Anatomy of an
Epidemic: Psychiatric Drugs and the Astonishing Rise of Mental Illness in
America
Abstract
Over the past 50
years, there has been an astonishing increase in severe mental illness in the
United States. The percentage of Americans disabled by mental illness has
increased five-fold since 1955, when Thorazine—remembered today as psychiatry’s
first “wonder” drug—was introduced into the market. The number of Americans
disabled by mental illness has nearly doubled since 1987, when Prozac—the first
in a second generation of wonder drugs for mental illness—was introduced. There
are now nearly 6 million Americans disabled by mental illness, and this number
increases by more than 400 people each day. A review of the scientific
literature reveals that it is our drug-based paradigm of care that is fueling
this epidemic. The drugs increase the likelihood that a person will become
chronically ill, and induce new and more severe psychiatric symptoms in a
significant percentage of patients.
The modern era of
psychiatry is typically said to date back to 1955, when chlorpromazine,
marketed as Thorazine, was introduced into asylum medicine. In 1955, the number
of patients in public mental hospitals reached a highwater mark of 558,922 and
then began to gradually decline, and historians typically credit this emptying
of the state hospitals to chlorpromazine. As Edward Shorter wrote in his 1997
book, A History of Psychiatry, “Chlorpromazine initiated a revolution in
psychiatry, comparable to the introduction of penicillin in general medicine.”
(Shorter, 1997, p. 255). Haldol and other antipsychotic medications were soon
brought to market, and then antidepressants and antianxiety drugs. Psychiatry
now had drugs said to target specific illnesses, much like insulin for
diabetes.
However, since 1955,
when this modern era of psychopharmacology was born, there has been an
astonishing rise in the incidence of severe mental illness in this country.
Although the number of hospitalized mentally ill may have gone down, every
other metric used to measure disabling mental illness in the United States has
risen dramatically, so much so that E. Fuller Torrey, in his 2001 book The
Invisible Plague, concluded that insanity had risen to the level of an
“epidemic” (Torrey, 2001). Since this epidemic has unfolded in lockstep with
the ever-increasing use of psychiatric drugs, an obvious question arises: Is our
drug-based paradigm of care fueling this modern-day plague?
The Epidemic
The U.S. Department of
Health and Human Services uses “patient care episodes” to estimate the number
of people treated each year for mental illness. This metric tracks the number
of people treated at psychiatric hospitals, residential facilities for the
mentally ill, and ambulatory care facilities. In 1955, the government reported
1,675,352 patient care episodes, or 1,028 episodes per 100,000 population. In
2000, patient-care episodes totaled 10,741,243, or 3,806 per 100,000
population. That is nearly a four-fold per-capita increase in 50 years. (Table
1).
A second way to assess
this epidemic is to look at the number of disabled mentally ill in the country.
Up until the 1950s, the number of hospitalized mentally ill provided a rough
estimate of this group. Today, the disabled mentally ill typically receive a
disability payment either from the Social Security Disability Insurance (SSDI)
program or the Supplemental Security Income (SSI) program, and many live in
residential shelters or other subsidized living arrangements. Thus, the
hospitalized patient of 50 years ago receives either SSDI or SSI today, and
this line of evidence reveals that the number of disabled mentally ill has
increased nearly six-fold since Thorazine was introduced.
In 1955, there were
559,000 people in public mental hospitals, or 3.38 people per 100,000
population. In 2003, there were 5.726 million people who received either an SSI
or SSDI payment (or from both programs), and were either disabled by mental
illness (SSDI statistics) or diagnosed as mentally ill (SSI statistics).[i]
That is a disability rate of 19.69 people per 100,000 population, which is
nearly six times what it was in 1955. (Table 2.)
It is also noteworthy
that the number of disabled mentally ill has increased dramatically since 1987,
the year Prozac was introduced. Prozac was touted as the first of a second
generation of psychiatric medications said to be so much better than the old.
Prozac and the other SSRIs replaced the tricyclics, while the atypical
antipsychotics (Risperidone, Zyprexa, etc.) replaced Thorazine and the other
standard neuroleptics. The combined sales of antidepressants and antipsychotics
jumped from around $500 million in 1986 to nearly $20 billion in 2004 (from
September 2003 to August 2004), a 40-fold increase. [ii]During this period, the
number of disabled mentally ill in the United States, as calculated by the SSI
and SSDI figures, increased from 3.331 million people to 5.726 million.[iii]That
is an increase of 149,739 people per year, or 410 people newly disabled by
mental illness every day. (Table 3).
