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A willfully maintained ignorance of the reality of antipsychotic withdrawal syndrome 10/22/2012

Posted by ALT in Mental Health Research, Pharmaceuticals, Psychosis.
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9 comments

SCIENCE. (Read that with a deep, booming, authoritative voice)

SCIENCE has achieved an exalted level of infallibility in our society. Start a sentence with “researchers say…” and you’ll not be questioned.  We mortals can only look to our pantheon of data collectors with wonder and awe. We dare not question their pronouncements, percentages.

“Blessed are the 64.3% of all statistics that are made up on the spot, for they shall make your argument mighty.”

Here’s the thing about SCIENCE as a new religion: the way it’s framed, there’s no faith involved. You’re not asked to believe anything. Instead, you’re given data, objective facts, supposedly THE TRUTH as derived through the scientific process. Either you accept the truth, or you deny it. But you can’t argue with it; the facts don’t lie, do they?

The Facts Don’t Lie; Researchers Do

Lie.  That’s an inflammatory word, not to be used lightly. It means willful deceit.

But what do we call deceit achieved by willfully maintained ignorance? Is that a lie?

Whatever it’s called, that’s what I witnessed time and time again during my employment with the Research Scientists of Children’s Mental Health: careful avoidance of any idea that challenged their painfully constructed, government-funded, biopsychiatric house of cards. And it’s what I saw this morning, staring up at me from a press release about a new study in the New England Journal of Medicine.

HEADLINE: Some with Alzheimer’s better off staying on antipsychotics (study)

Essentially, the study found that abrupt discontinuation of Risperdal doubled the risk of “relapse” (defined as a return of psychotic/aggressive symptoms), when compared to continuation of Risperdal. In the “Conclusions” section, the authors write:

In patients with Alzheimer’s disease who had psychosis or agitation that had responded to risperidone therapy for 4 to 8 months, discontinuation of risperidone was associated with an increased risk of relapse.

Sounds like they just demonstrated that going off antipsychotics can lead to withdrawal symptoms. 

But here’s how principal investigator Dr. D.P.Devanand, who currently has disclosed financial ties to Janssen (makers of Risperdal), Novartis, and Eli Lilly (makers of Zyprexa), interpreted this data:

Caregivers should be aware of the increased mortality associated with these medications in people with dementia… [However] if a patient is taking an antipsychotic and doing reasonably well without any major side effects, they should stay on it.

- D.P. Devanand, principal investigator

Caregivers SHOULD be aware of the increased mortality associated with antipsychotics and dementia patients.  A black box warning issued by the FDA for antipsychotics risperidone, olanzapine, and aripirazole reads (in part) “Elderly patients with dementia-related psychosis treated with atypical antipsychotic drugs are at an increased risk of death compared to placebo… These drugs are not approved for the treatment of patients with dementia-related psychosis.”

Caregivers should ALSO be aware of a long and scandalously illegal history of off-label promotion of these drugs to treat dementia when they were not and are not approved for this purpose. Fines for dementia-related off-label marketing prosecuted under the False Claims Act alone have totaled almost $2 billion. And who can forget Lilly’s clever sales pitch for the use of Zyprexa in nursing homes, “5 at 5”?

Lilly even devised a LTC sales slogan used nationwide – ‘5 at 5 pm,’ which was shorthand for dosing elderly [nursing home] patients with 5 milligrams of Zyprexa at 5 pm to keep patients calm throughout the night… It’s particularly disturbing that such a potent drug, with so many serious adverse side effects, was so blatantly abused in a vulnerable patient population whose health is already at risk. [A]t many nursing homes this potent antipsychotic was essentially used as a ‘chemical restraint’ for the elderly for whom Zyprexa had no other health benefit.

-Brian Kenney, attorney for the plaintiffs in Zyprexa whistleblower suit resulting in a $1.415 billion fine for off-label marketing

 ONE MORE THING caregivers should be aware of that Devanand et al. neglected to mention:

Antipsychotic Discontinuation Syndrome (IE, withdrawal)

When a person whose brain is accustomed to the presence of an antipsychotic agent abruptly stops ingesting that agent, discontinuation syndrome (withdrawal) is a very likely result. The brain attempts to maintain normal dopaminergic function in the presence of a dopamine-suppressing chemical (antipsychotic) – it does this by significantly enhancing dopaminergic activity.  When the chemical is removed from the equation, there is no longer a counterbalance for the dopamine-enhancing adjustment built up over time in the brain. This is the probable cause of antipsychotic withdrawal symptoms, which can include both psychosis and aggression.

Even in the case of gradual discontinuation of the drug, withdrawal may occur – but take it away abruptly, and you’re essentially guaranteed a display of withdrawal symptoms in a significant portion of the study population.

So Devanand’s study really isn’t all that newsworthy. His data plainly shows that stopping the use of antipsychotics can cause a withdrawal reaction, which is what the FDA-approved label essentially already says – “To prevent serious side effects [read: withdrawal], do not stop taking ZYPREXA suddenly.” And a 2006 literature review summing up many antipsychotic discontinuation studies shows the same thing:

There is evidence to suggest that the process of discontinuation of some antipsychotic drugs may precipitate the new onset or relapse of psychotic episodes. Whereas psychotic deterioration following withdrawal of antipsychotic drugs has traditionally been taken as evidence of the chronicity of the underlying condition, this evidence suggests that some recurrent episodes of psychosis may be iatrogenic.

- Joanna Moncrieff, in “Does antipsychotic withdrawal provoke psychosis? Review of the literature on rapid onset psychosis (supersensitivity psychosis) and withdrawal-related relapse

Here’s the ground-breaking bit: Devanand and co-authors chose not to describe what they observed during the course of the study as “withdrawal” – that word is studiously avoided in the press release and abstract.* Rather, here’s how the results are characterized: the risk of “relapse” should antipsychotic medication be abruptly discontinued is evidence of the need for elderly patients to keep taking their Risperdal.

A classic case of willfully maintained ignorance.

Is it possible that Devanand and co-authors are ignorant of the concept of “withdrawal,” its causes, its symptomatology? Is it possible that they haven’t read the FDA-approved label for Risperdal, haven’t familiarized themselves with the scientific literature surrounding the discontinuation of antipsychotics, and are therefore innocent in their public charactarization of the results of their study as “relapse” best treated with continued use of Risperdal? Yes, it’s possible. It’s even likely that these authors averted their eyes from a mere glimpse of any such information, given the strong financial incentives and conflicts of interest disclosed in conjunction with the publication of this article.

But that’s a shaky foundation to build your innocence on.

The foolish man builds his house upon the sand; the wise man builds his house upon a rock. 

   


* I’d like to tell you the word “withdrawal” is entirely absent from the article itself (and I highly suspect it is!) but, even though this is a publicly funded National Institutes of Health study, the article is not freely available to the funders (we, the people) and I have been thwarted in my attempts to obtain it. Big bonus points if you send it to me.

