Dignity of Elders: Carole Hayes Collier — Madness Radio

Why are nearly a third of all elders in nursing homes given anti-psychotic drugs, despite life threatening side effects? Are medications being used as chemical restraints? Can nursing homes be places of dignity — or should they be abolished? Carole Hayes-Collier was diagnosed schizophrenic at 19 and left to a lifetime of hospitalization. When she recovered, the abuses she witnessed inspired her to join the Gray Panthers and dedicate her life to elder rights and mental health.

Listen here:

●  Prescription Abuse Seen In U.S. Nursing HomesPowerful Antipsychotics Used to Subdue Elderly

●  Gray Panthers

●  The Campaign to STOP Chemical Restraints in Nursing Home

Download this talk at Madness Radio

Numbing of our emotions and what happens to adolescents who develop that way?

Psych drugs damage ability to love/bond

I’ve posted some variation of this post twice before. I felt moved to post it again since I had a conversation with a journalist friend who is thinking about this issue too. My last paragraph in this piece speculated about what antidepressants do to pre-pubescent and adolescent kids. What happens when the normal drive for sex and orgasm and romantic love is muted or altogether absent because the kids are on SSRI or SNRI antidepressants (and/or other psych drugs)? My friend talked with an adolescent counselor and she’s noticed that these kids are strangely uninterested in romantic love and sometimes even appear to be asexual. That is ALARMING and it’s right in line with what my speculative fears suggested. I don’t have much more to say about the topic but would like to raise the issue that more people may start to think about this very serious problem that effects a far too large percentage of our young population.

The post as it was to begin with started out with Helen Fisher’s work which lays a good foundation for the point about the kids:

Helen Fisher is an anthropologist who has looked at how antidepressants effect romantic love, falling in love and most importantly ongoing attachment. The conclusion being that the love response and the human instinct for attachment are profoundly messed up. Antidepressants don’t just create sexual dysfunction, they wreak havoc with the whole emotional system that creates attachment to other human beings. In my experience it is not only the antidepressants that do this. As far as I can tell all psychiatric drugs do it. As is often the case antidepressants are more commonly studied when the mainstream is being considered. The fact is, however and unfortunately, that neuroleptics are going mainstream. Historically, neuroleptics (antipsychotics) and the other psych meds aren’t taken by as many “normal” people as the antidepressants do so they haven’t been studied by this woman who is basically making a social commentary. Someday perhaps such studies will extend to include all psychotropics, as there are more and more people effected by all these classes of drugs.

Below is from an article in the LA times about Fisher’s work from a few years ago:

Couples think about the other obsessively – on a roller coaster of euphoria when together, longing when apart.

“It’s temporary insanity,” says Helen Fisher, an evolutionary anthropologist at Rutgers University.

Now, from her studies of the brains of lovers in the throes of the initial tumble, Fisher has developed a controversial theory. She and her collaborator, psychiatrist J. Anderson Thomson of the University of Virginia, believe that Prozac, Zoloft, Paxil and other antidepressants alter brain chemistry so as to blunt the intense cutting edge of new love.

Fisher and Thomson, who describe their theory in a chapter in the book, “Evolutionary Cognitive Neuroscience,” aren’t talking just about the notorious ability of the drugs to damp sexual desire and performance, although that, they believe, plays its part. They think the drugs also sap the craving for a mate – perhaps even the brain’s very ability to fall in love.

And here is a video of her speaking on the same topic but emphasizing different things which I think are more important:

This fact alone about psychiatric drugs is enough to undermine society. Don’t think this doesn’t effect parent’s ability to love and bond with their children. And then when you think about all the kids on these drugs who simply don’t develop normally. Teenage hormones are part of growing up. What happens when you skip that developmental stage? What happens if you never enter it at all due to a lifetime of being on drugs? We are stopping the human experience from happening.

