“Depression is really a chemical imbalance of the brain” – just one more branch on the eugenics tree 12/03/2012Posted by ALT in Activism, Depression, Mental Health News.
Tags: chemical imbalance, depression, eugenics, mental health, Prozac, serotonin, stigma, suicide
Two Northwestern professors (Cristina Traina and Laurie Zoloth) wrote an article in response to a college student’s suicide, entitled “Culture stigmatizing mental illness must change.” It reads, in part:
Learning to accept your limits is learning what it means to be human. Realize that although difficult events can trigger depression and suicide, depression is really a chemical imbalance in the brain. You can no more adjust this balance than a diabetic can will their body to make more insulin or a person with low thyroid production can think themselves out of fatigue. At the physical level, the brain, like any organ, can become unable to function properly — in this case, to imagine that there are other futures beyond the intensity, or the injustice, or the pain of this moment.
What can you do for yourself and your friends? First, get rid of the stigma around depression, suicidal thoughts and treatment for mental illness. We need to learn to talk about mental illness like we talk about cancer, a serious emotional and physical crisis that can be treated, whose sufferers need support and decency and understanding as they face a life-threatening illness. Depression and anxiety are more common than asthma. You wouldn’t stigmatize a friend for using her inhaler; she shouldn’t feel shame if she uses Prozac to function, too.
I had to respond.
TO: Cristina Traina and Laurie Zoloth
CC: Editors, Northwestern Daily and Huffington Post College
SUBJECT: Response to your article: “Culture stigmatizing mental illness must change”
In your recent Huffington Post article (Culture stigmatizing mental illness must change), you wrote that “depression is really a chemical imbalance in the brain.” I understand this was not an academic publication – but could you provide a citation to back this up?
You’ll find it impossible to do so; because this mantra, this advertising slogan is about as scientific as the statement that “the best part of waking up is Folgers in your cup!” The best? Really?
Meanwhile, let me provide with you with a few citations of my own:
[Antidepressant] advertising campaigns have revolved around the claim that SSRIs correct a chemical imbalance caused by a lack of serotonin… Contemporary neuroscience research has failed to confirm any serotonergic lesion in any mental disorder, and has in fact provided significant counterevidence to the explanation of a simple neurotransmitter deficiency… In fact, there is no scientifically established ideal “chemical balance” of serotonin, let alone an identifiable pathological imbalance.
- from Lacasse, J.R. & J. Leo (2005) Serotonin and Depression: A disconnect between the Advertisements and the Scientific Literature.
A serotonin deficiency for depression has not been found.
- Psychiatrist Joseph Glenmullen, clinical instructor of psychiatry at Harvard Medical School, in Prozac Backlash (2000)
Although it is often stated with great confidence that depressed people have a serotonin or norepinephrine deficiency, the evidence actually contradicts these claims.
- Professor Emeritus of Neuroscience Elliot Valenstein, in Blaming the Brain (1998), which reviews the evidence for the serotonin hypothesis.
But I am not writing merely to correct a factual error in your post – there’s more.
When an advertising gimmick is touted as scientific fact and even entered into the canon of “common sense,” there are bound to be some serious consequences. Consider:
- Rather than helping us “learn what it means to be human,” as you say, the chemical imbalance theory actually tells us that some people are born with brains that don’t function properly. That are, in some fundamental way, pathological. Put another way, there are the mentally fit and the mentally unfit. Sound familiar? To any student of late 19th/early 20th century eugenic thought in the West, it would sound mighty familiar.
- The theory also supports another common biopsychiatric fallacy: that an individual with a mental health diagnosis will need to take psychiatric medications for the rest of his/her life, to “correct the imbalance,” as the story goes. Long-term use of most classes of psychotropic drugs (including antidepressants, antipsychotics, and mood stabilizers) not only comes with serious, LIFE-THREATENING adverse effects, but can actually serve to make what could be rare occurrences of severe mental emotional/distress chronic and repeating. In some cases, this remains true even after withdrawal from the offending chemical agent. (see Robert Whitaker’s Anatomy of an Epidemic for chapters of information devoted to this astonishing truth).
- Finally, the chemical imbalance theory takes nearly all agency away from the individuals who are suffering from mental/emotional distress – they become the victims of whatever their faulty, off-balance brains inflict on them. You write that a person “can no more adjust this [depression-inducing chemical im]balance than a diabetic can will their body to make more insulin or a person with low thyroid production can think themselves out of fatigue.” How horrible if this were so! The kinder truth is there are many strategies a distressed individual can employ that are not purely chemical or pharmaceutical, but rather make use of the mind, will, spirit, and being. That empower, enliven, and entail a joyful discovery of strength, stamina, and RESILIENCY within the human being, who is indeed FIT TO LIVE in whatever way he/she chooses!
