Preventive Psychiatry E-Newsletter # 224
Excerpts from Robert Whitaker's Anatomy of an Epidemic:
Psychiatric Drugs and the Astonishing Rise of Mental Illness in America
Ethical Human Psychology and Psychiatry, Vol. 7, Number 1, Spring 2005
Full article, with extensive documentation, accessible at:
http://psychrights.org/index.htm
Excerpted, with minimal editing, by Gary G. Kohls, MD, Duluth, MN
The percentage of Americans disabled by mental illness has increased
fivefold since 1955, when Thorazine ˆ remembered today as psychiatry‚s
first "wonder" drug ˆ was introduced into the market.
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.
E. Fuller Torrey, in his 2001 book The Invisible Plague, concluded that
insanity had risen to the level of an epidemic. This epidemic has
unfolded in lockstep with the ever-increasing use of psychiatric drugs.
The number of disabled mentally ill has increased nearly six-fold since
Thorazine was introduced.
The number of disabled mentally ill has also increased dramatically
since 1987, the year Prozac was introduced.
Anti-psychotics, antidepressants, and anti-anxiety drugs create
perturbations in neurotransmitter functions. In response, the brain goes
through a series of compensatory adaptations. 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 50% or more. After a few weeks, the patient‚s brain is functioning in
a manner that is qualitatively as well as quantitatively different from
the normal state.
Conditions that disrupt brain chemistry may cause delusions,
hallucinations, disordered thinking, and mood swings ˆ the symptoms of
insanity. Infectious agents, tumors, metabolic and toxic disorders and
various diseases could all affect the brain in this manner. Psychiatric
medications also disrupt brain chemistry. Psychotropic drugs increase
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 (= Anti-psychotics = Anti-schizophrenics = Major Tranquilizers)
In an NIMH (National Institute of Mental Health) study, short-term (6
weeks) anti-psychotic drug-treated patients were much improved compared
to placebo (75% vs. 23%). However patients who received placebo
treatment were less likely to be re-hospitalized over the next 3 years
than were those who received any of the three active phenothiazines.
Relapse was found to be significantly related to the dose of the
tranquilizing medication the patient was receiving before he was put on
placebo ˆ the higher the dose, the greater the probability of relapse.
Neuroleptics increased the patients‚ biological vulnerability to
psychosis. A retrospective study by Bockoven also indicated that the
drugs were making patients chronically ill.
There were three NIMH-funded studies conducted during the 1970s that
examined this possibility (whether first-episode psychotic episodes
could be treated without medications), and in each instance, the newly
admitted patients treated without drugs did better than those treated in
a conventional manner (i.e. with anti-psychotic drugs).
Patients who were treated without neuroleptics in an experimental home
staffed by nonprofessionals had lower relapse rates over a 2-year period
than a control group treated with drugs in a hospital. Patients treated
without drugs were the better functioning group as well.
The brain responds to neuroleptics ˆ which block 70% to 90% of all D2
dopamine receptors in the brain ˆ 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 becomes more biologically vulnerable to psychosis and is at
particularly high risk of severe relapse should he or she abruptly quit
taking the drugs.
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 that just the normal course of
the illness.
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).
In the mid 1990s, several research teams reported that the drugs cause
atrophy of the cerebral cortex and an enlargement of the basal ganglia.
The drugs were causing structural changes in the brain. The drug-induced
enlargement of the basal ganglia was associated with greater severity of
both negative and „positive‰ (schizophrenic) symptoms. 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.
Antidepressants
The story of antidepressants is a bit subtler, and it leads to the same
conclusion that these drugs increase chronic illness over time.
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%.
At the end of 16 weeks (in a study comparing cognitive behavior therapy,
interpersonal therapy, the tricyclic antidepressant imipramine and
placebo) 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%).
Antidepressants were making people chronically ill, just like the
anti-psychotics were. In 1985, a U.K. group reported that in a 2-year
study comparing drug therapy to cognitive therapy, relapse was
significantly higher in the pharmacotherapy group. Long-term use of
antidepressants may increase the patient‚s biochemical vulnerability to
depression and thus worsen the course of affective disorders. An
analysis of 27 studies showed that whether one treats a depressed
patient for 3 months of 3 years, it does not matter when one stops the
drugs. The longer the drug treatment, the higher the likelihood of relapse.
Benzodiazepines
Xanax (a benzodiazepine class „minor‰ tranquilizer) patients got better
during the first four weeks of treatment; they did not improve any more
in weeks 4 to 8, and their symptoms began to worsen after that. 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.
Patients tapered off Xanax suffered nearly 4 times as many panic attacks
as the non-drug patients and 25% of the Xanax patients suffered from
rebound anxiety more severe than when they began the study.
Then and Now
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 have set up a revolving door and appear to be a
leading cause of injury and death.