The above paragraph was my speculation about the issue from three years ago. It seems that I was right to be concerned. I find this issue extremely problematic and disturbing and think it should become part of the dialogue about these drugs. Pass it on, people. Let’s not harm young people coming of age in the psychopharmaceutical age. Let’s halt the direction it’s been going in and start learning to support these kids and everyone who takes these drugs in new ways.

My husband read this post and made this comment which I thought well worth sharing:

Very good post and a profound issue. You used the phrase “undermine society” and I would make that even stronger and say destroy society. If epidemiological studies were done, I would expect there is a direct correlation between the number of people living alone and the number on antidepressants (and other psych meds). I suspect that America (perhaps more than other countries) has blinkers on when it comes to acknowledging mass isolation as a problem because so much value is attached to autonomy. It’s as though if everyone is doing there own thing, then everyone is enjoying their freedom — except this is a freedom that atomizes society. Instead of their being one society, there is now a universe of societies-of-one, each separated by lifeless space.

“The seriously mentally ill die, on average, 25 years earlier than the general population…”

(exploring the source of a statistic)

Are you familiar with this oft-quoted statistic: “people with serious mental illness served by the public mental health system die, on average, 25 years earlier than the general population”?  You see it everywhere – for example in TIME magazine, USA Today, and throughout the mental health blogosphere.

It comes from this 2006 report on mortality and morbidity in the seriously mentally ill population published by the National Association of State Mental Health Program Directors [NASMHPD].  The report also contains several other [less frequently quoted but no less powerful] statistics.  Consider:

  • suicide accounts for 30% of excess mortality [in the population suffering from “serious mental illness”], but 60% of premature deaths are due to other causes such as cardiovascular and pulmonary disease, obesity, and smoking – causes which are in some ways preventable.
  • people diagnosed with schizophrenia are 2.7X more likely to die of diabetes than the general population; 2.3X more likely to die of cardiovascular disease, 3.2X more likely to die of respiratory disease, and 3.4X more likely to die of infectious disease.  All of these causes of death are exacerbated by the following risk factors – obesity, smoking, diabetes, hypertension, and dyslipidemia [high blood cholesterol] – which are, again, significantly more prevalent amongst this population.

These are shocking things for science to say, surely a kind of gauntlet thrown at the feet of this population and those who serve/support/love them.

Methinks a champion is required; and this guy is probably NOT it.

What causes this shocking mortality/morbidity problem, and what can be done?

Are you thinking what I’m thinking?

In light of all that we’ve recently learned about psychotropic medications, antipsychotics in particular (causing brain shrinkage, diabetes, obesity, heart disease, et al): does the NASMHPD report have the guts to honestly own up to the fact that most of the abovementioned risk factors can often be traced back directly to the psychotropic medications so glibly prescribed to this population?  Actually, they do a pretty good job, acknowledging all of the following:

Residence in group care facilities and homeless shelters (exposure to TB [tuberculosis] and other infectious diseases as well as less opportunity to modify individual nutritional practices)… symptoms associated with serious mental illness [such as] feelings of hopelessness and powerlessness, learned helplessness…

Psychotropic medications may mask symptoms of medical illness and contribute to symptoms of medical illness and cause metabolic syndrome… [and] polypharmacy [is] identified as a risk factor for sudden death.

(from the 2006 NASMPHD report on mortality in the mental health population)


Seeing such promising signs – a willingness to acknowledge these usually unspoken-of risk/causative factors – I eagerly turned to the “Policy Recommendations” section…

Only to be severely disappointed.  Nothing addresses the risk factors listed above.  NOTHING.

[alright – they did briefly mention a tool used in New York State hospitals to insure folks weren’t prescribed 3 or more antipsychotic medications at the same time but that was just a subordinate clause in a very long sentence buried near the bottom of page 47… and I feel that’s just a tad inadequate, don’t you?]