A Biological Cause for
the Epidemic
The notion that
psychiatric drugs work by balancing brain chemistry was first raised in the early
1960s. Once Thorazine and the standard neuroleptics were shown to block
dopamine activity in the brain, researchers hypothesized that schizophrenia was
caused by too much of this neurotransmitter. Thus, the neuroleptics—by blocking
the dopamine receptors—helped normalize the brain’s dopamine system. Since the
tricyclics raised norephinephrine and serotonin levels in the brain,
researchers reasoned that depression was caused by low levels of these brain
chemicals. Merck, meanwhile, marketed its antianxiety drug Suavitil as a “mood
normalizer.” These normalizing claims suggested that the drugs were indeed
curative of biological ailments.
However, this
hypothesis—that the drugs balanced abnormal brain chemistry— never panned out.
Although the public may still be told that the drugs normalize brain chemistry,
the truth is that researchers did not find that people with schizophrenia had
overactive dopamine systems (prior to being medicated), or that those diagnosed
with depression suffered from abnormally low levels of serotonin or
norephinephrine. As U.S. Surgeon General David Satcher acknowledged in his 1999
report on mental health, the causes of mental disorders “remain unknown”
(Satcher, 1999, p.102).
Yet, scientists have
come to understand how the drugs affect the human brain, at least in terms of
their immediate mechanisms of action. In 1996, the director of the National
Institute of Mental Health, neuroscientist Steven Hyman, set forth a paradigm
for understanding how all psychiatric drugs work. Antipsychotics,
antidepressants, and antianxiety drugs, he wrote, “create perturbations in
neurotransmitter functions” (Hyman and Nestler, 1996, p. 153). In response, the
brain goes through a series of compensatory adaptations. For instance, Prozac
and other SSRI antidepressants block the reuptake of serotonin. In order to
cope with this hindrance of normal function, the brain tones down its whole
serotonergic system. Neurons both release less serotonin and down-regulate (or
decrease) their number of serotonin receptors. The density of serotonin
receptors in the brain may decrease by fifty percent or more. As part of this
adaptation process, Hyman noted, there are also changes in intracellular
signaling pathways and gene expression. After a few weeks, Hyman concluded, the
patient’s brain is functioning in a manner that is “qualitatively as well as
quantitatively different from the normal state.”
In short, psychiatric
drugs induce a pathology. Princeton neuroscientist Barry Jacobs has explicitly
made this point about SSRIs. These drugs, he said, “alter the level of synaptic
transmission beyond the physiologic range achieved under (normal)
environmental/biological conditions. Thus, any behavioral or physiologic change
produced under these conditions might more appropriately be considered
pathologic, rather than reflective of the normal biological role of serotonin.”
(Jacobs, 1991). Once psychiatric drugs are viewed in this way, it is easy to
understand why their widespread use would precipitate an epidemic of mental illness.
As E. Fuller Torrey wrote in The Invisible Plague, conditions that “disrupt
brain chemistry may cause delusions, hallucinations, disordered thinking, and
mood swings—the symptoms of insanity” (Torrey, 2001, p. 315). He noted that
infectious agents, tumors, metabolic and toxic disorders, and various diseases
could all affect the brain in this manner. What Torrey failed to mention is
that psychiatric medications also “disrupt brain chemistry.” As a result, their
long-term use is bound to be problematic, and that is precisely what the
research literature reveals: Their use increases the likelihood that a person
will become chronically ill, and they cause a significant percentage of
patients to become ill in new and more severe ways.
Turning Patients
Chronically Ill
Neuroleptics
The study that is
still cited today as proving the efficacy of neuroleptics for curbing acute
episodes of schizophrenia was a nine-hospital trial of 344 patients conducted
by the National Institute of Mental Health in the early 1960s. At the end of
six weeks, 75% of the drug-treated patients were “much improved” or “very much
improved” compared to 23% of the placebo patients. (Cole, Klermn et al., 1964).
However, three years
later, the NIMH reported on one-year outcomes for the patients. Much to their
surprise, they found that “patients who received placebo treatment were less
likely to be rehospitalized than those who received any of the three active
phenothiazines” (Schooler, Goldberg et al., 1967, pp. 991). This result raised an
unsettling possibility: While the drugs were effective over the short term,
perhaps they made people more biologically vulnerable to psychosis over the
long run, and thus the higher rehospitalization rates at the end of one year.
