Why antipsychotics are a bad idea if you don't have psychosis

[crayzyMed]

First lets make clear that if you do have psychotic symptoms which are interfering with your life and the med helps them, then the benefit-risk ratio is acceptable.

Refuse neuroleptics for off-label disorders for the following reasons.

1) Incosistent evidence based on small pilot study's wich hasnt been replicated in bigger study's AFAIK, as an example:

J Clin Psychiatry. 2005 Oct;66(10):1289-97.
Olanzapine/fluoxetine combination for treatment-resistant depression: a controlled study of SSRI and nortriptyline resistance.
Shelton RC, Williamson DJ, Corya SA, Sanger TM, Van Campen LE, Case M, Briggs SD, Tollefson GD.

Department of Psychiatry, Vanderbilt University, Nashville, TN 37212, USA. richard.shelton@vanderbilt.edu
Comment in:

Evid Based Ment Health. 2006 May;9(2):42.
Abstract
BACKGROUND: This 8-week, double-blind, multicenter study was undertaken to replicate, in a larger sample of patients with treatment-resistant major depressive disorder (MDD; DSM-IV criteria), the results of a pilot study of the olanzapine/fluoxetine combination.

METHOD: The study was begun in August 1999. The primary entry criterion was a history of failure to respond to a selective serotonin reuptake inhibitor (SSRI). Patients (N = 500) who subsequently failed to respond to nortriptyline during an open-label lead-in phase were randomly assigned to 1 of 4 treatment groups: olanzapine (6-12 mg/day) plus fluoxetine (25-50 mg/day) combination, olanzapine (6-12 mg/day), fluoxetine (25-50 mg/day), or nortriptyline (25-175 mg/day). The primary outcome measure was baseline-to-endpoint mean change in score on the Montgomery-Asberg Depression Rating Scale (MADRS).

RESULTS: At the 8-week study endpoint, MADRS total scores decreased by a mean 8.7 points from baseline (28.5) with the olanzapine/fluoxetine combination, 7.0 points from baseline (28.4) with olanzapine (p = .0, 8.5 points from baseline (28.4) with fluoxetine (p = .84), and 7.5 points from baseline (28. with nortriptyline (p = .30), with no significant differences among the therapies. The olanzapine/fluoxetine combination was associated with significantly (p < or = .05) greater improvement (decrease) in MADRS scores than olanzapine at weeks 2, 4, 6, and 7; than fluoxetine at weeks 2 through 5; and than nortriptyline at weeks 1 through 4. A post hoc analysis of a subgroup of patients who had an SSRI treatment failure during their current MDD episode (N = 314) revealed that the olanzapine/fluoxetine combination group had a significantly (p = .005) greater decrease in MADRS scores than the olanzapine group at endpoint. Safety data for the olanzapine/fluoxetine combination were similar to those for its component monotherapies.

CONCLUSIONS: The olanzapine/fluoxetine combination did not differ significantly from the other therapies at endpoint, although it demonstrated a more rapid response that was sustained until the end of treatment. The results raised several methodological questions, and recommendations are made regarding the criteria for study entry and randomization.

2) Long term risks, wich includes a permanent movement disorder wich is no joke.

Tardive dyskinesia and new antipsychotics.
Correll CU, Schenk EM.

The Zucker Hillside Hospital, North Shore Long Island Jewish Health System, Glen Oaks, NY 11004, USA. ccorrell@lij.edu
Abstract
PURPOSE OF REVIEW: To provide an update on tardive dyskinesia rates in patients treated with first-generation or second-generation antipsychotics in studies published since the last systematic review in 2004. RECENT FINDINGS: Across 12 trials (n = 28 051, age 39.7 years, 59.7% male, 70.9% white, followed for 463 925 person-years), the annualized tardive dyskinesia incidence was 3.9% for second-generation antipsychotics and 5.5% for first-generation antipsychotics. Stratified by age, annual tardive dyskinesia incidence rates were 0.35% with second-generation antipsychotics in children, 2.98% with second-generation antipsychotics versus 7.7% with first-generation antipsychotics (P < 0.0001) in adults, and 5.2% with second-generation antipsychotics versus 5.2% with first-generation antipsychotics (P = 0.865) in the elderly (based almost exclusively on one retrospective cohort study). In four adult studies (n = 2088, age 41.2 years, 71.2% male, 62.0% white), tardive dyskinesia prevalence rates were 13.1% for second-generation antipsychotics, 15.6% for antipsychotic-free patients, and 32.4% for first-generation antipsychotics (P < 0.0001). SUMMARY: Current evidence supports a lower tardive dyskinesia risk for second-generation antipsychotics than for first-generation antipsychotics. Tardive dyskinesia incidence was higher with second-generation antipsychotics than previously reported, possibly due to recent studies with relatively short mean durations and use of nonstandard tardive dyskinesia definitions.