Here’s what they do instead:


Policy Recommendations?  Change the language, of course…

The “Policy Recommendations for Providers and Clinicians” section starts out with some powerful and exciting language: mentally ill people must be assisted in finding “hope for tomorrow” and to “understand the hopeful message of recovery.”  They must be “enabled to engage as equal partners in care and treatment” and “empowered.”

But what is really meant is that the language must be changed so that these things are implied, while treatment remains largely the same.  Here is how NASMHPD recommends achieving a “partnership with the people we serve:”

Agree on a Treatment Plan

“Adherence” is the goal because it implies sticking to a collaboratively developed plan, as opposed to the more directive term “compliance.”  Six specific actions can increase the likelihood of adherence: keep the regimen simple, write out treatment details, give specifics about the expected benefits of treatment and the timetable, prepare the patient for side effects and optional courses of action, discuss obstacles to moving forward with the regimen, and get patient feedback.

(from the 2006 NASMHPD report)

So “partnership” between providers and “consumers” is to be achieved by a mere change of language (from “compliance” to “adherence”), which no longer implies the directive (ie use of force), power flowing from provider to patient.  Never mind that involuntary commitment and treatment of the mentally ill is as frequent a practice as ever, and that a patient’s supposed mental competence/ability to provide informed consent is often judged solely on the basis of the patient’s willingness to “adhere” to whatever lucrative treatment the doctor prescribes (take for example the strange case of Paul Henri Thomas, who was competent as long as he said “yes” to expensive ECT treatments, but was immediately “incompetent” upon refusing treatment).

What’s more, from the NASMHPD’s above use of the terms “regimen” and “side effects,” it’s clear they’re mainly talking abouttreatment centered on medication.

So in an almost incomprehensibly illogical turn of events, the NASMHPD first acknowledges that psychotropics and polypharmacy are causative factors for the increased mortality rate of the seriously mentally ill population, and then strongly emphasizes in the policy recommendations section the importance of compliance with/adherence to medication regimes!

What’s the big deal?

Ok. So the NASMHPD put out a lousy report in 2006 that, while acknowledging the mortality rate for the mentally ill population, failed to make good policy recommendations addressing its own listed causative/risk factors… so what?

What it boils down to is there’s a reason this statistic is quoted so often (a reason apart from its shocking nature).  The NASMHPD report forms the very foundation of some of the most important nationwide “official” mental health initiatives — and what I mean by that are SAMHSA [Substance Abuse and Mental Health Services Administration] and DHHS-funded [Department of Health and Human Services] initiatives.  These initiatives are meant to address the issue of mortality of the seriously mentally ill population; but they’re also taking their cues from the fatally flawed “Policy Recommendations” section… and that’s not a good thing.  In fact, it’s the most self-defeating setup imaginable.

[to make comments, visit the original post here]

Off-label marketing: the competition for “biggest corporate fine” gets juicy

It is so important to admit when you’re wrong.  So here goes…

When I wrote that Astra-Zeneca paid the biggest corporate fine in American history ($520 million) for the off-label marketing of Seroquel, an atypical antipsychotic [I wrote that here]; I was wrong.

(NOTE: off-label marketing is the promotion of a drug – whether amongst patients, doctors, or other professionals – for uses that are not FDA-approved)


In early 2009, Eli Lilly paid an even bigger corporate fine — $1.4 billion — for the illegal off-label marketing of its star atypical antipsychotic, Zyprexa.  Off-label marketing is quite the trend these days; fines since 2004 total over $7 billion (and growing), yet pharmaceutical companies continue the practice unabated.

This chart contains a list of some of the worst offenders of recent years.  Note the surprising number of drugs with applications in the mental health field (both on- and off- label).  Actually, if you were to include the number of drugs which address psychosomatic symptoms of PTSD like auto-immune responses, fibromyalgia, and Irritable Bowel Syndrome, mental health drugs would be in the majority.

There’s an unwritten business plan.  They [pharmaceutical companies] are drivers that knowingly speed.  If stopped, they pay the fine, and then they do it again.