In the wake of that
disturbing report, the NIMH conducted two medication-withdrawal studies. In
each one, relapse rates rose in correlation with neuroleptic dosage before
withdrawal. In the two trials, only 7% of patients who were on placebo relapsed
during the following six months. Twenty-three percent of the patients on less
than 300 mg of chlorpromazine daily relapsed following drug withdrawal; this
rate climbed to 54% for those receiving 300-500 mg and to 65% for patients
taking more than 500 mg. 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” (Prien, Levine et al., 1971, pp. 22).
Once again, the
results suggested that neuroleptics increased the patients’ biological
vulnerability to psychosis. Other reports soon deepened this suspicion. Even
when patients reliably took their medications, relapse was common, and
researchers reported in 1976 that it appeared that relapse during drug
administration was greater in severity than when no drugs were given (Gardos
and Cole, 1977). A retrospective study by Bockoven also indicated that the
drugs were making patients chronically ill. He reported that 45% of patients
treated at Boston Psychopathic Hospital in 1947 with a progressive model of
care did not relapse in the five years following discharge, and that 76% were
successfully living in the community at the end of that follow-up period. In
contrast, only 31% of patients treated in 1967 with neuroleptics at a community
health center remained relapse-free over the next five years, and as a group
they were much more “socially dependent”—on welfare and needing other forms of
support—than those in the 1947 cohort (Bockoven and Solomon, 1975).
With debate over the
merits of neuroleptics rising, the NIMH revisited the question of whether newly
admitted schizophrenia patients could be successfully treated without drugs.
There were three NIMH-funded studies conducted during the 1970s that examined
this possibility, and in each instance, the newly admitted patients treated
without drugs did better than those treated in a conventional manner. In 1977,
Carpenter reported that only 35% of the non-medicated patients in his study
relapsed within a year after discharge, compared to 45% of those treated with
neuroleptics (Carpenter, McGlashan et al., 1977). A year later, Rappaport
reported that in a trial of 80 young male schizophrenics admitted to a state
hospital, only 27% of patients treated without neuroleptics relapsed in the
three years following discharge, compared to 62% of the medicated group
(Rappaport, Hopkins et al., 1978). The final study came from Mosher, head of
schizophrenia research at the NIMH. In 1979, he reported that patients who were
treated without neuroleptics in an experimental home staffed by
nonprofessionals had lower relapse rates over a two-year period than a control
group treated with drugs in a hospital. As in the other studies, Mosher
reported that the patients treated without drugs were the better functioning
group as well (Bola and Mosher, 2003; Mathews, Roper et al., 2003)
The three studies all
pointed to the same conclusion: Exposure to neuroleptics increased the
long-term incidence of relapse. Carpenter’s group defined the conundrum:
There is no question
that, once patients are placed on medication, they are less vulnerable to
relapse if maintained on neuroleptics. But what if these patients had never
been treated with drugs to begin with? We raise the possibility that
antipsychotic medication may make some schizophrenic patients more vulnerable
to future relapse than would be the case in the natural course of the illness
(Carpenter and McGlashan, 1977, pp. 19).
In the late 1970s, two
physicians at McGill University in Montreal, offered a biological explanation
for why this was so (one that fits with the paradigm later outlined by Hyman).
The brain responds to neuroleptics—which block 70-90% of all D2 dopamine
receptors in the brain—as though they are a pathological insult. To compensate,
dopaminergic brain cells increase the density of their D2 receptors by 30% or
more. The brain is now “supersensitive” to dopamine, and this neurotransmitter
is thought to be a mediator of psychosis. The person has become more
biologically vulnerable to psychosis and is at particularly high risk of severe
relapse should he or she abruptly quit taking the drugs (Chouinard, Jones et
al., 1978; Chouinard and Jones, 1980). The two Canadian researchers concluded:
Neuroleptics can
produce a dopamine supersensitivity that leads to both dyskinetic and psychotic
symptoms. An implication is that the tendency toward psychotic relapse in a
patient who had developed such a supersensitivity is determined by more than
just the normal course of the illness. (Chouniard, Jones, et al., 1978, pp.