3) Possibility of even higher risk when those drugs are being used offlablel, still need to check the full text of this one:

Curr Drug Saf. 2010 Jul 2;5(3):263-6.
Safety considerations of the use of second generation antipsychotics in the treatment of major depression: extrapyramidal and metabolic side effects.
DeBattista C, DeBattista K.

Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA. debattista@stanford.edu
Abstract
Second generation antipsychotics (SGAs) are increasingly employed in the treatment of depression. Adjunctive aripiprizole and olanzapine/ fluoxetine combination (OFC) have been approved in the US in the treatment of depression. Quetiapine also appears to be poised for an FDA approval as an adjunctive treatment for resistant depression. Historically, first generation antipsychotics were thought to carry an enhanced risk of certain side effects in the treatment of mood disorders, including an enhanced risk of extrapyramidal symptoms (EPS). The second generation antipsychotics are also known to be associated with a variety of metabolic side effects. The use of SGA in a depressed population may pose risks that differ from use in other conditions such as bipolar disorder and schizophrenia. In this paper, the risk of extrapyramidal and metabolic side effects is reviewed in depressed patients treated with second generation antipsychotics.

[crayzyMed]

Continued

Eur Psychiatry. 2010 Oct 29. [Epub ahead of print]
Cardiovascular and metabolic risk in outpatients with schizoaffective disorder treated with antipsychotics: Results from the CLAMORS study.
Bobes J, Arango C, Aranda P, Carmena R, Garcia-Garcia M, Rejas J; on behalf of the CLAMORS Study Collaborative Group.

Medicine Department, Psychiatry Area, University of Oviedo, Centro de Investigación Biomédica en Red de Salud Mental CIBERSAM, C/Julián Clavería, 6, 33006 Oviedo (Asturias), Spain.
Abstract
AIM: To assess the coronary heart disease (CHD) risk and prevalence of the metabolic syndrome (MS) in patients with schizoaffective disorder (SD) receiving antipsychotics.

METHODS: Patients meeting DSM-IV criteria for SD and receiving antipsychotic treatment were recruited in a retrospective, cross-sectional, multicenter study (the CLAMORS study). MS was defined as at least three of the following components: waist circumference greater than 102cm (men)/greater than 88cm (women); serum triglycerides greater or equal to 150mg/dl; HDL cholesterol less than 40mg/dl (men)/less than 50mg/dl (women); blood pressure greater or equal to 130/85mmHg; fasting blood glucose greater or equal to 110mg/dl. The 10-year CHD risk was assessed by the Systematic coronary risk evaluation (SCORE) (cardiovascular mortality) and Framingham (any cardiovascular event) functions. Clinical severity was assessed using the PANSS and CGI-S scales.

RESULTS: A total of 268 valuable patients with SD (127 men, 48.1%), 41.9±12.3years (mean±S.D.), were analyzed. The 10-year overall cardiovascular mortality and CV-event risk were 0.8±1.6 (SCORE) and 6.5±6.8 (Framingham), respectively. A high/very high risk of any CV event (Framingham≥10%) was associated with severity [CGI-S=3-4; OR: 4.32 (1.15-16.26), P=0.03)]. MS was present in 26.5% (95%CI: 21.2-31. of subjects, without gender differences, but significantly associated with patient's impression of severity: CGI=3-4; OR=1.90 (0.83-4.36), and CGI=5-7; OR=3.13 (1.06-9.24), P=0<0.001, and age [OR=1.91 (1.09-3.34), P<0.024)].

CONCLUSIONS: CHD risk and MS prevalence were high among patients with SD, being MS prevalence associated with age and severity of disease.

Side effects of antipsychotic agents--neuroleptic malignant syndrome.
Cvjetković-Bosnjak M, Soldatović-Stajić B.