(Lon Schneider, University of Souther California professor and off-label marketing researcher)

This aptly titled Washington Post piece, “When drug makers’ profits outweigh penalties,” explores the issue in a bit more depth — essentially the fines amount to only a fraction of pharma’s profits, and seem to be operating more as bribes than fines.  I guess if you’re powerful enough, it pays to misbehave.  Never mind that others are paying with their lives.

[to make comment, visit the original post here]

FDA safety alert — Antipsychotic drugs: Treatment During Pregnancy and Potential Risk to Newborns


From the FDA Safety  Alert site

Including Haldol, FazaClo, Fanapt, Clozaril, Risperdal, Zyprexa, Seroquel, Abilify, Geodon, Invega, Loxitane, Moban, Navane, Orap, Saphris, Stelazine, Thorazine, Symbyax
[Posted 02/22/2011]


ISSUE: FDA notified healthcare professionals that the Pregnancy section of drug labels for the entire class of antipsychotic drugs has been updated. The new drug labels now contain more and consistent information about the potential risk for abnormal muscle movements (extrapyramidal signs or EPS) and withdrawal symptoms in newborns whose mothers were treated with these drugs during the third trimester of pregnancy.

The symptoms of EPS and withdrawal in newborns may include agitation, abnormally increased or decreased muscle tone, tremor, sleepiness, severe difficulty breathing, and difficulty in feeding. In some newborns, the symptoms subside within hours or days and do not require specific treatment; other newborns may require longer hospital stays.

BACKGROUND: Antipsychotic drugs are used to treat symptoms of psychiatric disorders such as schizophrenia and bipolar disorder.

RECOMMENDATION: Healthcare professionals should be aware of the effects of antipsychotic medications on newborns when the medications are used during pregnancy. Patients should not stop taking these medications if they become pregnant without talking to their healthcare professional, as abruptly stopping antipsychotic medications can cause significant complications for treatment.

Healthcare professionals and patients are encouraged to report adverse events or side effects related to the use of these products to the FDA’s MedWatch Safety Information and Adverse Event Reporting Program:

  • Complete and submit the report Online: www.fda.gov/MedWatch/report.htm
  • Download form or call 1-800-332-1088 to request a reporting form, then complete and return to the address on the pre-addressed form, or submit by fax to 1-800-FDA-0178

Antipsychotic drugs, thyroid, and cardiac death — by Grace Jackson MD

Grace Jackson MD has written two of the most important critical books on psychiatric drugs, Drug-Induced Dementia: a perfect crime and Rethinking Psychiatric Drugs: A Guide for Informed Consent. You can read posts about these books here and here.

I’m in an email group with Grace Jackson. She answered a question in the group about neuroleptics and the ways they can lead to premature death with an emphasis on thyroid function. I asked her if I could publish her response. She graciously added references to the piece so that now there is a reading list at the end.

Reply to question about antipsychotic drugs, thyroid, and cardiac death:

There are many mechanisms through which antipsychotic drugs cause or contribute to premature death.  Thyroid hormone excess or deficiency would be only one potential mechanism.

When physicians speak of the “endocrine” system, they generally think about the HPA axis =   hypothalamus, pituitary (gland), adrenal (glands).

The word endocrine means “inside secretion”   >>  The organs of the body which are part of the “endocrine” system release chemical mediators that travel into the bloodstream until they hit receptors / targets in other parts of the body.

Dopamine is made by many cells of the body, and is not generally considered to be an  endocrine hormone (endocrine chemical that exerts effects at a distance).  Under normal metabolic conditions, dopamine suppresses the pituitary [specifically, the anterior pituitary] gland’s production and release of prolactin.   When dopamine levels fall, the anterior pituitary is “released” from inhibition >> hence, prolactin levels climb.   This is why many antipsychotic drugs cause gynecomastia (breast enlargement), lactation (milk production and secretion), and infertility.   High levels of prolactin have also been linked to osteoporosis and cardiac disease, and == in some studies — to breast cancer.  There are a few published studies which demonstrate a correlation between abnormally high levels of prolactin and autoantibodies against the thyroid.

