Are neuroleptics helpful to anyone?

"jake" wrote in message
...


Do the benefits of use of neuroleptics ever outweigh the harm they cause?

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"A : Surrounding issues of the social and political use of neuroleptic
medications.
B : Drug induced diseases and side effects of neuroleptic
medications.
C : Critiques of the newer so-called "atypical antipsychotics".
D : Critiques of the way neuroleptic drugs are tested and approved.
E : Alternatives to using neuroleptic drugs
F : Other sources and links.

A : Surrounding issues of the social and political use of neuroleptic
medications.

It is no longer clear that the benefits of neuroleptic drugs outweigh
the costs, even though a majority of psychiatrists, and all drug
companies and HMOs, have persuaded themselves that this is the case.
Biopsychiatry so dominates the whole field of mental illness that it
is difficult to view the field from a different perspective.
Psychiatrists seem to focus exclusively on medications
and "symptoms."

As psychiatry has become markedly preoccupied with the 'objective', a
gradual disregard of the subjective dimension of our patients'
experience has followed. This disregard for mentally ill patients'
accounts of their subjective experience is based on the notion that
these accounts are unreliable, since these patients suffer from
disturbed thinking and communication. Researchers have systemically
avoided studying the role played by patients subjective responses to
neuroleptics.

Neuroleptics are used to "straighten out the brain" of patients with
various thought disorders, bi-polar disorder and schizophrenia.
Textbooks of psychiatry and review articles claim that the
neuroleptics have a specific antipsychotic effect, especially on the
so-called positive symptoms of schizophrenia, such as hallucinations
and delusions, marked incoherence, and repeatedly bizarre or
disorganized behavior. Their widespread use for social control in
such a wide variety of people and institutions makes the claim that
they are specific for schizophrenia ridiculous. For example, there is
scattered evidence that neuroleptic drugs are administered
indiscriminately to a majority of the elderly who are confined in
convalescent and board and care homes. ". neuroleptic medications are
used in 39% to 51% of elderly institutionalized patients" (Lancetot,
et al, 1998). These figures refer only to anti-psychotic drugs. If
anti-depressants and other tranquilizers were included, the figures
would be much higher. It may be that neuroleptic drugs are being used
as chemical straitjackets for a large majority of the confined
elderly.

There is one further problem connected with the biological approach,
the way it is used with vulnerable populations. It seems likely that
it is frequently being used to control or manage children, confined
aged persons, and women, rather than to help them. It is clear that
the drug Ritalin is being used widely to control children that
teachers find difficult to manage (Breggin 1998, Diller 1998;
DeGrandpre 1999; Walker 1998 ).

Given the over-all picture of the lack of proof of genetic causation,
the chaos of diagnosis, the small average efficacy and dangerous side-
effects of neuroleptic drugs, and their abuse in vulnerable
populations, why hasn't the biological approach been overthrown? The
economics of drug use supplies part of the answer. It has been
extremely profitable for drug companies to exaggerate the efficacy of
neuroleptic drugs, and to play down their brief effectiveness and
destructive side effects. Also, neuroleptic drugs give psychiatrists
a competitive edge over other professionals who treat mental
disorder, since only psychiatrists can prescribe them. Patients
families have bitterly rejected the idea that family relationships
may be a cause of their relatives' mental disorder. Biological
psychiatry, as they interpret it, seems to relieve them of dealing
with shame and guilt, and indeed, from any concern with their own
behavior, emotions and relationships. It leaves their family
systems, no matter how slightly or extremely dysfunctional,
inviolate.

B: Drug induced diseases and side effects of neuroleptic
medications.

Neuroleptics, which include the older antipsychotics and the
newer "atypical" antipsychotics such as olanzapine, have an
extraordinary range of drug-induced diseases. The newer atypical
antipsychotics are said to differ in that they have a lower risk of
the potentially fatal diseases EPS and tardive dyskinesia (1% as
opposed to 5%). However, if administered for as little as three
months, even in low dosages, it has been known for many years that
any of these types of medications will sooner or later cause severe
neurological damage (ie tardive dyskinesia). But the milder, less
perceptible forms of tardive dyskinesia occuring in a high proportion
of patients are the most worrying effects from the patients'
perspective, and are usually talked down by professionals and
dismissed as 'moderate' side effects. Very little is written in
professional sources about the apathy, disinterest, and other
lobotomy-like effects of the drugs.