Clinical Centre of Vojvodina, Novi Sad. minacvjet@mynsn.net
Abstract
Summary - Neuroleptic malignant syndrome is a rare, potentially life-threatening complication which is an unpredictable, idiosyncratic reaction to antipsychotics. In patients receiving traditional antipsychotics, neuroleptic malignant syndrome occurs with an incidence of 0.2-3.3%. However, neuroleptic malignant syndrome also appears in patients treated with atypical antipsychotics, especially Clozapine. A possible cause of neuroleptic malignant syndrome is blockade of dopamine receptors in the nigrostriatal tracts or hypothalamic nuclei. If signs and symptoms of the Neuroleptic malignant syndrome are identified in time, full recovery is possible. This is a report of a female patient with neuroleptic malignant syndrome treated by traditional antipsychotics. As soon as neuroleptic malignant syndrome symptoms were recognized, the antipsychotic drugs were discontinued, symptomatic therapy was initiated and symptoms of neuroleptic malignant syndrome disappeared. However, the patient's psychotic symptoms persisted and an atypical antipsychotic was administered. During the next few days the psychotic symptoms gradually disappeared and the patient accomplished good recovery.

Mov Disord. 2010 Oct 30;25(14):2475-6.
Neuroleptic malignant syndrome with aripiprazole in Huntington's disease.
Gahr M, Orth M, Abler B.

PMID: 20669301 [PubMed - indexed for MEDLINE]

Publication Types, MeSH Terms, Substances
LinkOut - more resources

chiatr Danub. 2011 Mar;23(1):101-4.
Weight gain induced with olanzapine in adolescent.
Graovac M, Ružić K, Rebić J, Dadić-Hero E, Kaštelan A, Frančišković T.

University Psychiatric Clinic Rijeka, Clinical Hospital Centre Rijeka, Department of Psychiatry and psychological medicine, School of Medicine, Cambierieva 17/7, 51000 Rijeka, Croatia, mirjana.graovac@ri.t-com.hr.
Abstract
Children and adolescents are being treated with antipsychotics more often than before, although the risk of adverse events in this age group still remains unclear. Because of increased use of antipsychotics in children and adolescents, their endocrine and metabolic side-effects (weight gain, obesity, and related metabolic deviations) are of particular worrying, especially within pediatric and adolescent population that appears to be at greater risk comparing with adults for antipsychotic-induced metabolic adverse events. In this work we will present the course of treatment of an adolescent girl with psychotic symptoms, within the clinical diagnosis of Organic delusional disorder, who had a considerable weight gain after one year of olanzapine treatment.

Antipsychotic treatment - side-effect and/or metabolic syndrome.
Dadić-Hero E, Ružić K, Grahovac T, Palijan TZ, Petranović D, Sepić-Grahovac D.

Community Primary Health Centre, Primorsko-goranska county, Rijeka, Croatia, elizabeta.dadic.hero@ri.t-com.hr.
Abstract
According to current medical opinion chronic mental diseases such as schizophrenia require life-long treatment. The choice of antipsychotics is an important treatment factor, since their side-effects often influence patients' compliance with treatment. Severe side-effects may cause the patients to reject such treatment, the latter being their right. In case a psychiatrist does not agree with the patient's decision to interrupt his antipsychotic treatment regardless its serious side-effects, the former should be persistent in convincing the patient to replace such drug with a more appropriate therapy.

[crayzyMed]

Continued

Expert Opin Drug Metab Toxicol. 2011 Mar 15. [Epub ahead of print]
Antipsychotic drug toxicology in children.
Caccia S, Clavenna A, Bonati M.

Mario Negri Institute for Pharmacological Research, Department of Molecular Biochemistry and Pharmacology, Via Giuseppe La Masa 19, Milan 20156, Italy silvio.caccia@marionegri.it.
Abstract
Introduction: There is an increasing use of antipsychotic drugs, particularly those of second- and third-generation, for a wide range of behavioral and affective disorders in pediatric and psychiatric practice. Limited data are available, however, regarding their safety and effectiveness, although children may be more vulnerable than adults to antipsychotic adverse effects because of developmental physiological changes that may affect their pharmacodynamic and pharmacokinetic profiles. Areas covered: This review covers the antipsychotics now specifically approved in major markets for children as well as those that are used in these patients for unapproved or off-label indications taking into account the potential differences in drug disposition and metabolism among children, adolescents and adults. MEDLINE and EMBASE international databases were searched for studies concerning the pharmacokinetics, efficacy and safety of first-, second- ('atypical') and third-generation antipsychotic agents. Expert opinion: Few studies have systematically monitored the safety of antipsychotics in young populations. Data concerning long-term side effects are especially limited, and a systematic benefit-risk evaluation is needed. When prescribing antipsychotics, physicians should, therefore, monitor patients closely for metabolic adverse events, hyperprolactinemia, extrapyramidal symptoms and corrected QT prolongation. Dose selection should include a careful consideration of the drugs' pharmacokinetic profiles and, when these are lacking therapeutic drug monitoring should be implemented as it is often a valid tool to optimize pediatric psychiatric practice.