1410)
Together, the various
studies painted a compelling picture of how neuroleptics shifted outcomes away
from recovery. Bockoven’s retrospective and the other experiments all suggested
that with minimal or no exposure to neuroleptics, at least 40% of people who
suffered a psychotic break and were diagnosed with schizophrenia would not
relapse after leaving the hospital, and perhaps as many as 65% would function
fairly well over the long-term. However, once first-episode patients were
treated with neuroleptics, a different fate awaited them. Their brains would
undergo drug-induced changes that would increase their biological vulnerability
to psychosis, and this would increase the likelihood that they would become
chronically ill (and thus permanently disabled.)
That understanding of
neuroleptics had been fleshed out by the early 1980s, and since then, other
studies have provided additional confirming evidence. Most notably, the World
Health Organization twice compared schizophrenia outcomes in the rich countries
of the world with outcomes in poor countries, and each time the patients in the
poor countries—where drug usage was much less—were doing dramatically better at
two-year and five-year followups. In India, Nigeria and Colombia, where only
16% of patients were maintained continuously on neuroleptics, roughly
two-thirds were doing fairly well at the end of the followup period and only
one-third had become chronically ill. In the U.S. and other rich countries,
where 61% of the patients were kept on antipsychotic drugs, the ratio of
good-to-bad outcomes was almost precisely the reverse. Only about one-third had
good outcomes, and the remaining two-thirds became chronically ill (Jablensky,
Sartorius et al., 1992; Leff, Sartorius et al., 1992).
More recently, MRI
studies have shown the same link between drug usage and chronic illness. In the
mid 1990s, several research teams reported that the drugs cause atrophy of the
cerebral cortex and an enlargement of the basal ganglia (Chakos, Lieberman et
al., 1994; Gur, Cowell et al., 1998; Madsen, Keiding et al., 1998). These were
disquieting findings, as they clearly showed that the drugs were causing
structural changes in the brain. Then, in 1998, researchers at the University
of Pennsylvania reported that the drug-induced enlargement of the basal ganglia
was “associated with greater severity of both negative and positive
symptoms”(Gur, Maany et al., 1998, pp. 1711). In other words, they found that over
the long term the drugs cause changes in the brain associated with a worsening
of the very symptoms the drugs are supposed to alleviate. The MRI research, in
fact, had painted a very convincing picture of a disease process: An outside
agent causes an observable change in the size of brain structures, and as this
occurs, the patient deteriorates.
Antidepressants
The story of
antidepressants is a bit subtler, and yet it leads to the same conclusion that
these drugs increase chronic illness over time. Even their short-term efficacy,
in terms of a benefit greater than placebo, is of a questionable sort.
In the early 1960s,
there were two types of antidepressants, monoamine oxidase inhibitors (MOAIs)
and tricyclics. However, MOAIs soon fell out of the favor because of dangerous
side effects and a 1965 finding by the Medical Research Council in the United
Kingdom that they were no more effective than placebo (Medical Research
Council, 1965). Four years later, the NIMH concluded that there was also reason
to doubt the merits of tricyclics. After reviewing the medical literature, NIMH
investigators determined that in “well-designed studies, the differences
between the effectiveness of antidepressant drugs and placebo are not
impressive.” About 61% of the drug-treated patients improved, versus 46% of the
placebo patients, producing a net drug benefit of only 15% (Smith, 1969).
This finding led some
investigators to wonder whether the placebo response was the mechanism that was
helping people feel better. What the drugs did, several speculated, was amplify
the placebo response, and they did so because they produced physical side
effects, which helped convince patients that they were getting a “magic pill”
for depression. To test this hypothesis, investigators conducted at least eight
studies in which they compared a tricyclic to an “active” placebo, rather than
an inert one. (An active placebo is a chemical that produces an unpleasant side
effect of some kind, like dry mouth.) In seven of the eight, there was no difference
in outcomes, leading investigators at New York Medical College to conclude
“there is practical value in viewing (psychotropics) as mere amplifiers or
inhibitors of the placebo effects” (Thompson, 1982).