MANUFACTURING MENTAL ILLNESS
It is well-known that all of the major classes of psychiatric drugs ˆ
anti-psychotics, anti-depressants, benzodiazepines, and stimulants for
ADHD ˆ can trigger new and more severe psychiatric symptoms in a
significant percentage of patients. It is easy to see this
epidemic-creating factor at work with Prozac and the other SSRIs.
Prozac quickly took up the top position as America‚s most complained
about drug. By 1997, 39,000 adverse-event reports about it had been sent
to Medwatch. These reports are thought to represent only 1% of the
actual number of such events, suggesting that nearly 4 million people in
the US had suffered such problems, which included mania, psychotic
depression, nervousness, anxiety, agitation, hostility, hallucinations,
memory loss, tremors, impotence, convulsions, insomnia and nausea.
The propensity of Prozac and other SSRIs to trigger mania or psychosis
is undoubtedly the biggest problem with these drugs. The American
Psychiatric Association warns that manic or hypomanic episodes are
estimated to occur in 8% to 20 % of patients treated with anti-depressants.
Anti-depressant-induced mania is not simply a temporary and reversible
phenomenon, but a complex biochemical mechanism of illness
deterioration. Yale researchers reported that 8.1% of all admissions to
a psychiatric hospital they studied were due to SSRI-induced mania or
psychosis.
Thus the SSRI path to a disabling mental illness can be easily seen. A
depressed patient treated with an anti-depressant 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
anti-psychotic to go along with the anti-depressant, and, once on a drug
cocktail, the person is well along on the road to permanent disability.
CONCLUSION
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 or
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.
NOTE: Robert Whitaker wrote the ground-breaking book, Mad In America:
Bad Science, Bad Medicine and the Enduring Mistreatment of the Mentally
Ill, a book that should be required reading for everybody, (check out
http://www.madinamerica.com/).
The purpose of the Preventive Psychiatry E-Newsletter (PPEN) is to
disseminate critical information that concerns mental health, especially
that which pertains to the root causes of mental ill health and its
prevention, information that is often not readily available in the
mainstream media. Most of the items that I pass on via the PPEN are
derived from other sources, which I believe to be accurate, but cannot
guarantee, and I do not accept responsibility for any errors or
omissions. I strive to provide references so that the reader can
independently evaluate the validity of the information in each issue.
Preventive Psychiatry E-Newsletter Editor - Gary G. Kohls, MD, Duluth, MN
Excerpts from Robert Whitaker's Anatomy of an Epidemic:
Psychiatric Drugs and the Astonishing Rise of Mental Illness in America
Ethical Human Psychology and Psychiatry, Vol. 7, Number 1, Spring 2005
Full article, with extensive documentation, accessible at:
http://psychrights.org/index.htm
Excerpted, with minimal editing, by Gary G. Kohls, MD, Duluth, MN
The percentage of Americans disabled by mental illness has increased
fivefold since 1955, when Thorazine ˆ remembered today as psychiatry‚s
first "wonder" drug ˆ was introduced into the market.
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.
E. Fuller Torrey, in his 2001 book The Invisible Plague, concluded that
insanity had risen to the level of an epidemic. This epidemic has
unfolded in lockstep with the ever-increasing use of psychiatric drugs.
The number of disabled mentally ill has increased nearly six-fold since
Thorazine was introduced.
The number of disabled mentally ill has also increased dramatically
since 1987, the year Prozac was introduced.
Anti-psychotics, antidepressants, and anti-anxiety drugs create
perturbations in neurotransmitter functions. In response, the brain goes
through a series of compensatory adaptations. 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 50% or more. After a few weeks, the patient‚s brain is functioning in
a manner that is qualitatively as well as quantitatively different from
the normal state.
Conditions that disrupt brain chemistry may cause delusions,
hallucinations, disordered thinking, and mood swings ˆ the symptoms of
insanity. Infectious agents, tumors, metabolic and toxic disorders and
various diseases could all affect the brain in this manner. Psychiatric
medications also disrupt brain chemistry. Psychotropic drugs increase
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 (= Anti-psychotics = Anti-schizophrenics = Major Tranquilizers)
In an NIMH (National Institute of Mental Health) study, short-term (6
weeks) anti-psychotic drug-treated patients were much improved compared
to placebo (75% vs. 23%). However patients who received placebo
treatment were less likely to be re-hospitalized over the next 3 years
than were those who received any of the three active phenothiazines.
Relapse was found to be significantly related to the dose of the
tranquilizing medication the patient was receiving before he was put on
placebo ˆ the higher the dose, the greater the probability of relapse.
Neuroleptics increased the patients‚ biological vulnerability to
psychosis. A retrospective study by Bockoven also indicated that the
drugs were making patients chronically ill.