Letter to the Editor: The “seriously mentally ill” are NOT dying 25 years earlier because of failure to seek/receive treatment 10/09/2012

Posted by ALT in Mental Health Awareness, Mental Health Research.
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7 comments

From: ALT
To: Online Editors, Amarillo Globe-News
Subject: Letter to the Editor concerning article “NAMI observes mental illness awareness week

To the editor:

I would like to inform you of a factual error in a recent article, “NAMI observes mental illness awareness week.”  You published the following statement:

“On average, people living with serious mental illness live 25 years less than the rest of the population. One reason is that less than one-third of adults and less than half of children with a diagnosed illness receive treatment.”

The source of the statistic cited in the first sentence is the NASMHPD [National Association of State Mental Health Program Directors] 2006 report entitled “Morbidity and Mortality in People with Serious Mental Illness.” This report lists multiple causes for increased mortality in the seriously mentally ill population.  Suicide is responsible for about 30% of premature deaths, but 60% are attributable to other causes: smoking, obesity/diabetes, alcohol and substance use, infectious diseases, the long-term use of psychotropic medications, and polypharmacy (the concurrent use of multiple psychotropic medications). Note that failure to access treatment for mental health issues is not listed as a causative factor.

The report makes clear that the use of psychotropic medications (especially atypical antipsychotic medications like Risperdal, Zyprexa, Seroquel, etc.) is causally linked to several of the most common causes of premature death amongst this population: cardiovascular disease, obesity and Type II diabetes.

On page 22: “the second generation antipsychotic medications have become more highly associated with weight gain, diabetes, dyslipidemia, insulin resistance and the metabolic syndrome.”

And on page 17: “Psychotropic medications … contribute to symptoms of medical illness and cause metabolic syndrome” and “Polypharmacy [is] identified as a risk factor for sudden death.

You will find that FDA-approved labels for these drugs (atypical antipsychotics) entered in the Physician’s Desk Reference list cardiovascular disease, diabetes, and weight gain as possible side effects. These adverse events are also very well substantiated both in the scientific literature and legally, through the courts.  As one example, Eli Lilly has settled about 30,000 personal injury lawsuits for almost $1.2 billion for failure to adequately inform doctors and the public about the known risk of developing diabetes and obesity when using Zyprexa.

Therefore, your statement that “one reason [for higher mortality rates] is that less than one-third of adults and less than half of children with a diagnosed illness receive treatment” is inconsistent with the source of the statistic it purports to explain. More fundamentally, it is factually incorrect.

Individuals from this population are dying from diseases whose onset was often a “side effect” of the antipsychotic medications they were prescribed, diseases that developed because they received medical treatment.

Please consider publishing a correction at your earliest convenience as an error of this kind is truly a matter of life and death.

Yours sincerely,

Alice Tremont
Mental health activist and writer
http://altmentalities.wordpress.com

CC: Patty Robertson and Angela Ellis, contacts for NAMI Texas Panhandle

***

More on that oft-quoted (and mis-quoted!) statistic here:

Also worth reading (in connection to “Mental Illness Awareness Week”) — David Oaks’ essay “Let’s stop saying mental illness!

How to INCREASE stigma in mental health — fight stigma the conventional way 09/10/2012

Posted by ALT in Bipolar, Depression, Mental Health Awareness, Mental Health Research.
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11 comments

Mental illness is a biological disease like any other… Schizophrenia is just like diabetes!

It is the mantra of mainstream psychiatry.

And the typical justification presented for the continued repetition of this mantra (despite its being patently false, both from a subjective and objective point of view) is the theory that characterizing “mental illness” as a brain disease reduces stigma.  The general public won’t blame afflicted individuals once they realize that it’s just a matter of faulty chemicals, a somewhat defective brain.  They won’t fear the disease if they believe that lifelong, routine injections of a necessary but missing chemical (like an insulin shot!) will solve the problem.

Here’s an example of the mantra (and its accompanying justification) in action, from Glen Close’s highly publicized “Bring Change 2 Mind” campaign to decrease the stigma of mental illnesses:

LEARN THE FACTS

One of the best ways you can help someone with mental illness is by understanding what it is – and what it isn’t.  After all, myths about mental illnesses contribute to stigma…

The fact is, a mental illness is a disorder of the brain – your body’s most important organ – and 1 in 6 adults lives with a brain-related illness including depression, bipolar disorder, PTSD and schizophrenia… And just as with most diseases, mental illnesses are no one’s fault.

- from the “Bring Change 2 Mind” website*

This organization has a celebrity spokesperson and billboards (!)

… so they must know what they’re talking about, right?

LEARN THE ACTUAL FACTS

FACT 1:  So-called mental illnesses (let’s call them “subjective experiences of mental and emotional distress”) CANNOT be reduced down to mere imbalances in brain chemicals. 

First of all, there’s NO KNOWN WAY to measure the balance of chemicals in someone’s brain.  No method of establishing what a so-called “normal” balance of chemicals would be.  Even if there WERE a method for measuring this, there’d be no reason to assume that this would somehow be universal across people of disparate genetic, biological, cultural, emotional, environmental backgrounds – which mainstream psychiatry seems bent on doing.

Second, numerous (far too numerous to list here!) studies show that a variety of factors besides “biological” ones – ie, the introduction of new chemicals, in the form of pharmaceuticals, into someone’s body – have a profound effect on the resolution of mental and emotional distress.  To list one simple example, outcomes for first-episode psychosis (typically leading to a diagnosis of “schizophrenia”) are very different in industrialized societies and non-industrialized societies, because the standard of care is different: industrialized societies emphasize medication as first-line and perhaps the only treatment, while non-industrialized societies emphasize social support and integration into the community combined with little or (more often) no medication.  Here’s another great article that goes through a few more examples of how culturally specific mental and emotional distress (and our reactions to it!) can be.

FACT 2:  The disease model explanation for so-called “mental illness” actually INCREASES STIGMA, while a psychosocial model explanation slightly DECREASES it.

That’s right, folks: the disease model, describing mental and emotional distress as mere chemical imbalances of the brain, is not only false – spreading that falsehood markedly increases stigma!  So when mainstream psychiatry claims it may need to tell a “white lie” about all this for the patients’ own good (reduce stigma, get folks to take their meds, etc.) they’re wrong again.

In 1997, Sheila Mehta of Auburn University conducted a simple experiment to test the stigma produced by a disease-based explanation of so-called “mental illness” and a psychosocial one.  55 male college students were enrolled in an experiment.  Each one was told that he and a partner would have to do a simple learning task – but the partner was actually a confederate in the study.  The confederate would disclose a mental illness to the subject, and then explain either that he had this illness because of “the kind of things that happened to me when I was a kid” [psychosocial] or that he had “a disease just like any other, which affected my biochemistry” [biochemical].