Predictive value of early changes in triglycerides and weight for longer-term changes in metabolic measures during olanzapine, ziprasidone or aripiprazole treatment for schizophrenia and schizoaffective disorder post hoc analyses of 3 randomized, controlled clinical trials.
Hoffmann VP, Case M, Stauffer VL, Jacobson JG, Conley RR.

Eli Lilly and Company, Lilly Corporate Center, Indianapolis, IN 46285, USA. vph@lilly.com
Abstract
The objective of this study was to determine if early changes in triglycerides and weight may be useful in predicting longer-term changes in weight and other metabolic parameters. Data were from three 24- to 28-week randomized, controlled studies comparing olanzapine to ziprasidone or aripiprazole for treatment of schizophrenia. Analyses were restricted to completers with fasting laboratory data at all protocol specified time points. Analyses were primarily descriptive and included mean changes and categorical outcomes. In all treatment groups, participants who did not experience a 20 mg/dL or greater increase in triglycerides at early time points were unlikely to experience a change of 50 mg/dL or more in triglycerides after 6 months. Negative predictive values were 83% to 95%. However, early change in triglycerides was not useful for predicting later change in glucose, cholesterol, or weight. Similarly, early weight change gave robust negative predictive values for longer-term weight change (≥10 kg), but not for change in glucose or cholesterol. Lack of early elevation in triglyceride concentrations was predictive of later lack of substantial increase in triglycerides in olanzapine-, ziprasidone-, and aripiprazole-treated participants. Lack of early elevation in weight was predictive of later lack of substantial increase in weight in all 3 treatment groups. Early monitoring of triglyceride concentrations and weight may help clinicians assess risk that individuals will experience significant increase in triglycerides or weight gain, allowing assessments of potential risks and benefits earlier in treatment. Clinical monitoring is advised throughout treatment for all patients.

Psychiatr Danub. 2010 Jun;22(2):373-6.
Changes in values of cholesterol and tryglicerides after weight loss during treatment with aripiprazole in a patient with schizophrenia - Case report.
Uzun S, Kozumplik O, Sedić B.

University Department, Vrapce Psychiatric Hospital, 10090 Zagreb, Croatia. suzana.uzun@gmail.com
Abstract
Metabolic syndrome can contribute to significant morbidity and premature mortality and should be accounted for in the treatment of mental disorders. Patients with schizophrenia are at risk of undetected somatic comorbidity. Patients with schizophrenia have metabolically unfavorable body composition, comprising abdominal obesity, high fat percentage and low muscle mass, leading to increased risk of metabolic and cardiovascular diseases. Smoking, poor diet, reduced physical activity and alcohol or drug abuse are prevalent in people with schizophrenia and contribute to the overall cardiovascular disease risk. Side effects of antipsychotics may cause diagnostic problems in deciding regarding the origin of particular symptoms (somatic illness vs. side effects) during treatment of psychotic disorders. Bearing in mind frequent comorbidity between of psychotic and somatic disorders, early recognition of such comorbidity is important, as well as the selection of antipsychotics. The aim of this article is to report a case of changes in values of cholesterol and tryglicerides after weight loss, during treatment with aripiprazole in a patient with schizophrenia. This case report emphasizes the importance of regular monitoring of values of cholesterol and tryglicerides during treatment with antipsychotics.

[millenniumman75]

CrayzyMed - you should have studied to become one of those pharmacological scientist dudes who put together medications .

I was on one for a brief period - mainly as a strong sleep aid. It was another drug that was WAY too strong for me. The lowest dose had me groggy all day. Thank goodness I was only on it for like three months. It was scary. There was some worry that I would have trouble without it, but I had no issues thank God.