You express a desire to reduce stigma in mental health – I think this is admirable. Unfortunately, several scientific studies have demonstrated without a doubt that the “chemical imabalance” theory of mental health issues has the opposite effect: it increases stigma.
For example, in 1997 Sheila Mehta of Auburn University conducted a simple experiment on stigma in mental health, comparing the “chemical imbalance” model to the psychosocial model (which acknowledges a broad variety of factors – including family, past trauma, diet, environment, etc. – as potential contributors to emotional distress).
55 male college students were enrolled, and each one was told that he and a partner would have to do a simple learning task. The partner was actually a confederate, who 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.” [See: Mehta, S. (1997). Is being “sick” really better? Effects of disease view of mental disorder on stigma]
Rather than learning “to talk about mental illness like we talk about cancer” by doing as you suggest and falsely promoting it as a merely physical problem of chemicals out of balance, I say we need to talk about mental and emotional distress in psychosocial context. AND in context of community, society. What is it about our culture, our rather toxic life on this planet, that makes people sick? And even more importantly, what can we as a society learn from these individual experiences of distress?
I take it you are sincere in your desire to help young people support each other in dealing with the distress that seems to hit so hard at the dawn of true adulthood. Surely, as scholars and seekers of knowledge, you recognize that truth, however complicated and elusive it may be, is vastly preferable to an oversimplified falsehood? Especially when that truth embraces the human potential to survive and thrive, while the falsehood embraces a technocratic romance with chemicals and a eugenical division of what were once human beings into groups of “fit” and “unfit” participants in this consumerist, sick culture.
If you want to help, tell the truth. If you’re not sure what the truth is, take the time to find out. Go slow, think critically, ask questions. Look for the roots of ideas, the beginnings of things, and then follow them from earth to sky – and all the branchings inbetween.
This will not be easy – psychiatry is a strange plant, indeed. But our community needs you to be more than just professors; we need you to be professors of TRUTH.
Can you? Will you?
Mental health writer and activist
I have received a response from one of the professors. She actually seems pretty open to considering what I said and has asked for time to research the information I shared. I’m not going to post her response yet because I’d like to win her trust — I think she really wants to dialogue! — but I hope to document our conversation here once it’s developed a bit more. I’m looking forward to a valuable exchange with her.
Tags: Dr. Allen Frances, mental health, paxil, Prozac, Seroquel, suicidality, violence
Dr. Allen Frances. We’ve been hearing his name a lot this past year, haven’t we? [and not in conjunction with his excellent tan!]
A fine specimen of “middle way” protesting, which poses as activsm for real psychiatric reform, but does little more than reinforce psychiatric treatment-as-usual, perhaps with a few Orwellian language shifts along the way. Here’s an instructive string of emails to prove the point — no DSM protest unless it’s Dr. Allen Frances APPROVED DSM protest.
Anyhow, in a recent blog for the Psychiatric Times (“Mass Murderer Psychobabble Misses Gun Policy Point“), he writes that “there is no indication that psychiatry can change the statistics of violence or the proclivity of the violent.”
I beg to differ, and wrote him an email to tell him so.
To: Allen Frances
Subject: Response to your recent “Psychiatric Times” Blog
Dear Allen Frances,
In a recent blog for the Psychiatric Times, you state that “psychiatry has no way to predict mass murder and no way to prevent it.” Hammering the point home later on, you write that “there is no indication that psychiatry can change the statistics of violence or the proclivity of the violent.”
Sir, I believe you are in error.
As you may be aware, there are many examples of psychotropic medications (commonly prescribed by psychiatrists to their patients) which list “suicidality,” or “suicidal ideation,” “acting aggressive, being angry, or violent,” “agitation,” and “mania,” as side effects in the Physician’s Desk Reference [PDR], a publication of the official FDA-approved labeling and information for all drugs. A violent combination of effects, don’t you agree?
For example, clonazepam (Klonopin) and lorazepam (Ativan), two common benzodiazepines, list “suicidal ideation” or “potential to commit suicide” as a side effect. Doctors are also cautioned about “paradoxical effects” – which could include aggression and hostility. The Medication Guide for Serqouel, an antipsychotic medication, lists “thoughts of suicide or dying,” “feeling very agitated or restless,” “new or worse irritability,” “acting aggressive, being angry, or violent,” “acting on dangerous impulses,” and “mania” as symptoms that may occur in conjunction with use of Seroquel – something to be brought up with a doctor immediately. And, perhaps most well-known of all, selective serotonin reuptake inhibitor [SSRI] antidepressants such as paroxetine (Paxil), fluoxetine (Prozac), and citalopram (Celexa) carry a black box warning about the potential to cause suicidality in children, adolescents, and young adults. Furthermore, a 2004 booklet published by the FDA (which is also inserted at the end of every antidepressant entry in the PDR) lists, under a heading entitled What to Watch Out For in Children or Teens Taking Antidepressants: “thoughts about suicide or dying,” “attempts to commit suicide,” feeling very agitated or restless,” “acting aggressive, being angry, or violent” as potential side effects.