It turned out the group presented with the biochemical explanation were far more likely to treat their partners harshly than the group presented with the psychosocial one.  Says Mehta, “The results of the current study suggest that we may actually treat people more harshly when their problem is described in disease terms.  We say we are being kind, but our actions suggest otherwise… Viewing those with mental disorders as diseased sets them apart and may lead to our perceiving them as physically distinct. Biochemical aberrations make them almost a different species.”

[Mehta, S. (1997).  Is being “sick” really better?  Effects of disease view of mental disorder on stigmaJournal of Social and Clinical Psychology, 16(4), 405-419.]

Later studies (like this one involving over 450 people in New Zealand) have replicated Mehta’s results and agreed with her conclusion.  What’s that mean? 

It’s actually SCIENTIFICALLY SOUND

unlike the disease-based “biochemical imbalance of the brain” theory, which has still not been proven true, in part or in whole, despite over 40 years of extremely well-funded studies directed towards that very specific purpose.

We do not know the causes [of any mental illness]. We don’t have the methods of ‘curing’ these illnesses yet.  

-Dr. Rex Cowdry, psychiatrist and director of National Institute of Mental Health (NIMH), 1995

[While] there has been no shortage of alleged biochemical explanations for psychiatric conditions…not one has been proven. Quite the contrary. In every instance where such an imbalance was thought to have been found, it was later proven false.

 -Dr. Joseph Glenmullen, Harvard Medical School psychiatrist

    

  

  


[today's dose of sarcasm will be footnoted]

*A few other goodies from the “Bring Change 2 Mind” website

An image of Glen Close and her BIPOLAR sister. 

See the difference – one person is NORMAL, and the other is BRAIN-DISEASED.  It says it on their shirts!  (Not stigmatizing at all…)   And for the mere price of $20 a pop you, too, can wear an anti-stigma shirt with your diagnosis printed clearly across the front, labeling you. 

Anyone? Anyone at all want to fight stigma by labeling and stigmatizing yourself?

I think this is a far better way to fight stigma — rip those labels up!

Beautiful lady and old hag at play on Bipolar Awareness Day! 06/27/2012

Posted by ALT in Bipolar, Depression, Mental Health Research, Pharmaceuticals.
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3 comments

Two studies with nearly identical data yield very different conclusions.  Beautiful lady or old hag?  Both collected data showing that individuals initially receiving a diagnosis of “depression” and treatment with antidepressants convert to “bipolar” diagnoses at an impressively high rate.

But the survey released today (in honor of the UK’s “National Bipolar Awareness Day”) by Bipolar UK portrays the data on conversion as evidence of misdiagnosis and the need for better awareness of bipolar disorder by mental health professionals, while this study from 2004 attributes conversion, not to misdiagnosis, but largely to antidepressants’ tendency to cause mania (it is a PDR-listed side effect, after all).

Is the rise of bipolar diagnoses in the US (a 56% increase in adults between 1996 and 2004) and Western Europe a largely iatrogenic phenomenon?

I decided to write Bipolar UK to ask them their thoughts on the matter.

***

From: ALT
To: the folks at Bipolar UK
Subject:  Enquiry Related to “Challenges to Diagnosis” Survey

Hello,

First, let me wish you a happy National Bipolar Awareness Day!

I read the executive summary of your recent survey of individuals diagnosed as “bipolar” with great interest.  I was particularly struck by two statistics you presented:

- 85% of respondents were diagnosed with and treated for depression before being diagnosed as bipolar

- 71% of those receiving delayed diagnosis felt that their symptoms had been made worse by antidepressants or sleeping pills

Your data reminds me of a widely cited 2004 study in which 87,920 individuals initially diagnosed with depression were followed for 5 years.  4182 eventually received a diagnosis of bipolar (“converted”) during the course of the study, and 81% of them were being treated with antidepressants.  The authors state in their analysis that “the conversion rate amongst antidepressant-treated patients (7.7% per year) was 3-fold that amongst unexposed patients (2.5% per year).”  These findings are quite consistent with yours.

Your interpretation of this data seems to be that the timely diagnosis of bipolar disorder is an area that needs improvement amongst mental health professionals, who currently are misdiagnosing many bipolar individuals with depression.

However, I would like to suggest to you another interpretation, one that the previously cited study puts forward.  Its authors state that “It has long been known that antidepressant medications can precipitate mania in vulnerable individuals” and that “treatment with antidepressants is associated with … conversion hazards.”  “Mania/hypomania” are also listed in the Physician’s Desk Reference as effects of both SSRIs and tricyclic antidepressants.  The PDR entry on imipramine (the very first tricyclic antidepressant) explicitly states “Manic or hypomanic episodes may occur; consider decrease until episode is relieved.”

Is it possible that many of the respondents to your survey, and many of the individuals you serve – in short, people with “bipolar” diagnoses – are dealing with an entirely iatrogenic phenomenon? 

On this inaugural “Bipolar Awareness Day,” I think it is vital that we pursue awareness, not only of the diagnostic criteria, but also of the very real possibility of diagnostic inflation that is iatrogenic in nature.

I look forward to hearing your thoughts on this.

Yours truly,

Alice Tremont
Writer, mental health activist
http://altmentalities.wordpress.com

 

People in mental or emotional distress more likely to consult a pastor than a psychiatrist 06/25/2012

Posted by ALT in Mental Health Research, Philosophy/Spirituality.
Tags: , , , ,
3 comments

In recent posts (here and here), I’ve asked some questions about the spiritual content of the psychotic visionary process, and the general tendency of mainstream psychiatry to deny – at all costs – that spiritual content as being in any way valid or “real.”   Though the very language we use to describe our dealings with mental and emotional distress acknowledges its roots in the spiritual world (“psychiatrist” literally means “soul healer“), our society’s standard response is fundamentally clinical, biopsychiatric, and entirely secular.   

Put simply, we do not acknowledge the possibility of mental and emotional distress as spiritual suffering; we claim it is wholly biological in kind.  An imbalance of neurotransmitters maybe, or a genetic problem. 

Or maybe a cat virus? That would be E. Fuller Torrey’s theory on the cause of schizophrenia. No joke.

But is this how people experience such distress – as a biological problem requiring a chemical solution?

Here’s a statistic (and a partial answer to my quesiton): people going through mental and emotional distress are more likely to consult with a pastor or religious counselor than any other type of professional, and it is often the only type of professional help they seek (in one study, only 10% of people who sought help from a clergy member were referred on to a mental health professional).

What kind of response do they get?  I’m sure it varies widely – this study reported that responses were often positive, but about 1/3 of mentally distressed folks who sought help from the church got a negative reaction, “abandonment or lack of involvement” being the most common.** 

On the flip side, this recent news story profiles a number of ways that churches across the country have attempted to reach out to folks with mental and emotional problems.

Some are offering home-cooked meals, personal hygiene items, and clothing, others do day programs with self-directed art, gardening, and other activities, or just a space to experience peace and quiet; all provide a culture of listening without judgment, a strong sense of community, and prayer.  The focus is on faith, hope, and the possibility of healing.