[crayzyMed]

Originally Posted by millenniumman75

CrayzyMed - you should have studied to become one of those pharmacological scientist dudes who put together medications .

Thx mate maybe i will, right now i'm putting my efford in helping people online.

[Medline]

Antipsychotics are being pushed for everything. You have a headache, acne or a broken heart? Take Seroquel, Zyprexa... and you're fine.

[crayzyMed]

Originally Posted by Medline

Antipsychotics are being pushed for everything. You have a headache, acne or a broken heart? Take Seroquel, Zyprexa... and you're fine.

Yes, sadly...

[Akane]

Antipsychotics are the only thing that work for me. Everything else I take is just icing on the cake. If you want zyprexa though you better have darn good insurance. It's an $800 prescription otherwise.

[MavenMI6Agent009]

Risperdal helped my hallucinations but i did gain a lot of weight on it though,

[Medline]

Originally Posted by MavenMI6Agent009

Risperdal helped my hallucinations but i did gain a lot of weight on it though,

You got an antipsychotic for a good reason, but some Pdocs give them away like candies.

[writingupastorm]

Originally Posted by crayzyMed

First lets make clear that if you do have psychotic symptoms which are interfering with your life and the med helps them, then the benefit-risk ratio is acceptable.

The benefit-risk ratio may be acceptable, but the benefit-side effect ratio is not. Especially in combination with the risk.

[Medline]

Originally Posted by crayzyMed

First lets make clear that if you do have psychotic symptoms which are interfering with your life and the med helps them, then the benefit-risk ratio is acceptable.

Originally Posted by writingupastorm

The benefit-risk ratio may be acceptable, but the benefit-side effect ratio is not. Especially in combination with the risk.

What's your point? Do you think people with schizophrenia shouldn't take antipsychotics because there are (long-term)-risks involved and the drugs have side effects? That makes no sense.

[Duke of Prunes]

They really do hand antipsychotics out like candy for all sorts of retarded reasons where they are definitely not suitable. I was offered risperidone once because I had a manic reaction to sertraline. The psychiatrist didn't even offer to take me off of it (even to put me on another SSRI) until I'd argued for half an hour about why I wasn't going to take risperidone. After all that, she offered to give me fluoxetine instead, and at that point I left, quit sertraline cold and swore off SSRIs and incompetent psychiatrists for good.

I know a couple of people on antipsychotics. One of them is on olanzapine (not sure what dose or what exactly it's for but I know it's definitely not for psychosis), and they are basically dead. They look like they're in their own little world, and when they're having a conversation, there's always a huge lag, like they're 10 seconds behind everybody. They also move very slowly and have strange facial movements; not serious ones that affect their speech, but small, strange oscillating vertical jaw/mouth movements, like they're cold and shivering, chattering their teeth.

A bit off topic but SSRIs are another class that are a total joke. I was never depressed, depersonalised, seriously anxious or messed up before I tried them, just a bit avoidant, brainfogged and inattentive, but here I am years later after one short trial of an SSRI still don't feel like myself. They might not be physically dangerous, unlike antipsychotics, but they can have pretty serious mental repercussions and they're almost as ubiquitous as ibuprofen.

[writingupastorm]

Originally Posted by Medline

What's your point? Do you think people with schizophrenia shouldn't take antipsychotics because there are (long-term)-risks involved and the drugs have side effects? That makes no sense.

Why does that not make sense? I said it pretty clearly and you repeated it.

[crayzyMed]

For those interesting in experimenting:

Antipsychotics are highly problematic meds because of their ability to induce a permanent movement disorder, verapamil could be a alternative without those problematic side effects.
Another alternative is rimonabant, while it can induce depression i beleive comorbid use of a antidepressant could be a safe and effective alternative for antipsychotics.

Eur J Pharmacol. 2001 Jan 26;412(2):139-44.
Behavioural and anti-psychotic effects of Ca2+ channel blockers in rhesus monkey.
Palit G, Kalsotra A, Kumar R, Nath C, Dubey MP.