As far as I know, there has never been a finding of dopamine receptors on the thyrotrophs of the anterior pituitary gland  (the ant. pit cells that make TSH).  However, studies in animals and humans have demonstrated mixed findings with respect to DOPAMINE and thyroid hormone balance  — several studies of dopamine agonists (such as bromocriptine) have demonstrated a suppressive effect on TSH secretion, but studies of dopamine antagonists have not always found an effect on TSH  or other thyroid-related hormones.     There have been few studies in antipsychotic-recipients that have tracked TRH, TSH, T4, T3, and autoantibody levels.

There is evidence in the published medical literature which supports causal links between many psychiatric drugs and thyroid hormone disruption:  most notably, SSRIs, TCAs (tricyclic antidepressants), lithium, and Seroquel >> all of which are linked to hypothyroidism;  however, some lithium patients have experienced hyperthyroidism.

As for neuroskeletal biology, this is a fairly “young” science —-  high levels of prolactin promote bone demineralization and bone thinning.   Stimulant drugs appear to affect bone morphogenetic proteins  (BMPs) >> ultimately, the stimulant effects on BMPs may represent a joint mechanism through which the drugs stunt bone growth (and brain development).  I have written about this in Drug-Induced Dementia.

Serotonergic drugs (SSRIs, some of the antihistamines, and TCAs) also inhibit bone growth and bone remodelling due to effects of serotonin on bone cells.  Anticonvulsants also accelerate bone density loss.

As for the cardiac toxicity of antipsychotic (and other) drugs, there is no one pathway. To my knowledge, there is no proven link between antipsychotic-induced changes in thyroid hormone metabolism and cardiac death.

Nevertheless, most of the dopamine antagonists appear to be cardiotoxic.  Some of this may be related to Drug Induced PPL (phospholipidosis) >> a phenomenon which results, literally, in cell digestion of the cardiac muscle tissue via autophagy.   Some of the damage may be caused by inflammatory changes (myocarditis, often due to eosinophilia).  Some of the damage may also be caused by hypoxia/ischemia >> starving the heart tissue of oxygen [i.e., high prolactin can contribute to platelet clumping > risk of clots or arterial narrowing;  hyperprolactinemia has also been found to promote blood vessel constriction, via B-adrenergic receptors and nitric oxide changes; in lab studies, prolactin has also been linked to smooth muscle cell proliferation in vascular cells].   Some of the damage may also be mediated by prolactin-related heart enlargement (cardiomegaly) >> the putative mechanism:   prolactin induced growth-hormone like effect on heart.

Several animal studies have demonstrated the cardiotoxic effects of antipsychotic drugs

For example:

Saito et al (1985  Heart Vessels Suppl) >> these investigators exposed 6 male Wistar rats to daily injections of thorazine for 30 days >> 30% of the animals experienced thickening of blood vessels (arterioles); all of the animals experienced damage to cardiac muscle fibers (fragmentation, swelling, fibrotic scarring).

Belhani et al (2006  Experimental and toxicologic pathology) >> these investigators exposed male and female New Zealand white rabbits to IM (intramuscular) injections of neuroleptics for 3 months:  drugs used included saline (control group), amisulpride, haloperidol, risperidone, olanzapine, levomepromazine,  and  two kinds of combinations. All of the antipsychotic drugs — all of them — resulted in cardiac lesions (damage) of variable magnitude.  Changes included disorganized fibers, myolysis (muscle disintegration), cell death (necrosis), and scar tissue (fibrosis).   Based on their discoveries, the authors recommended that all human patients receive an EKG and cardiac ultrasound (echocardiogram) PRIOR to beginning any antipsychotic drug therapy

It is important to remember that “NEUROGENIC” (brain-induced)  sudden death
remains a largely unexplored and undiscussed problem in dementia  and  in drug-induced dementia.  Although neurologists have finally started to ask the question:   how do anticonvulsants affect the process of  SUDEP    [sudden death in epilepsy]  >>  focusing upon brain-mediated  interruptions in signals to the heart and lungs  >>>>>
you will not find any psychiatrists  or neurologists asking this question about antipsychotic drugs.