With such confusion
over the efficacy of tricyclics hanging in the air, the NIMH launched an
ambitious long-term study of depression treatments in the early 1980s. Two
hundred thirty-nine patients were randomized into four treatment
groups—cognitive behavior therapy, interpersonal therapy, the tricyclic
imipramine, and placebo. The results were startling. At the end of 16 weeks,
“there were no significant differences among treatments, including placebo plus
clinical management, for the less severely depressed and functionally impaired
patients.” Only the severely depressed patients fared better on a tricyclic
than on placebo. However, at the end of 18 months, even this minimal benefit
disappeared. Stay-well rates were best for the cognitive behavior group (30%)
and poorest for the imipramine group (19%) (Elkin, 1990). Moreover, two
pharmacology researchers at the State University of New York, Seymour Fisher
and Roger Greenberg, concluded that if study dropouts were included in the
analysis, then the “results look even worse.” Patients treated with an antidepressant
were the most likely group to seek treatment following termination of the
initial treatment period, they had the highest incidence of relapse, and they
“exhibited the fewest weeks of reduced or minimal symptoms during the follow-up
period” (Greenberg and Fisher, 1997, pp. 147).
Once again, the
results led to an unnerving conclusion. Antidepressants were making people
chronically ill, just like the antipsychotics were. Other studies deepened this
suspicion. In 1985, a U.K. group reported that in a two-year study comparing
drug therapy to cognitive therapy, relapse “was significantly higher in the
pharmacotherapy group”(Blackburn, 1986). In 1994, Italian researcher Giovanni
Fava reviewed the outcomes literature and concluded that “long-term use of antidepressants
may increase the (patient’s) biochemical vulnerability to depression,” and thus
“worsen the course of affective disorders” (Fava, 1994). Fava revisited the
issue in 2003. An analysis of 27 studies, he wrote, showed that “whether one
treats a depressed patient for 3 months or 3 years, it does not matter when one
stops the drugs. A statistical trend suggested that the longer the drug
treatment, the higher the likelihood of relapse” (Fava, 2003, pp. 124).
Benzodiazepines
This same basic
paradox—that a psychiatric drug may curb symptoms over the short-term but
worsen the long-term course of the disorder—has been found to hold true for
benzodiazepines, at least when used to treat panic attacks. In 1988,
researchers who led the large Cross-National Collaborative Panic Study, which
involved 1,700 patients in 14 countries, reported that at the end of four
weeks, 82% of the patients treated with Xanax (alprazolam) were “moderately
improved” or “better,” versus 42% of the placebo patients. However, by the end
of eight weeks, there was no difference between the groups, at least among
those who remained in the study (Balanger, 1988). Any benefit with Xanax seemed
to last for only a short period. As a followup to that study, researchers in
Canada and the U.K. studied benzodiazepine-treated patients over a period of
six months. They reported that the Xanax patients got better during the first
four weeks of treatment, that they did not improve any more in weeks four to
eight, and that their symptoms began to worsen after that. As patients were
weaned from the drugs, a high percentage relapsed, and by the end of 23 weeks,
they were worse off than patients treated without drugs on five different
outcomes measures (Marks, 1993). More bad news of this sort was reported by
Pecknold in 1988. He found that as patients were tapered off Xanax they
suffered nearly four times as many panic attacks as the non-drug patients, and
that 25% of the Xanax patients suffered from rebound anxiety more severe than
when they began the study. The Xanax patients were also significantly worse off
than non-drug patients on a global assessment scale by the end of the study
(Pecknold, 1988).
Then and Now
Research by David
Healy, a prominent U.K. psychiatrist who has written several books on the
history of psychopharmacology, shows how this problem of drug-induced
chronicity plays out in society as a whole. Healy determined that outcomes for
psychiatric patients in North Wales were much better a century ago than they
are today, even though patients back then, at their moment of initial
treatment, were much sicker. He concluded that today’s drug-treated patients
spend much more time in hospital beds and are “far more likely to die from
their mental illness than they were in 1896.” “Modern treatments,” he said,
“have set up a revolving door” and appear to be a “leading cause of injury and
death” (Healy, Harris, et.al, unpublished paper. See also Healy, Harris, 2001).
Manufacturing Mental Illness
It is well known that
all of the major classes of psychiatric drugs—antipsychotics, antidepressants,
benzodiazepines, and stimulants for ADHD—can trigger new and more severe
psychiatric symptoms in a significant percentage of patients. This is the
second factor causing a rapid rise in the number of disabled mentally ill in
the United States. Moreover, it is easy to see this epidemic-creating factor at
work with Prozac and the other SSRIs.
Although serotonin has
been publicly touted as the brain’s mood molecule, in truth it is a very common
chemical in the body, found in the walls of the blood vessels, the gut, blood
platelets, and the brain. The serotonin system is also one that could be said
to be primitive in kind. Serotonergic neurons are found in the nervous systems
of all vertebrates and most invertebrates, and in humans their cell bodies are
localized along the midline of the brain stem. From their, their axons spread
up into the brain and down into the spinal cord. The first purpose of this
neuronal network is thought to be control of respiratory, cardiac, and
repetitive motor activity, as opposed to higher cognitive functions.