The sense of community and the loving support are big reasons why people are interested in accessing the clergy and church for help.

 Faith helps. Faith helps greatly. And coming to the church where everybody knows me, acknowledges that you’re there—that helps.

- Ruth Reskey, psychiatric survivor who accesses the clergy regularly for help (quoted here)

Another contributing factor could be the lack of mental health training that the clergy has received – they’re not trained in the art of diagnosis, and consequently, the art of over-pathologizing and stigmatizing.

But most of all…

We conclude that those coming to the clergy for help in times of psychological distress are seeking religious rather than psychological counseling. Spiritual help appears to be what they want.

-  from this study, showing that 41% of participants turned to clergy first for mental health needs [emphasis added]

I say, give the people what they want!


*This does vary quite a lot across cultures, however here are three studies [from disparate cultural groups] showing this is true in El Paso, Texas amongst Caucasian and Latino populations, amongst African Americans, and in Northern England.

**Rossa Forbes also has some excellent posts on this topic at Holistic Recovery from Schizophrenia.  Check them out here and here.

Photo credits: infobarrel.com

DSM critique in the New England Journal of Medicine is not what it seems 05/21/2012

Posted by ALT in DSM-5, Mental Health Research.
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1 comment so far

I heard the rumors of a fight, and I came a-running. 

Fisticuffs, you say? I’m in!

This morning, I read [here] that the following inflammatory remarks were published in this week’s New England Journal of Medicine:

 … [Only when psychiatrists address] psychiatric disorders in the same way that internists address physical disorders, explaining the clinical manifestations … by the causal processes and generative mechanisms known to provoke them … will psychiatry come of age as a medical discipline and a field guide [the DSM – Diagnostic and Statistical Manual] cease to be its master work.

- Paul McHugh, MD and Phillp Slavney, MD in the NEJM [emphasis added]

Damn, that’s cold.  And did I mention it was published in the New England Journal of Medicine (!), which is “one of the world’s most prestigious medical journals… cited in scientific literature more frequently than any other biomedical journal”?  All kinds of doctors, clinicians, and practitioners read this thing!

A big deal.

Sounds like the authors are saying mental illness is fundamentally NOT like diabetes, that psychiatry as a discipline will continue to suffer from its immaturity and crippling inferiority complex (“we wanna be scientists, too!”) as long as diagnosis doesn’t rest on a firmly established foundation of physical pathology, and that the DSM is a poor substitute for that kind of a foundation.

Them’s fighting words.  Words that might make the NEJM readership think twice before handing out diagnoses and their accompanying pharmacological interventions like the proverbial candy.

Don’t believe every rumor you hear

Having matured a bit from my high school days of running directly to join the ring of kids chanting “fight, fight, fight!”, I decided to get a little context.  Who are these guys -– researchers? psychiatrists? some other kind of doctors? — and what does the rest of their NEJM editorial say?

“These guys” are two psychiatrists, professors at the Johns Hopkins School of Medicine.  Paul McHugh, the lead author, is a rather famous one.  He’s attended Harvard, designed a famous cognitive test often used as a dementia/Alzheimer’s diagnostic tool (a mere 11 questions!), served on the Presidential Council of Bioethics under GW and on a lay panel put together by the Catholic Church to look into the abuse of young boys by priests – none of these things being very high recommendations in my book.  The two, together, have written a popular paperback for the general public entitled The Perspectives of Psychiatry which takes the biopsychiatric/disease-based approach to mental health.

And their editorial?  It starts off very nicely with a critique of the DSM-delineated “field guide” method of diagnosis – the main problem being that clinicians no longer think too long or hard about causation.  This promotes a “rote-driven” method of treating folks, and as the authors so rightly state “identifying a disorder by its symptoms does not translate into understanding it.”  Or treating it effectively, if long-term studies of schizophrenia outcomes are any indication.

But things go sour real fast as we get to the “what’s to be done about it” part.  We simply must establish causation for psychiatric disorders, and – guess what?—the authors have already done that! 

The causes of psychiatric disorders derive from four interrelated but separable families: brain diseases, personality dimensions, motivated behaviors, and life encounters.

-McHugh et al.

Good, good.

They have also helpfully sorted out some common psychiatric disorders into the four families, or “causal perspectives”:

It’s written in a table so it MUST be true!

Right there, in the NEJM (remember – prestigious medical journal read by everybody), we’ve got schizophrenia neatly categorized as “brain disease.” 

Oh, dear.

I diagnose thee… Flipfloppers!

Contrast the NEJM editorial with the polite phrasing the authors used in the aforementioned co-authored The Perspectives of Psychiatry, chapter 6:

The continuing failure to identify a particular cerebral pathology or pathophysiology in these disorders [manic depression and schizophrenia] undermines attempts to proclaim them as diseases with complete confidence.  They remain mysteries in the sense that a confirmation of their essential nature is lacking…

- authors Paul McHugh, MD and Phillp Slavney, MD in The Perspectives of Psychiatry [emphasis added]

And yet they feel comfortable, only a few years after these words were published, with proclaiming schizophrenia as a “brain disease,” without providing any citations for new, groundbreaking research whatsoever.  Clearly this “DSM critique” is not what it seems.

Middle way protestors all the way

As it turns out, these guys are total middle way DSM protestors – the only thing they’d like to fight is the bad public image of the DSM, not the institution of psychiatric diagnoses masquerading as science, and all of the poor treatment that goes along with such posturing (symptom suppression via pharmaceuticals, coercive treatment, et al.).

According to McHugh and Slavney, “no replacement of the criterion-driven diagnoses of the DSM would be acceptable; clinicians are too accustomed to them.”  Rather, the only solution is for everyone [clinicians, researchers, families, patients] to embrace their causation groupings – and for that to be coded and billable, too, one can only presume.

In no other field would you continue to reach for an admittedly blunt, ineffective tool simply because it’s “what people are used to.”  Surely there are some other possiblities?

I believe that there is another way – instead of fitting people and their “symptoms” into predetermined boxes, we could communicate with each unique individual, offering our support and encouragement (help) when it’s wanted, and offering our respectful non-interventionism and acknowledgement of the humanity of the suffering individual when our “help” is neither helpful nor desired.

I believe there is life after the DSM – and I’d like, as a society and a community, to live it!

Reflections on time spent as a “researcher” in the field of children’s mental health 02/16/2012

Posted by ALT in "An Insider's Perspective", Children's Mental Health, Mental Health Research.
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3 comments

For two years, I worked full time in the field of children’s mental health program evaluation and research as a “Research Project Coordinator.” My boss, the “Principal Investigator,” and I had been contracted to implement a standardized, predetermined program evaluation of what is called a “system of care” — a program that coordinates and delivers services to children with mental health challenges.   The system of care had been set up with money from SAMHSA [Substance Abuse and Mental Health Services Administration], part of the Department of Health and Human Services. 