There were three NIMH-funded studies conducted during the 1970s that
examined this possibility (whether first-episode psychotic episodes
could be treated without medications), and in each instance, the newly
admitted patients treated without drugs did better than those treated in
a conventional manner (i.e. with anti-psychotic drugs).
Patients who were treated without neuroleptics in an experimental home
staffed by nonprofessionals had lower relapse rates over a 2-year period
than a control group treated with drugs in a hospital. Patients treated
without drugs were the better functioning group as well.
The brain responds to neuroleptics ˆ which block 70% to 90% of all D2
dopamine receptors in the brain ˆ 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 becomes more biologically vulnerable to psychosis and is at
particularly high risk of severe relapse should he or she abruptly quit
taking the drugs.
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 that just the normal course of
the illness.
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).
In the mid 1990s, several research teams reported that the drugs cause
atrophy of the cerebral cortex and an enlargement of the basal ganglia.
The drugs were causing structural changes in the brain. The drug-induced
enlargement of the basal ganglia was associated with greater severity of
both negative and „positive‰ (schizophrenic) symptoms. 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.
Antidepressants
The story of antidepressants is a bit subtler, and it leads to the same
conclusion that these drugs increase chronic illness over time.
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%.
At the end of 16 weeks (in a study comparing cognitive behavior therapy,
interpersonal therapy, the tricyclic antidepressant imipramine and
placebo) 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%).
Antidepressants were making people chronically ill, just like the
anti-psychotics were. In 1985, a U.K. group reported that in a 2-year
study comparing drug therapy to cognitive therapy, relapse was
significantly higher in the pharmacotherapy group. Long-term use of
antidepressants may increase the patient‚s biochemical vulnerability to
depression and thus worsen the course of affective disorders. An
analysis of 27 studies showed that whether one treats a depressed
patient for 3 months of 3 years, it does not matter when one stops the
drugs. The longer the drug treatment, the higher the likelihood of relapse.
Benzodiazepines
Xanax (a benzodiazepine class „minor‰ tranquilizer) patients got better
during the first four weeks of treatment; they did not improve any more
in weeks 4 to 8, and their symptoms began to worsen after that. 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.
Patients tapered off Xanax suffered nearly 4 times as many panic attacks
as the non-drug patients and 25% of the Xanax patients suffered from
rebound anxiety more severe than when they began the study.
Then and Now
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 have set up a revolving door and appear to be a
leading cause of injury and death.
MANUFACTURING MENTAL ILLNESS
It is well-known that all of the major classes of psychiatric drugs ˆ
anti-psychotics, anti-depressants, benzodiazepines, and stimulants for
ADHD ˆ can trigger new and more severe psychiatric symptoms in a
significant percentage of patients. It is easy to see this
epidemic-creating factor at work with Prozac and the other SSRIs.
Prozac quickly took up the top position as America‚s most complained
about drug. By 1997, 39,000 adverse-event reports about it had been sent
to Medwatch. These reports are thought to represent only 1% of the
actual number of such events, suggesting that nearly 4 million people in
the US had suffered such problems, which included mania, psychotic
depression, nervousness, anxiety, agitation, hostility, hallucinations,
memory loss, tremors, impotence, convulsions, insomnia and nausea.
The propensity of Prozac and other SSRIs to trigger mania or psychosis
is undoubtedly the biggest problem with these drugs. The American
Psychiatric Association warns that manic or hypomanic episodes are
estimated to occur in 8% to 20 % of patients treated with anti-depressants.
Anti-depressant-induced mania is not simply a temporary and reversible
phenomenon, but a complex biochemical mechanism of illness
deterioration. Yale researchers reported that 8.1% of all admissions to
a psychiatric hospital they studied were due to SSRI-induced mania or
psychosis.
Thus the SSRI path to a disabling mental illness can be easily seen. A
depressed patient treated with an anti-depressant 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
anti-psychotic to go along with the anti-depressant, and, once on a drug
cocktail, the person is well along on the road to permanent disability.
CONCLUSION
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 or
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.
NOTE: Robert Whitaker wrote the ground-breaking book, Mad In America:
Bad Science, Bad Medicine and the Enduring Mistreatment of the Mentally
Ill, a book that should be required reading for everybody, (check out
http://www.madinamerica.com/).
The purpose of the Preventive Psychiatry E-Newsletter (PPEN) is to
disseminate critical information that concerns mental health, especially
that which pertains to the root causes of mental ill health and its
prevention, information that is often not readily available in the
mainstream media. Most of the items that I pass on via the PPEN are
derived from other sources, which I believe to be accurate, but cannot
guarantee, and I do not accept responsibility for any errors or
omissions. I strive to provide references so that the reader can
independently evaluate the validity of the information in each issue.
Preventive Psychiatry E-Newsletter Editor - Gary G. Kohls, MD, Duluth, MN
