazine at the start of the study, and 54% of these patients got worse after drug withdrawal. One hundred thirteen patients were on more than 300mg. of chlorpromazine at the start of the study, and 66% of these patients got worse after drug withdrawal. See: Relapse in Chronic Schizophrenics following Abrupt Withdrawal of Tranquilizing Medication, Prien, R. British Journal of Psychiatry, 115 (1968) 679-86.
In the second relapse study, the earlier finding that relapse rates rose in correlation with neuroleptics dosage was confirmed. Only 2 of 30 patients who were on placebo at the start of the study relapsed during the next 24 weeks (7%). Twenty-three percent of the 99 patients who were on under 300 mg. of chlorpromazine at the start of the study relapsed following drug withdrawal. Fifty-two percent of the 91 patients who were on 300 to 500 mg. of chlorpromazine at the start of the study relapsed following drug withdrawal, and sixty-five percent of the 81 patients who were on more than 500 mg. of chlorpromazine at the start of the study relapsed following drug withdrawal.
The researchers concluded: “Relapse was found to be significantly related to the dose of the tranquilizing medication the patient was receiving before he was put on placebo—the higher the dose, the greater the probability of relapse.” See: Discontinuation of Chemotherapy for Chronic Schizophrenics, Prien, R. Hospital and Community Psychiatry, 22 (1971), 20-23.
It seems paradoxical that drugs that ameliorate acute psychotic symptoms over the short term will actually increase the likelihood that a person diagnosed with schizophrenia will become chronically ill. But as we have just seen, that disturbing fact showed up in the very first outcome studies presented here.
In 1997 Ross Baldessarini of Harvard Medical School reviewed 145 of such clinical trials and found that the antipsychotic proved superior to a placebo in 83 % of them. The Brief Psychiatric Rating Scale (BPRS) adopted by the American Psychiatric Association was regularly employed in these trials. The APA eventually decided that a 20 percent reduction in total BPRS score represented a clinically significant response to a drug. Based on this measurement, an estimated 70 percent of all schizophrenia patients suffering from an acute episode of psychosis “respond” over a six week period, to an antipsychotic medication.
Once the NIMH investigators determined that the antipsychotics were efficacious over the short term they naturally wanted to know how long schizophrenia patients should stay on the medication.
To investigate this question, they ran studies that, for the most part, had the following design: Patients who were good responders to the medication were either maintained on the drug or abruptly withdrawn from it.
In 1995, Patricia Gilbert at the University of California at San Diego reviewed sixty-six relapse studies, involving 4,365 patients and found that 53 percent of the drug-withdrawn patients relapsed within ten months versus 16 percent of those maintained on the medication. Gilbert concluded that “The efficacy of these medications in reducing the risk of psychotic relapse has been well documented.” It was later discovered after repeating this study that when the drugs were gradually withdrawn, the relapse rate was only one-third as high as in the abrupt-withdrawal studies.
Based on these relapse studies, in a 2002 John Geddes, a prominent British researcher, wrote in an article in the New England Journal of Medicine, “Anti-psychotic drugs are effective in treating acute psychotic symptoms and preventing relapse.
Nevertheless, in 2007 the Cochrane Collaboration, an international group of scientists that doesn’t take funding from pharmaceutical companies, raised questions about the drug’s short-term efficacy.
They conducted a meta-analysis of all chlorpromazine-versus placebo studies in the scientific literature, and after identifying fifty of decent quality, they came to the following conclusion: (Most briefly, a meta-analysis study is one that combines the results of several studies that address a set of related research hypotheses. In the simplest form, this is normally by identification of a common measure effect size, for which a weighted average might be the output of a meta-analysis.)
They calculated that seven patients had to be treated with chlorpromazine to produce a net gain of one “global improvement” and that even this finding may be an overestimate of the positive and an underestimate of the negative effects of giving chlorpromazine.” These investigators noted that they were startled by their results. This was the first attempt to assess the long-term efficacy of these drugs when a long-term measure was applied.
Even if one accepts the objectivity of this clinical trial procedure many investigators have pointed to the large hole in this evidence base. Joseph Zubin warned that when it came to evaluating a therapy for psychiatric disorder, a six-week study induced a kind of scientific myopia.
“It would be foolhardy to claim a definite advantage for a specified therapy without a two-to five-year follow-up. A two year follow-up would seem to be the very minimum for the long-term effects.
Lisa Dixon, psychiatrists at the University of Maryland School of Medicine in 1995 went still further in her criticism. “Little can be said about the efficacy and effectiveness of conventional antipsychotics on nonclinical outcomes.” Well-designed long-term studies are virtually nonexistent, so the longitudinal impact of treatment with conventional antipsychotics is unclear.