Neuroleptics are treatments, not cures, which means that their
effects only last as long as the medication is continued to be taken
daily. Mounting clinical evidence and findings point to additional,
severe, adverse neurological changes in response to long-term
exposure to neuroleptics. These drugs' actions suppress certain brain
receptors (e.g., dopamine, glutamate), and when such drugs are
withdrawn, the drug-induced receptor changes are unmasked, causing an
acute "discontinuation syndrome"; they are highly addictive in a
sense, as withdrawal from them creates a sickness many times worse
than the original illness. Withdrawal or discontinuation syndromes
should normally be expected whenever drugs that significantly alter
brain function and trigger changes in neurochemistry are abruptly
withdrawn.

This withdrawal syndrome shows just how dangerous and dubious taking
antipsychotics over longer periods can be; the sedative and dulling
effects can create diverse personality disorders over time. Also,
varying forms of tolerance to the drugs usually develops after 2 to 3
months, so that the drug's actions become more and more clouded and
distorted the longer it is used.

All of this brings into question the toxicity of typical and atypical
antipsychotics. It also brings into question their mode of action :
although neuroleptics show some ability to prevent relapse in
schizophrenia, they have no direct positive effect on social
functioning. The drugs do not correct any "chemical imbalance in the
brain". In fact, they interfere with the nervous system to suppress
brain activity. Chronic neuroleptic use actually depresses social
functioning. Neuroleptics work by interfering with brain function in
a fundamental way. Not only do patients slowly lose their memories,
but they lose strength and physical coordination as well as the
ability to speak coherently. The patient becomes de-energized or de-
enervated. Will or volition is crushed, and passivity and docility
are induced. The patient complains less and becomes more manageable.
Despite the claims made for symptom cure, multiple clinical studies
document a non-specific emotional flattening or blunting effect.
Akinesia is a behavioral state of diminished motoric and psychic
spontaneity that is difficult to distinguish from the negative
symptoms of schizophrenia. Neuroleptics varyingly inhibit dopamine
and 5-HT nerve transmission in the frontal lobes and in the emotion-
regulating limbic system of the brain. This inhibition is no
different than surgical lobotomy. It is chemical lobotomy. The
frontal lobes and limbic system are the seat of higher human
functions such as love, concern for others, empathy, self-insight,
creativity, initiative, autonomy, rationality, abstract reasoning,
judgment, future planning, foresight, will power, determination and
concentration. Inhibition of this portion of the brain disrupts the
total behaviour of the patient. Chemically lobotomized patients lose
their personality. They become "robotic", verbally and physically
withdrawn, as the result of the damage caused to their frontal lobes
and limbic system. Typical changes are apathy, lack of initiative,
loss of memory and concentration, severe lethargy, emotional
indifference, loss of deeper feelings and tenderness, disinterest,
diminished concern, lack of spontaneity, reduced stamina and
emotional reactivity, and, in the extreme, a rousable stupor. In the
end, the patient looses control over his or her body. As one
psychiatrist noted of inpatients taking thorazine
(chlorpromazine) : "approximately half the patients were completely
immobile. One could move them about like puppets".

Although specific treatments do have recognizable different effects
on the brain, they share the capacity to produce generalized
dysfunction with some degree of impairment across the spectrum of
emotional and intellectual function. Because the brain is so highly
integrated, it is not possible to disable circumscribed mental
functions without impairing a variety of them. For example, even the
production of a slight emotional dullness, lethargy, or fatigue is
likely to impair cognitive functions such as attention,
concentration, alertness, self-concern or self-awareness, and social
sensitivity.

If psychosurgery, electroshock, or the more potent psychiatric drugs
were refined to the point of harmlessness, they would approach
uselessness. In biopsychiatry, unfortunately, it's the damage that
does the trick. The brain-disabling principle states that as soon as
toxicity is reached the drug begins to have a psychoactive effect,
that is, it begins to affect the brain and mind. Without toxicity,
the drug would have no psychoactive effect. The principle states that
all of the major psychiatric treatments exert their primary or
intended effect by disabling normal brain function. Neuroleptic
lobotomy, for example, is not a side effect, but the sought-after
clinical effect. It reflects impairment of normal brain function.

A very serious consequence is loss of self-critical monitering of
whatever one may be doing...impaired in the particularly dangerous
way that the person concerned is unaware of the process of
behavoiural deterioration to which he or she is being subjected. High
level psychological functioning may be the first to go under the
stress of poisons and pollutants...only therefore by looking for
impairments of functions immediately dependent upon the highest
levels for their control and coordination might any adverse effect be
detectable at all. It is a profound conceptual issue that has spent
more time in oblivian than in recognition. Psychiatric textbooks and
countless studies of neuroleptic treatment might not contain a single
mention of psychic indifference, the outstanding neuroleptic effect.
Suggestions that neuroleptic treatment mimic the effects of lobotomy
are rarer still, if non existent.