As one would expect,
perturbing this system—and to a degree that could be considered pathologic, as
Jacobs said—causes a wide range of problems. In Prozac’s first two years on the
market, the FDA’s Medwatch program received more adverse-event reports about
this new “wonder drug” than it had received for the leading tricyclic in the
previous 20 years. Prozac quickly took up the top position as America’s most
complained about drug, and by 1997, 39,000 adverse-event reports about it had
been sent to Medwatch. These reports are thought to represent only one percent
of the actual number of such events, suggesting that nearly four million people
in the U.S. had suffered such problems, which included mania, psychotic
depression, nervousness, anxiety, agitation, hostility, hallucinations, memory
loss, tremors, impotence, convulsions, insomnia, and nausea. The other SSRIs
brought to market caused a similar range of problems, and by 1994, four SSRIs
were among the top 20 most-complained-about drugs on the FDA’s Medwatch list
(Moore, 1997).
In terms of helping
fuel a rapid rise in the number of disabled mentally ill, the propensity of
Prozac and other SSRIs to trigger mania or psychosis is undoubtedly the biggest
problem with these drugs. In clinical trials, slightly more than one percent of
the Prozac patients developed mania, which was three times higher than the rate
for patients given a tricyclic (Breggin, 2003). Other studies have found much
higher rates of SSRI-induced mania. In 1996, Howland reported that 6% of 184
depressed patients treated with an SSRI suffered manic episodes that were
“generally quite severe.” A year later, Ebert reported that 8.5% of patients
had a severe psychological reaction to Luvox (fluvoxamine) (Breggin, 2003).
Robert Bourguignon, after surveying doctors in Belgium, estimated that Prozac
induced psychotic episodes in 5% to 7% of patients (Bourguignon, 1997). All of
this led the American Psychiatric Association to warn that manic or hypomanic
episodes are “estimated to occur in 5% to 20% of patients treated with
antidepressants” (Breggin, 2003)
As Italy’s Giovanni
Favi has noted, “Antidepressant-induced mania is not simply a temporary and
reversible phenomenon, but a complex biochemical mechanism of illness
deterioration” (Fava, 2003, pp. 126). The best available evidence suggests that
this is now happening to well more than 500,000 Americans a year. In 2001,
Preda and other Yale researchers reported that 8.1 percent of all admissions to
a psychiatric hospital they studied were due to SSRI-induced mania or psychosis
(Preda, MacLean et al., 2001). The federal government reported that there were
10.741 million “patient care episodes” in 2000; if 8% percent were SSRI-induced
manic or psychotic episodes, that would mean that 860,000 people suffered this
type of adverse reaction in 2000.
Thus, the SSRI path to
a disabling mental illness can be easily seen. A depressed patient treated with
an antidepressant suffers a manic or psychotic episode, at which time his or
her diagnosis is changed to bipolar disorder. At that point, the person is
prescribed an antipsychotic to go along with the antidepressant, and once on a
drug cocktail, the person is well along on the road to permanent disability.
Since Prozac was introduced in 1987, the number of disabled mentally ill in the
U.S. has risen by 2.4 million people, and given the risk of mania and psychosis
with the SSRIs, that increase was to be expected.
Conclusion
A century ago, fewer
than two people per 1,000 were considered to be “disabled” by mental illness
and in need of hospitalization. By 1955, that number had jumped to 3.38 people
per 1,000, and during the past 50 years, a period when psychiatric drugs have
been the cornerstone of care, the disability rate has climbed steadily, and has
now reached around 20 people per 1,000. (Table 2). As with any epidemic, one
would suspect that an outside agent of some type—a virus, a bacterial
infection, or an environmental toxin—was causing this rise in illness. That is
indeed the case here. There is an outside agent fueling this epidemic of mental
illness, only it is to be found in the medicine cabinet. Psychiatric drugs
perturb normal neurotransmitter function, and while that perturbation may curb
symptoms over a short term, over the long run it increases the likelihood that
a person will become chronically ill, or ill with new and more severe symptoms.
A review of the scientific literature shows quite clearly that it is our
drug-based paradigm of care that is fueling this modern-day plague.