After reviewing a robust number of such clinical trial results, Whitaker noted, “Evidence that the drugs might worsen long-term outcomes showed up in the very first follow-up study conducted by the NIMH, and then it appears again and again in the research literature over the next fifty years. Some of these researchers include: J. Cole, 1977, Bockover 1975, Rappaport 1978, W. Carpenter 1977, L. Mosher 2003, C. Harding 1994, M. Harrow 2007, World Health Organization 1998
Evidence that long-term recovery rates are higher for non-medicated patients appears in studies and investigations of many different types. It shows up in the randomized studies conducted by Rappaport, Carpenter, and Mosher; in the cross-cultural studies conducted by the World Health Organization; and in the naturalistic studies conducted by Harding and Harrow.
Once a new tool for studying brain structures came along called electro-magnetic resonance imagery (MRIs), investigators discovered that antipsychotics fail to maintain or increase the size of the frontal lope and the white matter found there. These morphological changes in the brain reflect a “progressive neurodevelopmental disorder” in the schizophrenic patient which is associated with negative symptoms and both cognitive and functional impairments, which antipsychotics fail to arrest. (See: Nancy Andreason, American Journal of Psychiatry, 2003.
Whitaker makes the point that for the most part, the psychiatric researchers who conducted these studies hoped and expected to find the reverse. They wanted to tell a story of drugs that help schizophrenia patients fare well over
Conclusion - Now to summarize, what does the long-term scientific mental health evidence tell us about the record of antipsychotic medication for the treatment of schizophrenia?
1.Beginning in 1961 using symptom-based rating scales in short term placebo studies researcher found 75 percent of the drug-treated patients to be “much improved” versus 23 percent of the placebo (non-medicated) patients.
Following this study hundreds of smaller studies produced similar results. Sixty-six such short-term studies were reviewed and found that 53 percent of the drug withdrawn patients relapsed within ten months versus 16 percent of those maintained on the medications. See: NIMH investigators, and Patricia Gilbert
2. The first 1967 one year-after hospital discharge study found that patients who received placebo (non-medicated) “were less likely to be re-hospitalized than those who received any of the three active phenothiazines. See: N. Schooler
3. In two drug withdrawal trials, both of which included patients who weren’t on any drug at the start of the study, relapse rates rose in correlation with drug dosage. The higher the dose the greater the probability of relapse. See: R. Prien
4. There is no good evidence that antipsychotics improve long-term schizophrenia global outcomes. See: Lisa Dixon and Emmanuel Stip
5. There is significance evidence that drugs might worsen long-term outcomes. See: Cole, Bockoven, Rappaport, Carpenter, Mosher, Harding, and the WHO.
6. There is long-term evidence that antipsychotics affect the brain, and why the drug-withdrawal studies have misled psychiatrists into believing that the drugs prevented relapse. See: Chouinard and Jones
7. There is long-term evidence research that randomized placebo studies show that recovery rates are higher for non-medicated patients. See: Rappaport, Carpenter, Mosher
8. There are long-term studies that indicate that drugs induce global brain dysfunction in a high percentage of patients over the long term. See: the tardive dyskinesia studies by
9. There is also evidence that antipsychotics cause morphological changes in the brain and that these changes are associated with a worsening of both positive and negative symptoms, and with functional and cognitive functioning as well. See: Andreasen MRI studies
10. There is long-term evidence showing how schizophrenic patients in the US are faring following their hospitalization. See: Martin Harrow’s NIMH funded 2007 fifteen-year follow-up global outcome study showing that 40 percent of schizophrenic patients off antipsychotics recovered, versus 5 percent of the medicated patients.
At the 2008 APA conference Harrow stated: I conclude that patients with schizophrenia not on antipsychotic medication for a long period of time have significantly better global functioning outcomes than those on antipsychotics.”
(There is long-term evidence-based study that demonstrates that seven patients had to be treated with chlorpromazine to produce a net gain of one “global improvement.” versus a mere symptomatic short-term benefit. See: The 2007 Cockrane Collaboration.)
Chapter 7: The Benzo Trap
When Hoffmann-La Roche brought Valium to the market in 1963, advertising it in particular to women, and from 1968 to 1981, it was the bestselling drug in the Western world. Valium was preceded by Miltown which was often referred to as “mother’s little helper.” During this same period the number of people admitted to mental hospitals, psychiatric emergency rooms, and mental health outpatient clinics soared.
First discovered by George Beard in 1869 he described the condition as ”tired nerves” and defined the symptoms as consisting of worry, fatigue, and insomnia. He later also named the condition “neurasthenia.” Sigmund Freud first began treating neurasthenia in 1895 and soon announced that Beard’s disease of dread and worry were psychological in origin rather than tired nerves. He began to write about anxiety neurosis in women which he theorized arose in a large part form their unconscious repression and sexual desires and fantasies. Until the onset of Benzodiazepines psychiatry was a profession for those who treated mad patients in thee asylum.