Iatrogenic (Treatment-Caused) Helplessness : Brain dysfunction, such
as a chemical or surgical lobotomy syndrome, renders people much less
able to appreciate or evaluate their mental condition. Surgically
lobotomized people often deny both their brain damage and their
personal problems. They will loudly declare, "I'm fine, never been
better," when they can no longer think straight. Superficially, the
denial looks so sincere that prolobotomists cite it to justify the
harmlessness of the treatment. "A few of the hospital patients, and a
majority of the people I knew as outpatients, told me that they were
undoubtedly helped by their drugs, often spectacularly. In
questioning them closely about drug effects, I usually found that
these subjects were convinced to the point that they were impatient
with my detailed questions. Some reminded me of persons who had had
a religious conversion. They sang the praises of their drugs, and
were not cooperative in responding to questions." - Thomas Scheff,
1999

On the contrary, neuroleptics subject almost every system in the body
to impairment. Research, including a recent study, indicates that
these drugs are "toxic to cells in general". Clozaril, an atypical
antipsychotic, was banned in some European countries because it
caused so many fatalities; but the escalating power of drug companies
subsequently led to its approval by the FDA in the United States.

The brain does not welcome psychiatric medications as nutrients.
Instead, the brain reacts against them as toxic agents and attempts
to overcome their disruptive impact. For example, when Prozac
induces an excess of serotonin in the synaptic cleft, the brain
compensates by reducing the output of serotonin at the nerve endings
and by reducing the number of receptors in the synapse that can
receive the serotonin. Similarly, when Haldol reduces reactivity in
the dopaminergic system, the brain compensates, producing
hyperactivity in the same system by increasing the number and
sensitivity of dopamine receptors.

Neuroleptics have blatantly poisonous properties because part of
their function is the same as that of nerve gas and insecticide in
causing an abnormal build up of acetylcholine. In fact the very
molecular base of one class of neuroleptics called phenothiazines is
used as an insecticide!

In the 1995 Milwaukee heat wave, officials said the heat caused or
contributed to 60 deaths. Among them were about 18 people who were
taking anti-psychotic drugs that block the body's ability to release
heat. Heat intolerance is another major side effect of antipsychotic
medications.

Searching the Medline database for reviews of neuroleptic-induced
neuropathology (drug-induced changes in the structure of brain cells)
published between 1996 and 2000, this author located only two such
articles (Harrison, 1999; Jesteet al, 1999), compared to nearly two
dozen on the neuropathology of schizophrenia. Although various subtle
and not-so-subtle anatomical changes are regularly observed in the
brains of a minority of schizophrenic patients, the neurotoxic
effects of drugs loom large as causative or contributing factors.
During the last five years only, a dozen studies have reported
neuropathological changes, such as hypertrophy of the cerebral cortex
and volume loss in the forebrain of the hypothalamus, as direct
consequences of treatment with typical and newer neuroleptics, in
rodents, cats, nonhuman primates, and humans (e.g., Frazier et al.,
1996; Gur et al., 1998; Halliday et al., 1999; Lohr et al 2000;
Selemon et al 1999). This work only adds to the overwhelming
experimental and clinical evidence implicating neuroleptics as direct
causes of tardive dyskinesia, a movement disorder which usually
persists indefinitely even after drugs are withdrawn.

C : Critiques of the newer so-called "atypical antipsychotics"

Supportive statements notwithstanding, evidence has existed since the
arrival of atypical antipsychotics to illustrate what has been a
recurring pattern in psychiatry: as an older treatment falls into
disrepute, the benefits of a newer treatment are overstated (Cohen,
1994). There are now scores of reports of EPS such as severe
dyskinesias and dystonias (e.g., Ahmed et al., 1999), severe
akathisia (e.g., Jauss et al., 1998), neuroleptic malignant syndrome
(Al-Waneen, 2000; Karagianis et al 1999; Stanfield & Privette, 2000),
as well as tardive dyskinesia (TD) (e.g., Ananth & Kenan, 1999;
Spivak & Smart, 2000) associated with nearly every atypical drug on
the market. In a 2000 study by Modestin et al of 200 patients treated
for several years with older neuroleptics or with clozapine, the
authors conclude: "On the whole, long-term relatively extensive use
of clozapine has not markedly reduced the prevalence of
extrapyramidal syndromes in our psychiatric inpatient population. In
particular, we failed to demonstrate a beneficial effect of clozapine
on prevalence of TD". As to the unique therapeutic profile of the
newer drugs, the authors of a meta-analysis of 52 randomized
controlled trials with 12,649 subjects (Geddes et al, 2000) comparing
six atypical antipsychotics with conventional ones (usually
haloperidol or chlorpromazine), concluded :
"There is no clear evidence that atypical
antipsychotics are more effective or are better tolerated than
conventional antipsychotics [and further], many of the perceived
benefits of atypical antipsychotics are really due to excessive doses
of the comparator drug used in the trials.... Overall, no evidence
was identified to suggest that any individual atypical antipsychotic
had a specific effect on either positive or negative symptoms"