Regrettably, every time I am interviewed by journalists about  “premature death” in patients who take antipsychotic drugs ,  I  mention BRAIN MEDIATED  DEATH. The journalists never include my comments, apparently because they cannot grasp the concept  that the brain  controls the  heart and the lungs  …………. [of course, cardiologists and pulmonologists want neurologists to believe that the heart and lungs control the brain ]……..

hope this information is helpful to you —–  I’ll post a few references for those who would like to read more.


Selected Readings:

Belhani, D. et al (2006). “Cardiac lesions induced by neuroleptic drugs in the rabbit,” Experimental and Toxicologic Pathology 57:207-212.

Curtarelli, G. and Ferrari, C. (1979). “Cardiomegaly and heart failure in a patient with prolactin-secreting pituitary tumor.” Thorax 34:328-331.

Emiliano, ABF and Fudge, JL (2004). “From Galactorrhea to Osteopenia: Rethinking Serotonin-Prolactin Interactions.” Neuropsychopharmacology 29:833-846.

Fineschi, V. et al (2004). “Sudden cardiac death due to hypersensitivity myocarditis during clozapine treatment.” International Journal of Legal Medicine 118(5):307-309.

Frassati, D. et al (2004). “Hidden cardiac lesions and psychotropic drugs as a possible cause of sudden death in psychiatric patients: a report of 14 cases and review of the literature.” Canadian Journal of Psychiatry 49(2):100-105.

Gitlin, M. et al (2004). “Peripheral thyroid hormones and response to selective serotonin reuptake inhibitors.” Journal of Psychiatry and Neuroscience 29 (5):383-386.

Kelly, DL et al (2008). “Cardiac-related findings at autopsy in people with severe mental illness treated with clozapine or risperidone.” Schizophrenia Research 107:134-138.

Livingston, C and Rampes, H (2006). “Lithium: a review of its metabolic adverse effects.” Journal of Psychopharmacology 20:347-355.

Molinari, C. et al (2007). “Prolactin induces regional vasoconstriction through the beta2-adrenergic and nitric oxide mechanisms.” Endocrinology 148(8):4080-4090.

Saito, K. et al (1985). “Chlorpromazine-induced cardiomyopathy in rats,” Heart Vessels Suppl 1:283-285.

Sauro, MD and Zorn, NE (1991). “Prolactin induces proliferation of vascular smooth muscle cells through a protein kinase C dependent mechanism.” Journal of Cell Physiology 148 (1):133-138.

Wallaschofski, H. et al (2008). “PRL as a Novel Potent Cofactor for Platelet Aggregation.” Journal of Clinical Endocrinology and Metabolism 86 (12):5912-5919.

Witchel, HJ et al (2003). “Psychotropic drugs, cardiac arrhythmia, and sudden death.” Journal of clinical Psychopharmacology 23(1):58-77.

No mental health without physical health (from the Lancet)

Just sharing the fact that the gross degradation that this class of psychiatric drug causes is being talked about in the Lancet. Granted they still make the assumption that these drugs are “necessary” much more often than they are. The fact that the dialog is happening though is good if also long overdue.