Primate Behaviour Laboratory, Division of Pharmacology, Central Drug Research Institute, Post Box 173, 226001, Lucknow, India. root@cscdri.ren.nic.in
Abstract
The potential utility of Ca2+ channel blockers in the treatment of various psychiatric disorders has been recently suggested. In the present study, the behavioural and anti-psychotic effects of Ca2+ channel blockers were investigated in unrestrained rhesus monkeys (Macaca mulatta) living together in a colony. The different behaviours categorised as social, solitary and abnormal were video recorded and analysed. Graded doses of verapamil (5-20 mg/kg, i.m.) and nimodipine (7.5-30 mg/kg, p.o.) produced a mild decrease in social and solitary behaviour without producing any cataleptic posture in the tested monkeys. In order to determine potential antipsychotic effects, Ca2+ channel blockers were studied in the model of amphetamine-induced psychosis. Amphetamine, at the dose of 2 mg/kg, i.m., induced suppression of approach, contact, grooming, and feeding, whilst vigilance (checking), stereotyped behaviour and oral hyperkinesia were increased in the monkeys. Pre-treatment with verapamil (10 and 20 mg/kg, i.m.) significantly suppressed amphetamine-induced hypervigilance, stereotypy, oral hyperkinesia and tachypnoea but was unable to reverse other amphetamine-induced behavioural effects. Nimodipine showed insignificant anti-psychotic effects at both 15 and 30 mg/kg doses. These results suggest that verapamil has a definite antipsychotic effect without any extrapyramidal side effects and thus may be of clinical significance in the treatment of psychosis.

World J Biol Psychiatry. 2010 Mar;11(2 Pt 2):208-19.
Potential antipsychotic properties of central cannabinoid (CB1) receptor antagonists.
Roser P, Vollenweider FX, Kawohl W.

Research Group Clinical and Experimental Psychopathology, Department of General and Social Psychiatry ZH West, Psychiatric University Hospital Zurich, Zurich, Switzerland.
Abstract
Delta(9)-Tetrahydrocannabinol (Delta(9)-THC), the principal psychoactive constituent of the Cannabis sativa plant, and other agonists at the central cannabinoid (CB(1)) receptor may induce characteristic psychomotor effects, psychotic reactions and cognitive impairment resembling schizophrenia. These effects of Delta(9)-THC can be reduced in animal and human models of psychopathology by two exogenous cannabinoids, cannabidiol (CBD) and SR141716. CBD is the second most abundant constituent of Cannabis sativa that has weak partial antagonistic properties at the CB(1) receptor. CBD inhibits the reuptake and hydrolysis of anandamide, the most important endogenous CB(1) receptor agonist, and exhibits neuroprotective antioxidant activity. SR141716 is a potent and selective CB(1) receptor antagonist. Since both CBD and SR141716 can reverse many of the biochemical, physiological and behavioural effects of CB(1) receptor agonists, it has been proposed that both CBD and SR141716 have antipsychotic properties. Various experimental studies in animals, healthy human volunteers, and schizophrenic patients support this notion. Moreover, recent studies suggest that cannabinoids such as CBD and SR141716 have a pharmacological profile similar to that of atypical antipsychotic drugs. In this review, both preclinical and clinical studies investigating the potential antipsychotic effects of both CBD and SR141716 are presented together with the possible underlying mechanisms of action.

[Medline]

Originally Posted by writingupastorm

Why does that not make sense? I said it pretty clearly and you repeated it.

So people with schizophrenia should have a miserable life or die because of their disorder altough they could be treated with antipsychotics? Do you have any idea how the "treatment" of those people looked like before chlorpromazine was available?

[LALoner]

I have one close friend who takes anti psychotics and she's damn glad they work and she doesn't have hallucinations anymore. If you don't need them don't take them but some people consider them life savers.

[crayzyMed]

Originally Posted by LALoner

I have one close friend who takes anti psychotics and she's damn glad they work and she doesn't have hallucinations anymore. If you don't need them don't take them but some people consider them life savers.

True

[writingupastorm]

After having experienced them first hand I don't believe they have any medical value whatsoever. Those people could learn how to embrace their hallucinations and look at them positively, and so could the people who are pressuring them to take medication. Medication isn't the only option. Life as a depressed zombie isn't real life. People are pressured to take medication for a hallucination or delusion when they are in a vulnerable state, then after they're on the medication they no longer have the wherewithal to even decide what they want out of life. Their view of what's important is now skewed because of a decision they were pressured to make in a vulnerable state. I wish there could be a mass class action lawsuit on all their behalves. It's disgusting.

[Medline]

Yeah, whatever...