Any community that received funds from SAMHSA to start one of these “systems of care” – and there were over 144 of them! – had to agree to implement the full data collection protocol, which required in-depth multiple choice interviews be administered to about 250 families. Researchers were also expected to access extensive school records, court records, and medical records from the community mental health center.  Again, these research methods were implemented over and over, in every one of those 144 funded communities.

In short, the “Children’s Mental Health Initiative” (as SAMHSA calls it) is the largest standardized children’s mental health research project ever conducted.  The datasets collected by this massive undertaking  – nearly 20 years’ worth of data on tens of thousands of families – are owned by the government and managed by a contracted firm called ICF International, which, oddly enough, also has extensive contracts with the Departments of Defense and Homeland Security.  Go figure.

So that was the project, and I was its local coordinator.  I worked extensively with the regulatory agencies that protect human research subjects’ rights to get their approval for our proposed “research methods.”  I called potential participants and, following the script, assured them that being in the study was a chance for “their voice to be heard” and to “ensure that other children with challenges like their child’s could get services, too.”  I conducted interviews with mothers, grandmothers, uncles, and the children themselves (when they were old enough to be in the study).  I attended children’s mental health research conferences where we presented our data and listened to other communities present theirs’.  I attended numerous meetings in our designated area of evaluation (the community, we always called it), listening to social workers and other helping professionals talk endless circles around the project, its goals, its implementation, and something they called sustainability.

Sustainability inspired complicated emotions in these folks.  Each and every person employed by the system of care would lose his job in 5 years (that’s when the federal funding ran out), if the specter of sustainability was not made more substantial.

Now, a federally funded “system of care” is a real gravy train.  A community mental health center thus financed can easily employ twice as many, perhaps even three times as many, social workers and “helping professionals” as before.  Some people were literally paid to do nothing more than exist and lend the program more credibility by their impressive titles; the “Technical Assistance Coordinator” and “Social Marketing Associate” come to mind.  And then there were the fantastic perks: free trips to “conferences” at lovely resort destinations (how’s Tampa in late February/early March sound?), fancy business lunches provided on a near weekly basis (they call it “community engagement”), and, best of all, business cards that say you’re making a difference in children’s lives – a real boost to the self-esteem, which is priceless, isn’t it?  

Most of the staff seemed to know that they couldn’t keep riding the gravy train forever, but the burning question – would they even have jobs in 5 years? – had to be answered.  So sustainability was a real presence in those meetings, a creditor who couldn’t be evaded forever, or a god that must be appeased. 

But what’s the one thing that nobody – not even the gods – can question?  SCIENCE.  It’s objective.  It’s proven.  It’s Fact.  Science as published in peer-reviewed, “scholarly” articles, as glossily summarized in abstracts and press releases, as cited by thousands who have never read the research in its entirety.  If you choose to discount it, then you’re an irrational being, not worthy of consideration.

So science, in the form of program evaluation, was the answer to the sustainability question.  The system of care needed research that “proved” it was “effective,” that justified its continued existence, and that generated visually stimulating graphs with lines that went up (it really was that simple).  With their irrefutable SCIENCE in hand, they would apply for new grants, secure renewed funding, and keep the gravy train chugging along.  This was not just the local solution to the sustainability problem – it was national and it was built right into the Children’s Mental Health Initiative by SAMHSA from the very beginning. 

This, by the way, is a classic example of a synthetic Hegelian dialectic put in place by an institution to achieve its pre-determined goals with a semblance of grassroots mobilization; otherwise known as the “problem-reaction-solution” paradigm.  In this case, it went something like this:

  • Problem: in 5 years you won’t have a job
  • Reaction: I can’t miss a mortgage payment! What do I do?
  • Solution: justify the continued existence of your job by participating in and encouraging a truly massive data collection initiative, the depths and true purpose of which you know nothing about, an undertaking that under different circumstances you might question critically…

It hits home at a very personal level.  The threat of losing your job is literally a threat to your survival (and in the case of most of these employees, a threat to the survival of their children).  Animal — and maternal — instincts are activated, and critical thinking is no longer a part of the equation.

A critical thinker would question the protocol that SAMHSA gave us.  Is it appropriate to ask a parent to “list 5 things you don’t like about your child,” or “True or False: I turned out to be a worse parent than I thought,” (as we did in every interview)?  Is this “data” of any scientific value whatsoever?  Why must the protocol as a whole be so incredibly negative, pathologizing, and stigmatizing?  What is all this data really for, and what is the true purpose of the data collection exercise?

Such questions were taboo.  If someone insisted on asking them anyway, they were met with simple, pat answers, such as “it [the protocol] is not perfect, but it will help us help kids.”

We were doing it in the name of job security.  We were doing it to survive.  Problem-Reaction-Solution.

In countless meetings, workshops, and teleconferences, our mission as evaluators and “research scientists” was made clear to us: we needed to prove that the system of care was effective to ensure more funding, on both the local and national levels.

Obviously, with this being the setup, bias in our research was maximized from the very beginning.  In the script I read to potential participants in the study (which was “officially approved” by the Human Subjects Institutional Review Board), I was instructed to say: “We’re hoping to prove that the system of care works.  That way, similar programs can be funded in the future.”  From the first moment of contact, participants were notified what outcomes we, the researchers, expected.

Amazingly, many families would agree to the first interview.  Few agreed to a second, however (there were supposed to be 5 per family; one every 6 months).  They knew something was up.

Nevertheless, the data collection project went forward more or less as planned – continues on nationally to this day.   

And so I return, now, to those questions I wasn’t allowed to ask at the time: What was all that data really for? 

Sometimes we said it was to prove that the system of care improved outcomes for children and families involved in it, but that’s not the answer.  Wouldn’t we have stopped to ask the families what “improvement” meant to them if that were the nature of our quest?

Other times, when we professionals were talking amongst ourselves, we said it was to secure more funding; but that could easily have been achieved with far less data then we collected during the burdensome, 2 ½ hour long interviews.  The annual report to Congress, the supposed culmination of our efforts, was usually only 15-20 pages long, with only very small portions of the data we collected represented in its primary colored pie graphs.

Why did SAMHSA need to win our compliance with this effort so clearly deserving of critique?

What is the true purpose of the data collection enterprise?

New “research” claiming antidepressants don’t cause suicidality in children is fraudulent 02/07/2012

Posted by ALT in Mental Health Research, Pharmaceuticals.
Tags: , , , , , , , ,
2 comments

Meet Dr. Robert D. Gibbons:

He’s a “research scientist.”  A published author.  A professor of psychiatry.  An honored faculty member at the University of Chicago.

And he’s recently published one of the most dishonest and fradulent bits of “research” I have ever seen.

In his newest article, “Suicidal Thoughts and Behavior with Antidepressant Treatment: Reanalysis of the randomized placebo-controlled studies of fluoxetine and venlafaxine,” published yesterday in the Archives of General Psychiatry, he claims to have proven…

(drumroll please)

SSRIs do NOT cause an increased risk of suicide in children.