Once researches in the United States and the United Kingdom determined that Benzos did not provide any durable relief from anxiety, an obvious question arose: Do these drugs when taken on a continual basis, worsen the very symptoms they are supposed to treat? In 1991 Karl Rickels at the University Pennsylvania School of Medicine reported on a three year follow-up study. Rickels reported on a group of anxious patients and found that those who had successfully gotten off the drugs were doing “significantly” better than those who had failed to so.
A few years later he was back with another study and found that when long-term users withdrew from Benzos, they became more alert, more relaxed, and less anxious, and this change was accompanied by improved psychomotor functions.
Soon Canadian investigators found that benzo usage led to a fourfold increase in depressive symptoms. In England Aston observed that those who stay on the drugs tend to become more ill. Many patients find that anxiety symptoms gradually increase over the years despite continuous benzo use, and panic attack, agoraphobia may also appear for the first time. David Knott, a physician at the University of Tennessee, warned in 1976 that, “I am very convinced that Valium, Librium and other benzo drugs of that class cause damage to the brain. He discovered damage to the cerebral cortex which appeared to become a permanent condition. Other adverse symptoms of Benzos include trouble focusing, rembering things, learning new material and solving problems.
Chapter 8: An Episodic Illness Turns Chronic
Although a handful of European physicians may have sounded the alarm about the changing course of depression in the late 1960s and early 1970s, it wasn’t until 1994 that an Italian psychiatrist, Giovanni Fava, from the University of Bologna, pointedly announced that it was time for psychiatry to confront this issue. Neuroleptics had been found to be problematic over the long term, the benzodiazepines had, too, and now it looked like the antidepressants were producing a similar long-term record. In a 1994 Editorial in Psychotherapy and Psychosomatics, Fava wrote:
“I wonder if the time has come for debating and initiating research into the likelihood that psychotropic drugs actually worsen, at least in some cases, the progression of the illness which they are supposed to treat. In several more articles that followed, Fava offered a biological explanation for what was going on with the antidepressants. Like antipsychotics and benzodiazepines, these drugs perturb neurotransmitter systems in the brain. This leads to compensatory processes that oppose the initial acute effects of a drug…” When drug treatment ends, these processes may operate unopposed, resulting in appearance of withdrawal symptoms and increased vulnerability to relapse. A statistical trend suggested that the longer the drug treatment, the higher the likelihood of relapse, Fava noted.
Fava also wondered what was the outcome for people who stayed on antidepressants indefinitely. Weren’t they also relapsing with great frequency? He summed up the problem in this way:
“Antidepressant drugs in depression might be beneficial in the short term, but worsen the progression of the disease in the long term, by increasing the biochemical vulnerability to depression. Use of antidepressants drugs may propel the illness to a more malignant and treatment unresponsive course.”
Finally, Scott Patten, from the University of Calgary, plumbed a large Canadian health database to assess the five-year outcomes of 9,508 depressed patients, and he determined that the medicated patients were depressed on average nineteen weeks each year, versus eleven weeks for those not taking the drugs. These findings, Patten wrote, were consistent with Giovanni Fava’s hypothesis that, “antidepressant treatment may lead to a deterioration in the long-term course of mood disorders.
Returning to someone closer to home, William Coryell and his NIMH-funded colleagues studied the six year “naturalistic” outcomes of 547 people who suffered a bout of depression and they found those who were treated for the illness were three times more likely than the untreated group to suffer a “cessation” of their “principal social role” and nearly seven times more likely to become “incapacitated.”
Whitaker presents several demonological and long-term studies relating to the second generation of antidepressants or SSRIs. Here due to both time and space I will cite just one of the long-term studies by J. Moncrieff. “Trends in sickness benefits in Great Britain and the contribution of mental disorders. Both in the United States and in Great Britain scientists observed that following the arrival of the SSRIs, the number of citizens disabled by depression dramatically increased.
In Britain the number of days on incapacity due to depression and neurotic disorders jumped from 38 million in 1984 to 117 million in 1999, a threefold increased.
Chapter 9: The Bipolar Boom
Do antidepressants worsen the long-term course of bipolar disorder?
Frederick Goodwin and Robert Post’s latest book, Manic Depressive Illness, which is considered the bible in the field of bipolar disorders. At the 2008 APA conference, Goodwin gave this bottom-line summary.
Bipolar outcomes had noticeably worsened in the past twenty years. He went on to tell why. Today, we have a lot more rapid cycling, a lot more lithium resistance, and a lot more lithium treatment failures than there was previously. Regrettably today that most bipolar patients get an antidepressant before they ever get exposed to a mood stabilizer.
