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Are neuroleptics helpful to anyone?
"jake" wrote in message ... Do the benefits of use of neuroleptics ever outweigh the harm they cause? *********************************** "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".)" |
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