In spite of all of the following…

  • the FDA’s 2004 analysis of 9 selective serotonin reuptake inhibitors [SSRIs] and numerous Adverse Drug Reports [ADRs], and their subsequent insistence on black box warnings for all SSRIs about the risk of suicide in children and young adults taking these drugs…
  • the independent research of numerous others
  • the testimony at congressional hearings and the overall abundance of anecdotal data from families who will never be whole again because a loved one not predisposed to suicide suddenly committed the act in a violent and brutal way after beginning SSRI “therapy” (Here are a few people’s stories, shared during a congressional hearing in 1991.  There are many, many more)…
  • the data from the drug companies’ own trials [see below] …

…Gibbons boldly declares that “no evidence of increased suicide risk was observed in youths receiving active medication [SSRIs].”

I heard it this morning on NPR’s Morning Edition.  Hundreds of thousands of other Americans did, too.

And it is a deadly falsehood.

Let me be quick about this, because time is of the essence.  If even one child’s physician does as Gibbons urges and …

[reassess] the risk-benefit estimation for using antidepressants for major depressive disorder in all ages…

- Gibbons, in his Archives of General Psychiatry article

… a life could be lost, and that’s no exaggeration.  Because the fact of the matter is

SSRIs DO increase the risk of suicide in children

(and adults, too, for that matter), and pharmaceutical companies have known it from the very beginning.  This is true of multiple companies, but it is very well documented in the case of Eli Lilly.

They’ve known it all along

1. From the beginning, Eli Lilly executives noted Prozac’s (fluoxetine) propensity to cause agitation, aka akathisia, which research suggests is the causative factor in SSRI-related suicides.  It was recognized that akathisia put trial participants at increased risk for suicide.  This internal memo from the late 80s (later obtained by Peter Breggin through the “Freedom of Information Act”) is rather instructive:

Some patients have converted from severe depression to agitation within a few days.  In one case the agitation was marked and the patient had to be taken off the drugs.  In future studies, the use of benzodiazepines [tranquilizers] to control agitation will be permitted.
– Ray Fuller, “inventor” of Prozac, in internal Eli Lilly memo

Permitted by Lilly, not the FDA, I might add.

Which brings me to my next point…

2.  Lilly introduced the use of tranquilizers during the clinical trials to counteract the agitating and stimulating effects of Prozac.  This, of course, is not allowed by FDA regulations.

And furthermore:

After Eli Lilly submitted all of its clinical trials to the FDA, the agency’s evaluation showed Prozac to have little or no benefit, especially when the illegitimately tranquilized patients were removed from the clinical trial data… Instead of throwing out the bogus trials, negating any possibility of Prozac being approved, the accommodating federal agency allowed the tranquilized patients to be counted as if they were legitimate participants in the drug trials.  Then, and only then, did the clinical trials demonstrate effectiveness for Prozac – and even that was marginal at best.

- Peter Breggin, in Medication Madness, chapter 18: “Drug Companies on Trial”

But there’s more…

3.  Lilly routinely masked suicide and suicidal ideation in the clinical trials by calling it something else

An Eli Lilly internal memo written in 1990 (again obtained by Dr. Peter Breggin through the FOIA) reveals that Lilly researchers openly acknowledged employing this tactic.  From Claude Bouchy, a German employee, to Leigh Thompson in the United States:

Finally, on a very simple and non scientific basis, I personally wonder whether we are really helping the credibility of an excellent ADE [Adverse Drug Event] system by calling “overdose” what a physician reports as suicide attempt and calling “depression” what a physician reports as suicide ideation…Of course by the end of the day we will do what we are told to do…

- Eli Lilly employee and Prozac research Claude Bouchy in 1990 [emphasis added]

So, Lilly researchers routinely labeled suicidal ideation as “depression” in their adverse event reports during the clinical trials.  Remember that as you read this:

From my FOIA inquiries to the FDA, I had found that the initial drafts of the Prozac label had listed “depression” and “abnormal thoughts” as two of the three most commonly reported adverse reactions

- Peter Breggin, in Medication Madness, chapter 18: “Drug Companies on Trial” [emphasis added]

Let me get this straight: Lilly researchers were instructed to mask incidents of suicidality and suicidal ideation by calling them “depression.”  And then “depression” was reported as one of the top 3 adverse effects of Prozac?

Interestingly, at least one Lilly researcher could not escape the ethical and moral consequences of this action.  In a second 1990 memo, Bouchy expressed these sentiments:

I do not think I could explain to the BGA [German regulatory agency], to a judge, to a reporter or even to my family why we would do this especially on the sensitive issue of suicide and suicide ideation.

- Eli Lilly employee and Prozac researcher Claude Bouchy in 1990

5.  And, when all else failed, Lilly just threw out the suicide data altogether.

In 2005, several more Eli Lilly documents were forwarded by an anonymous source to a highly esteemed medical publication, the British Medical Journal.  The most damning of all of these, from 1985, was an internal analysis of one of the early Prozac placebo-controlled clinical trials that showed a significant increase in suicide attempts for the subjects taking Prozac.

12 suicide attempts were found in the Prozac group, compared to one in each of the control groups (one control group received placebo; the other received a tricyclic antidepressant).  The company’s hired research consultants simply decided to throw out six of the 12 suicide attempts.  Of course, this still leaves a 6:1 ratio between Prozac and control groups’ incidences of suicide…

Why am I telling you all this?

First, it is proof that even Lilly’s very biased trials, even her own paid “researchers,” could not hide the fact that Prozac does indeed increase the risk of suicidality amongst the people who take it.

And, second, because Gibbons reports in his article that he used 3 datasets, one of which was

The “complete longitudinal data for RCTs [randomized control trials] of fluoxetine hydrochloride conducted by Eli Lilly & Co.”

In other words, his assertion that “there is no evidence of increased suicide risk … in youths receiving active medication [SSRIs]” is based on the faulty data described above. In fact, he proudly boasts that he used “all industry trials of Prozac!”

This study avoided the problem of publications being biased in favor of positive clinical trials by examining all industry trials of fluoxetine and venlafaxine.

- Gibbons, in his Archives of General Psychiatry article

Gibbons claims that from the combined 3 datasets (including the Prozac clinical trials) “there were relatively few suicide attempts and suicides (a total of 20 attempts and 2 suicides in 21 patients among 9185 patients across all age cohorts and drugs).”  But we know from just the few snippets posted above that in one study of one drug [Prozac] 12 suicide attempts were recorded.

The numbers simply do not add up.

Revealingly, Gibbons goes on to report that:

An additional 6 suicidal events were identified from AERs [Adverse Event Reports], 4 attempts and 2 suicides… of the 2 suicides one was by an adult receiving fluoxetine and the other was a geriatric patient receiving placebo.

- Gibbons, in his Archives of General Psychiatry article

Very well.  But how many “overdoses” were there?