Nassir Ghaemi, from Tufs Medical Center agreed that antidepressants can cause manic switches and turn patients into rapid cyclers, and may actually increase the amount of time they spend in depressive episodes. He went on to say that the literature tells us that “the number of episodes is associated with more cognitive deficits. ”We are building more episodes, more treatment resistance, more cognitive dysfunction, and there is data showing that if you have four depressive episodes, unipolar or bipolar, it doubles your late life risk of dementia. Long-term outcomes for bipolar disorder have dramatically worsened in the pharmacotherapy era.
In Robert Whitaker’s segment on, Bipolar Before Lithium, he summarized it best. “Given what the scientific literature revealed about the long-term outcomes of medicated schizophrenia, anxiety, and depression, it stood to reason that the drug cocktails used to treat bipolar illness were not going to produce good long-term results.
The increased chronicity, the functional decline, the cognitive impairment, and the physical illness, all of these can be expected to show up in people treated with a cocktail that often includes an antidepressant, an antipsychotic, a mood stabilizer, a bensodiazepine, and perhaps a stimulant, too.
Chapter 10: An Epidemic Explained
We are now coming to the close of our examination of the long-term outcomes literature for the major psychiatric disorders for adults. I would like to leave with you the fifteen year long-term findings for manic depressive patients conducted by Martin Harrow from 1975 to 1983. Harrow followed four different groups: Schizophrenia on meds, manic-Depressive on meds, schizophrenia off meds, and maniac-depressive off meds. Here briefly were his findings:
Over the long-term, the manic depressive patients who stopped taking psychiatric drugs fared pretty well. At the end of two years, they were still struggling with their illness. Then they began to improve, and by the end of the study their collective scores fell into the “recovered” category on Harrow’s global assessment scale. The recovered patients were working at least part-time, they had acceptable social functioning, and the were largely asymptomatic.
In contrast the manic depressive patients who stayed on their psychiatric medications did not fare so well. At the end of two year they remained quite ill, so much so they were now a little bit worse than the schizophrenia patients off meds. Then, over the next two and one half years, while the manic-depressive and schizophrenia patients who were off meds improved, the manic-depressive patients who kept taking their pills did not, such that by the end of 4.5years, they were doing markedly worse than the other three groups.
We all know that schizophrenia is the worse mental disorder with the worst long-term prognosis. Nevertheless in this long term NIMH-funded study, the manic-depressive group on medications had the worse long-term outcomes. While their counterparts who were off medication fared the best at the end of this fifteen year study.
Chapter 11: The Epidemic Spreads to Children
I would like to conclude this review of the psychiatric literature this morning by now turning our attention to our children. The prescribing of psychiatric drugs to children and adolescents is a recent phenomenon, as relatively few youth were medicated prior to 1980. This will also give us the opportunity to put Robert Whitaker’s thesis to the same test as we have applied to the four previous major disorders. Will we find, in the scientific literature and in societal data, that the medicating of children and teenagers is doing more harm than good? Is it putting many children who initially may be struggling with a relatively minor problem---a disinterest in school, or a bout of sadness – onto a path that leads to lifelong disability?
The diagnosing and medication of mental disorders for our children with depression was nearly nonexistent until Prozac and other SSRIs were brought to market and touted as wonder drugs. The percentage of children so medicated tripled between 1988 and 1994, and by 2002 one in every forty children under nineteen years of age in the US was taking an antidepressant.
Fifty years ago, physicians virtually never saw manic-depressive illnesses in preteens, and they rarely diagnosed it in adolescents. Suddenly pediatricians and psychiatrists began prescribing Ritalin to hyperactive children, and suddenly the medical journals began running case reports of manic children. This problem grew as the prescribing of Ritalin increased, and then it exploded with the introduction of the SSRIs.
Research has since showed that both of these drugs trigger bipolar symptoms in children and adolescent cents on a regular basis. Whitaker concludes that these are the two outside agents fueling the epidemic. It should be remembered that they do perturb normal brain function. The manic children showing up at hospital emergency rooms have dopaminergic and serotonergic pathways that have been altered by the drugs and are now functioning in an “abnormal” manner.
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 roles 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% of the total.
This epidemic is even hitting pre school 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 the, rising from 22,453 in 2000 to 65,928 in 2007.
Twenty years ago, our society began regularly prescribing psychiatric drugs to children and adolescents, and now one of every fifteen Americans enters adulthood with a “serious mental illness.” Continuing to quote Whitaker, “The medicating of children has now become commonplace only a short time ago, and already it has put millions onto a path of lifelong mental illness.”
Now having reviewed the mental health outcome or evidenced-based literature let me conclude by saying a few things that these outcome studies have to say. First we have learned that antipsychotic drugs can help patients better manage their most acute symptoms early in the onset of the disorder.
(The conclusion of this paper will briefly highlight the most significant findings contained in these long term outcome studies for each of the four major disorders and for children. This paper remains a work in progress.)
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