Although the newer atypical antipsychotics developed over the last
decade may have a lower risk of EPS and tardive dyskinesia, they are
associated in varying degrees with sedation, cardiovascular and liver
enzyme abnormalities, anticholinergic effects, extreme weight gain
(30lbs to 50lbs) which significantly increases the risk for diabetes,
sexual dysfunction, NMS, seizures, mania, and (in the case of
clozapine) agranulocytosis. Creators of the newer atypical
antipsychotics, such as Eli Lilly (olanzapine) and Zeneca
(quetiapine) themselves also warn of many side effects. The more
serious adverse reactions identified in the warnings, like
agranulocytosis (Novartis, 1998, p. 8) and neuroleptic malignant
syndrome (Janssen, 1998, p. 1124), may cause sudden death. The
advertisements also warn about laboratory evidence which indicates
the new drugs are carcinogens (Eli Lilly, 1998, p. 310) and mutagens
(Zeneca, 1998, p 284). Despite the claims from some quarters that
tardive dyskinesia is not a problem with atypicals most of the
advertisements warn that these drugs do cause the disease. An
advertisement for Risperdal warns clearly of this risk (Janssen,
1998).

The manufacturers also warn about the possibility of adverse mental
and behavioural reactions. Many of these psychiatric reactions are
the very disorders that prophylactic treatment with the drugs is
intended to prevent. An advertisement published by Zeneca
Pharmaceuticals, for instance, after warning about an extraordinary
variety of ways their new atypical quetiapine can induce ill-health,
identifies "Other Adverse Events Observed During the Pre-Marketing
Evaluation of Seroquel". These include:
"abnormal dreams, dyskinesia, thinking abnormal,
tardive dyskinesia, vertigo, involuntary movements, confusion,
amnesia, psychosis, hallucinations, hyperkinesia, libido increased,
urinary retention, incoordination, paranoid reaction, abnormal gait,
myoclonus, delusions, manic reaction, apathy, ataxia,
depersonalisation, stupor, bruxism, catatonic reaction, hemiplegia"
(Zeneca, 1998).

A clozapine advertisement also warns about the risk of a variety of
drug-induced negative and positive symptoms like loss of speech,
amentia, delusions/hallucinations and paranoia (Novartis, 1998). If
treatment with atypical neuroleptics can sometimes induce psychosis,
hallucinations and delusions, as is frankly being admitted in
advertisements for the drugs, questions most definitely arise about
the application of these drugs as prophylactics against psychosis.

D : Critiques of the way neuroleptic drugs are tested and approved

Substantial evidence exists to suggest that the quality of research
on the psycho-pharmacological treatment of thought disorders has been
uniformly poor, or is conducted in such a way as to make results of
drug trials and other studies appear in the best light possible for
the tested drugs, or studiously ignores important research directions
that might highlight negative effects of drug treatment.

Although the last five decades have seen a vast number of studies of
functional mental disorder, there is as yet no substantial, verified
body of knowledge in this area. At this writing, there is no rigorous
and explicit knowledge of the cause, cure, or even a coherent
classification of the symptoms of functional mental disorders (such
as schizophrenia, depression, anxiety disorders, etc). An example is
the study of symptom clusters by Strauss (1979). He compared the
actual cluster of symptoms that each of 217 first admission patients
displayed with the diagnostic syndromes. He concluded that the
clusters of "the vast majority [of the patients] fall between
syndromes." That is to say, that the symptoms of the large majority
of actual patients do not cohere the way the DSM organizes them,
suggesting that, in this fundamental respect, the problems that
psychiatrists treat do not seem to fit into the medical model of
disease.

There are a vast number of systematic studies that seem at first
glance to testify to the effectiveness of neuroleptic drugs. These
are almost all what is called randomized clinical trials (RCTs). A
group of patients with similar diagnoses are divided randomly into
two subgroups. One subgroup, the treatment group, receives the drug,
the other, the control group, get an inert substance disguised as a
medication, a "placebo". The design requires that the administration
of the substances be "blind"; that is, neither the patients nor the
doctors know which are the drugs and which placebos. If the
subgroups are set up at random, and if the participants are "blind",
then any change in the treatment group larger than the control group
can be confidently ascribed to the effects of the drug.