Funny—he doesn’t say.

A little more on Gibbons

As it turns out, he’s been advocating for the use of antidepressants in children for a long time.

Even after the FDA released its black box warning in 2004 regarding this class of drugs’ propensity to cause suicidal ideation in children, Gibbons was arguing for continued, widespread prescription of these drugs.

In his 2007 Psychiatric Times article, “SSRI Prescribing Rates and Adolescent Suicide: Is the Black Box Hurting or Helping?,” (which draws almost exclusively on data from another “scholarly” article of his with equally dubious origins) Gibbons loudly proclaims:

The effect of the black-box warning has been to lower antidepressant prescription rates, which in turn has resulted in more untreated depression and a corresponding increase in suicide rates for children and adolescents. The FDA sought to improve treatment of depression, but an overall decline in diagnosis and treatment of depression implies that the black-box warning did not achieve this goal, and the decline is consistent with the possibility that the black-box warning has had the opposite effect.

- Gibbons (2007) “SSRI Prescribing Rates and Adolescent Suicide: Is the Black Box Hurting or Helping?”

Did I mention his “proof” for this assertion has dubious origins?

As the New York Times reported about a week later, the study Gibbons cited (his own) was – plain and simple – fraudulent.

While suicide rates for Americans ages 19 and under rose 14 percent in 2004, the number of prescriptions for antidepressants in that group was basically unchanged and did not drop substantially, according to data from the study.

“There doesn’t seem to be any evidence of a statistically significant association between suicide rates and prescription rates provided in the paper” for the years after the F.D.A. warnings, said Thomas R. Ten Have, a professor of biostatistics at the University of Pennsylvania.

- from the 2007 NYT article “Experts Question Study on Youth Suicide Rates

Gibbons did do some fancy maneuvering in an attempt to rebut this critique of his “work” about a year later – which fell flat, it seems —  but it is beyond the scope of this article to follow the trail much further than we already have.

In Conclusion…

Gibbons has a history of publishing academic articles based on faulty datasets.  He also has a history of drawing false conclusions from those faulty datasets.

In other words, he just makes shit up.

And it’s all in support of his favorite cause: getting kids to use antidepressants, and getting physicians, parents, and everyone else to re-evaluate “the risk-benefit estimation for using antidepressants.”

You know what?  I agree with him.  Let’s all evaluate the “risk-benefit estimation” together, shall we?

What are the risks of allowing Lilly and other SSRI producers to run their clinical trials in such a blatantly immoral and fraudulent fashion? 

What are the risks of allowing pharmaceutical companies to hide, for years, the overwhelming evidence that SSRIs cause suicidality? 

And what are the benefits of letting one man – with a proven track record of fraudulent research in the service of pharmaceutical companies – re-open the debate on what is essentially a dead (and deadly) issue?

Antidepressants cause suicide and suicidal ideation in patients of all ages, children included.

End of story.

And no fanciful, fraudulent “meta-analysis” of the faultiest clinical trials ever conducted is going to change that.

NPR resurrects “chemical-imbalance-causes-depression” theory, because it wanted to live 01/31/2012

Posted by ALT in Mental Health News, Mental Health Research, Pharmaceuticals.
Tags: , , , , , , ,
3 comments

Did you hear this?  I heard it, too.  The whole mental health blogosphere heard it.  And, understandably, we got excited. 

FINALLY — the truth comes out on a major news network (NPR): a so-called “serotonin imbalance” in the brain has never been scientifically linked with depression, and this false theory was used for years to sell SSRIs (selective serotonin reuptake inhibitors – modern antidepressants) to a lot of people out there as a scientifically proven, biological cure to their biopsychiatric problems.  Meanwhile, news of the appalling “side” effects of the drugs (suicidal and homicidal ideation in at the very least 5% of patients) was squelched, and literally thousands of people lost their lives in SSRI-related suicides and homicides.

After hearing all this, one would assume that we were done with that whole “chemical-imbalance-in-the-brain-causes-depression” thing.  We have established that the theory is false.  It’s a dead (and deathly) issue.  Right?

WRONG.

Turns out that little NPR piece is part of a series.  The second installment of which ran on “Morning Edition” today.

And the biopsychiatric idea that a chemical imbalance of some kind MUST cause depression – and that ameliorating this chemically/pharmaceutically must therefore CURE depression – is alive and well.  In only a week’s time, NPR has managed to resurrect it.  You see, it wanted to live.  Or at the very least, pharma wants it to.

I Wanted To Live

’I Wanted To Live': New Depression Drugs Offer Hope For Toughest Cases” is the name of the piece, and it is a simple reiteration of the serotonin/Prozac storyline, only with a new neurotransmitter/miracle drug combo: glutamate/Ketamine.

Zarate [a “research scientist”] sees depression as a bit like a leaky faucet in the brain. There are different ways to stop the leak, he says. “You can go straight to the faucet and you can fix it,” he says. “Or you can go to the water plant and shut down the water plant. The end result will be the same.”

The current antidepressants act in a way that is like shutting down the water plant, Zarate says. It takes a long time for the water to stop flowing through the miles of pipes that eventually lead to the leaky faucet.

He thinks the reason is that these drugs act primarily on the brain chemicals serotonin, norepinephrine and dopamine. Ketamine acts on a chemical called glutamate, which is much closer to the problem, Zarate says.

- from the NPR story “I Wanted to Live.”

So let me get this straight:

Last week we learned that a serotonin imbalance in the brain does not cause depression.  Scientists were confused on this point for some unspecified length of time because Prozac, a miracle/blockbuster drug that somehow “cures” depression, raises serotonin levels in the brain.  Scientists understandably put two and two together and assumed that higher serotonin levels = no depression because Prozac presumably also = no depression.  (Never mind that Prozac and other SSRIs have since been proven to be no better than placebo). 

At some point, scientists figured out their theory was incorrect, or at best oversimplified to the point of being false [a distinction they insist on making!], but they continued to present it to patients as fact “for the patients’ own good” so the patients would take their meds.  Which scientists still insisted “worked” to “cure” depression.  (Again, no better than placebo.)

One week later, in the next installment of the series, we learn two things:

1.  NPR has changed the story about serotonin – now it does work to cure depression by addressing problems in brain chemistry.  [Never mind what they said last week!]

Traditional antidepressants like Prozac work on a group of chemical messengers in the brain called the serotonin system. Researchers once thought that a lack of serotonin was the cause of depression, and that these drugs worked simply by boosting serotonin levels.

Recent research suggests a more complicated explanation. Serotonin drugs work by stimulating the birth of new neurons, which eventually form new connections in the brain. But creating new neurons takes time — a few weeks, at least — which is thought to explain the delay in responding to antidepressant medications.

- from “I Wanted to Live.”

It works, but it works real slow.