A snippet from the article in the Lancet:

No mental health without physical health

Figures published by the Archives of General Psychiatry on Feb 7 will be of deep concern to every mental health practitioner. In their systematic review of early cardiometabolic outcomes, Debra Foley and Katherine Morley set out the dramatic effects of antipsychotics on the physical health of those taking them for the first time. The authors record, for example, that “the average weight gain after 6 to 8 weeks taking olanzapine was 5 to 6 kg”, and that “at 8 weeks, there was a significant increase in insulin level, insulin resistance, and glucose, cholesterol, triglyceride, and C peptide levels across clozapine, olanzapine, risperidone and sulpiride combined but no significant difference between drugs”.

In any other scenario, the responsible physician’s response would be to seek an alternative. However, for mental health professionals, the mainstay of treatment for psychotic illness is—as it has been for over half a century—antipsychotic medication. read the rest (emphasis mine)

Antipsychotics increase risk of heart disease

This fact is of course obvious if one stops and thinks about the fact that antipsychotics, more appropriately called, neuroleptics (since they’re used for all sorts of things and often do not stop psychosis), cause metabolic syndrome in a very large number of users.

The fact that the drugs cause diabetes and obesity is widely known. So since diabetes and obesity often cause heart disease this is of course not surprising and is well known among those of us that look at the risks these drugs pose on a regular basis. The fact that it’s being reported explicitly in the mainstream media though, is a first.

Also known by underreported is that people on these drugs have a life-span of up to 25 years less then the rest of the population. This article refers to that as well.

Antipsychotic medications, which have raised red flags in the past, may increase the risk of heart disease in as little as a few months, a new study says.

Among the people taking these drugs are patients with schizophrenia, who tend to have shorter-than-average life spans. So the role of antipsychotics in heart disease needs to be addressed, said co-author Debra Foley, senior lecturer at the Center for Youth Mental Health at the University of Melbourne in Australia.

Researchers have already reported that newer antipsychotics are associated with an increased risk of diabetes. The Food and Drug Administration put out warnings on this danger in 2004.

According to the new study, published in the Archives of General Psychiatry, patients taking antipsychotics tended to gain weight after one month and had increases in their cholesterol levels after three to four months.

Obesity, high cholesterol, and diabetes all increase the risk of heart disease.

“This change in risk is evident early in the course of treatment, within several weeks of continuous use, but may continue to alter over several years,” Foley told Reuters Health in an email. The “risk varies depending on the specific drug taken and how long it is taken for,” she added.

About one in 100 adults in the U.S. has schizophrenia, according to the National Institute of Mental Health.

But antipsychotic drugs are also given to some patients with bipolar disorder, personality disorders, or anxiety, said Dr. Karen Graham, assistant professor of psychiatry at the University of North Carolina School of Medicine. She was not involved in the study. read the rest here

Antipsychotics often cause chronicity/long-term disability

Robert Whitaker has a page on his website that puts an entire history of the damning evidence of neuroleptics together on one page. This is only one class of psychotropic. Similar sorts of aggravating results can be found with the other classes of psychiatric drugs as well. Below is the introduction to the page. What follows is an arsenal of information that should give pause to anyone considering the use of these drugs for themselves or for their loved ones. What may be appropriate for a crisis may not in any way be appropriate for long term maintenance care. We see too in these studies that people do indeed recover, but much more frequently when they can be drug free.

The long-term outcomes literature for antipsychotics, which has been compiled over a period of nearly 50 years, consistently tells of drugs that increase the likelihood that a person diagnosed with schizophrenia will become chronically ill.

A. The Chronicity Problem Becomes Apparent (1960s-1970s)

It seems paradoxical that drugs that ameliorate acute psychotic symptoms over the short term will increase the likelihood that a person so treated will fare poorly over the long term. But that disturbing fact showed up in the very first outcome studies, and has continued to show up ever since. take a look at the extensive list of studies with links here

A couple of days ago Whitaker covered the news about antipsychotics causing the brain to shrink as well on his blog at Psychology Today.

For extensive interpretation of these studies as well as a look at real people in case studies buy and read Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs, and the Astonishing Rise of Mental Illness in America

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