The usually positive results of these studies is thought to
demonstrate two points: First that psychoactive drugs are more
effective than the placebos used in the control groups, and that
their effectiveness is due to the correction of biological deficits
in the patients. However it is important to note that even if these
results are accepted at face value, the average difference in effect
between the drug and the placebo group in the typical study is not
large, and often short-lived, as shown in studies over time.
Typically, in repeat studies done from four months to eight months
after the initial one, the average advantage of the treatment group
over the control group has decreased or even disappeared. Since we
are dealing with averages among many patients, this is not to say
that there aren't strong positive and negative, and even no effects
on individual patients. To summarize: even accepting the validity of
the RCTs, most neuroleptic drugs are only slightly and briefly more
effective than placebos. The decreasing effectiveness over time is
suggestive of a placebo effect.

In recent years there have been a sizable number of studies that
challenge the standard interpretation of the RCT studies, that
neuroleptic drugs, in themselves, are more effective than inert
substances, and that their effectiveness is due to the correction of
biological deficiencies. It now appears that most RCTs are not truly
blind, because most of the participants can make accurate guesses as
to whether the patient is receiving a psychoactive drug. Shapiro and
Shapiro (1997, Table 9.1) reviewed 27 studies that asked doctors,
patients, and "raters" (outside observers) to guess who was receiving
the drug. On average, 93% of the doctors, 73% of the patients, and
67% of the raters could accurately guess the active agent. Doctors,
patients, and raters can use physical effects, taste, color, texture,
and dissolvability to guess. Especially for the patient, the
physical effects on the body often reveal the active drugs, since
many of them are powerful stimulants, sedatives, or emotion
blockers. The drug companies who conduct most of the RCTs seldom try
to make a close match between the drug and the placebo, because they
think it is not sufficiently important to warrant investing in the
complex task of precise matching.

E : Alternatives to using neuroleptic drugs

A diversity of helpful treatments are lost as a result of the medical
profession's scheduling of drugs. And crude attempts to outlaw the
use of drugs not produced, marketed or supplied by international
industries have further devided the rich & poor, the strong & the
weak. Exorphins (Exogenous endorphins) such as opoids, are an
example. Some physicians have recommended opoids for diverse mental
illnesses. A recent review of controlled studies of patients in the
acute phase of schizophrenia showed that neuroleptics perform no
better than opoids or sedatives. But there is little profit from
generic opoids for the pharmaceutical profession, especially when
compared to drugs like prozac, and branching out there use would only
increase their spillage over to the drug black-market (which would
thus begin channelling more profit away from there hands). People
with illnesses such as chronic pain syndrome, who could benefit from
opoids, are left out of the equation. Many groups have been formed
over the last 10 years to fight for the human rights of these
patients, but to little or no avail, as the pharmaceutical profession
increasingly succeeds in its "drug-information abuse", and its
creation of fictitious diseases such as "chemical dependency" & "drug
abuse"; Addiction is itself addicted. The following sentences
describing ways opoids can work are quickly flushed back to where
they came from by the medical profession :
Exorphins & endorphins (endogenous painkillers which are produced by
our own bodies) have many extremely silent abilities. They can
suppress an individual's overflowingly painful, habituative, energies
in the spine & bodily nervous system, leaving more 'offset' energy
for the mind.

Links to medical articles about opioids and their use as a treatment
of various psychiatric conditions :
http://www.geocities.com/HotSprings/...ticlemenu.html
http://www.opioids.com/antidepressant/history.html
http://groups.google.com/groups?selm=t1b5n9n7qki594%
40corp.supernews.com&oe=UTF-8&output=gplain

F : Other sources and links

a) http://www.academyanalyticarts.org/scheff.html ("Biological
Psychiatry and Labeling Theory" - Thomas Scheff, 1999)
b) http://www.namiscc.org/Research/2002/SocialWork.htm
("Research on the Drug Treatment of Schizophrenia" - David
Cohen, 2002)
c) http://psychrights.org/Research/Dige...ninplacebo.pdf
("A critique of the use of neuroleptic drugs in psychiatry" -
David Cohen)
d) http://groups.google.com/groups?hl=e...=UTF-8&oe=UTF-
8&selm=EsHwDF.JD6%40world.std.com
e) http://www.dsuper.net/~styan/neurolep.htm
f) http://www.sntp.net/drugs/tranquilizers.htm (Excerpt from Peter
Breggin's book, "Toxic Psychiatry".)"