2.  This new drug – ketamine – works, too, but it works BETTER and FASTER!

Ketamine, in contrast, activates a different chemical system in the brain — the glutamate system. Researcher Ron Duman at Yale thinks ketamine rapidly increases the communication among existing neurons by creating new connections. This is a quicker process than waiting for new neurons to form and accomplishes the same goal of enhancing brain circuit activity.

- from “I Wanted to Live.”

I need hardly add that the author of this story did not cite any of the research studies referred to above.  He did, however, include these pretty pictures which successfully distracted my attention from the lack of documentation for his outrageous claims by looking so very “scientific” and “official.”

Look at the pretty pseudoscience!

Just kidding.  I’d like to see proof, not pictures.

Hope

The story’s headline promises to give us hope.  Here is what the author has to offer, at the close:

The goal of the NIH [National Institutes of Health] experiments with ketamine, riluzole and scopolamine is to identify compounds that pharmaceutical companies can use as molecular models to develop an entirely new class of antidepressants… Drug companies have taken notice. Several are now working on glutamate drugs for depression.

- from “I Wanted to Live.”

I guess we’re supposed to hope that pharma can patent this new chemical and sell it using a recycling of the old SSRI pitch? (As NPR has already begun to do for them…)

Are we supposed to hope that drug companies will conduct fair research trials on this new class of antidepressants, that they will accurately report the results of these trials, that they will be ethical in addressing concerns about adverse drug events in or out of court?

Let me try that on for size….

Nope.  I don’t feel hopeful.  Not in the least bit.

I’d rather hope for something else.

I hope I never again have to hear another repetition of this ridiculous, thousand-fold lie about mere “chemical imbalances” being the cause of this thing we call “depression.”  (Or any “mental illness,” for that matter.)

I hope that people dealing with depression will be allowed to make their own, fully informed choices about treatment. 

I hope they will be told the truth – that antidepressant drugs have been proven to cement depression into a chronic state, when an unmedicated and honest interaction with the problem often allows it to pass and to then stay in the past.  [more on all of that here.]

I hope that their family members and friends will be their cheerleaders and confidants, and they will find wholesome and healthy ways to address the root causes that their depression arises from.  

Because depression is not merely “of the body,” a simple biological imbalance and nothing more.  It is a mind-body phenomenon, it is subjectively real, it is connected to the world, and it is oftentimes a message about the world. 

A message we should each process, understand, and integrate in our own way, in our own time.

My conversation with a “Research Scientist” continues 04/05/2011

Posted by ALT in "An Insider's Perspective", Mental Health Research.
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3 comments

If we knew what we were doing, it wouldn’t be called Research.

(Albert Einstein)

this quote being the only decoration which hangs in the office of my boss, the Research Scientist

I remember the day I first crossed the threshold of his office – for my job interview.  That quote, framed and prominently displayed in an otherwise bare office, gave me pause.  “Is that supposed to be cute?” I thought. 

I wondered if Albert Einstein ever even said that.  And if he did, does it somehow make more sense — and sound more like something a believer in research/science would say — in German?  Or in context?

What kind of a researcher would make this his motto, even as a joke? 

But then I turned my attention to the man in front of me.  Destitute and desperate for a job at the time, I did my best to put these questions aside and form a good opinion of the Research Scientist who had the power to radically change my position and my general outlook. 

I really wanted that job.

2 years later, after gaining a sickening familiarity with his research “methods,” I’ve got a much better handle on what that quote means to him.  I think he takes a great deal of comfort in it.  If Albert Einstein, the standard cultural trope for “genius” and “scientist,” thought this – then maybe he cut corners, only examined data that was convenient (writing off the rest as “faulty” or whatever), and just plain made shit up sometimes, too!   By pulling Einstein down to a comfortable level of mediocrity, this Research Scientist is suddenly in much better company.  It’s not quite “I’m just as good as Einstein!” – it’s more like “Einstein was just as bad as I am!”

What a dumbass.

   

PART II to our conversation

Our second conversation on the childhood bipolar “fact” sheet took place on Friday.  And I spent the weekend pondering.  You see, I realized that he probably never read the sheet all the way through.  I inferred this from his lack of knowledge of what it said beyond the first two paragraphs – which I had read to him over the phone — and his mistaken attribution of the sheet to NAMI. 

He didn’t read it to protect his carefully maintained ignorance/innocence.  Basically, if he didn’t know what it said, he wouldn’t be convinced that ethically, morally, something needed to be done.  And he would therefore maintain his innocence.  [I told you I’m familiar with his methods!] 

What to do?  How to provoke some actual critical thinking about this?  He likes to think with his self-preservation gut (prime directive: preserve ignorance/innocence).  How to get beyond those very formidable defenses against data and reach the actual Research Scientist with conscience? 

I thought I’d give it one more shot.

This time, I went with email.  It would appear less confrontational, and maybe not trigger those strong defensive responses.

***

From: ALT
Sent: Monday, April 04, 2011 8:19 AM
To: Research Scientist
Attachments: bipolar info sheet.pdf

Research Scientist,

See attached to learn my objections to the childhood bipolar info sheet. I welcome your comments or questions. I hope you will give this information all the attention an “issue close to your heart” deserves.

I think your use on Friday of the phrase “company line” was very appropriate. These inaccuracies certainly promote a company line – lifelong, chronic illness never to be cured but only to be suppressed with an ever‐changing cocktail of expensive, patented drugs. It is a very convenient narrative for a pharmaceutical company.

But we are not a company. We are “researchers,” are we not?

Sincerely yours,

ALT

***

His response (in about a minute!):

You cannot understand how close this issue is to me. SO forgive me if I do not meet your expectations related to this.

***

That’s it. 

What I’d like to say to this Research Scientist (if the conversation weren’t so clearly over) is that it’s not about “my expectations.”  It’s not about me at all.  It’s about doing what’s right for the families and youth who will be affected by this information.

 

March on, Soldier.  But what are you fighting for?

Did you know that in police or heavily militarized states (Mexico, as one of many examples), where soldiers and policeman treat much of the country as an occupied territory, the citizens and populace as enemies – a policeman or soldier is never stationed in his hometown, or even home region?  They are stationed as far away from home as possible.

Why?

Because there are some things people typically just won’t do to their brothers, relatives, childhood companions.   Point a gun in their faces.  Dehumanize them.  Treat them as fundamentally “other.”  Kill, rape, terrorize.

But strangers?  Folks that look different?  And in the case of Mexico, speak different languages?  Come from radically different cultural heritages? 

Yeah.  You can train soldiers to do it to them.  Incrementally, step-by-step.  It can be done. 

I shared this information, long ago, with my boss the Research Scientist.  And then I mentioned the fact that nearly all of his research projects take place far from where he lives.  One is a 3 hours’ drive away; another is 18 hours. He’s often told me that observation troubles him. 

Why is it so easy to think of him as a mercenary? 

When it comes to childhood bipolar disorder, whose “company line” is he soldiering, guarding with his silence?  He styles himself as a children’s mental health advocate, but what is he really fighting for?

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