The list of psychotropic drugs indicated in causing restlessness, agitation, aggression, suicidality, and violence goes on, as I’m sure you know.
There is also a legal precedent acknowledging the reality of drug-induced suicidality and homicidality. Are you familiar with the case of Tobin v. SmithKline Beecham? Donald Schell, a 60-year-old man with no psychiatric history, was having trouble sleeping. His physician prescribed him Paxil, and 48 hours later he murdered his wife, daughter, and granddaughter—then shot himself. The court awarded $8 million in damages and wrote in its opinion that “Paxil can cause some individuals to commit suicide and/or homicide,” and that “Paxil was the proximate cause of the homicides and suicides involved in this litigation.”*
You may be interested to know that the legal definition of proximate cause is “the primary cause of injury… proximate cause produces particular, forseeable consequences without the intervention of any independent or unforeseeable cause.”**
In other words, the court ruled that Paxil was the primary cause of Schell’s violent actions, and this was a forseeable consequence of his taking Paxil.
Bearing all of this in mind, I think the statement that “there is no indication that psychiatry can change the statistics of violence or the proclivity of the violent” is erroneous. There is, in fact, something very simple psychiatrists can do:
stop prescribing drugs that, by their manufacturers’ own admissions, cause people to become aggressive, angry, violent, and suicidal.
Mental health activist and writer
Not a member of the Church of Scientology
Not an “antipsychiatrist” (very much pro- “soul healing,” in fact)
* Tobin v. SmithKline Beecham Pharmaceuticals, 164 F.Supp.2d 1278, 1284.
** West’s Enyclopedia of American Law, Second Edition. (2008).
New “research” claiming antidepressants don’t cause suicidality in children is fraudulent 02/07/2012Posted by ALT in Mental Health Research, Pharmaceuticals.
Tags: antidepressants, black box warning, Eli Lilly & Co., FDA, Peter Breggin, Prozac, Robert D. Gibbons, SSRIs, suicide
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…
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.
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.
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.
Tags: chemical imbalance, chemical imbalance in the brain, depression, ketamine, NPR, Prozac, selective serotonin reuptake inhibitors, SSRIs
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?
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.”
Just kidding. I’d like to see proof, not pictures.
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.
Tags: antidepressant, antipsychotic, branding, marketing, pharmaceutical, Prozac, Seroquel
Each word has an entire volume of history attached to it. Where does it come from? How was it used in other places, other times? Tracing the ancestry of a word through etymology reveals ancient understandings of the need for and role of such a word in a culture and tracks philosophical shifts over time on a societal level [exhibit A: compare the ancient, etymological meaning of “psychiatry” to current uses].
A word with no history, springing up “full-grown” and pregnant with meaning, is an anomaly with a specific function: it serves, not a culture attaching meaning to its life-world, but the sole purposes of its creator. It delivers a very specific message — cut out of context, simplified, compelling — from its master to all who invoke its power.
PROZAC. SEROQUEL. ZYPREXA.
We’re talking about branding.
Pharmaceutical companies have inserted new words into the language of mental wellness, words with no etymological ancestors. Words that are designed, above all else, to sell.
What effect does this have our culture’s conversation about mental health?
The perfect name = “the perfect beast”
Pharmaceutical companies start working with branding consultants as early as 3 years out, searching for that perfect name, the one that will:
find a fresh way into the hearts and minds of customers … redefine and own the conversation… ignite the passions of customers… propel itself through the world on its own, becoming a no-cost, self-sustaining PR vehicle.
WHOA. Let’s process for a moment: that “hearts and minds” phrase is a clear reference to LBJ’s counter-insurgency efforts in the Vietnam War (though it, too, has an interesting history which long predates American imperial activities). “Beast,” too, is an interesting word choice – slightly apocalyptic to my ears – though an appropriate description of a self-propelled, insentient thing doing the PR bidding of its masters.
Costly research has shown that:
- hard letters with an edge (P,T, and K) convey effectiveness
- X is perceived as scientific
- L,R, and S are calming
- Z means speed
Additionally, the name is most effective if it contains some pre-existing elements of meaning; then there is less of a need to create a new meaning through marketing and advertising.
All this points towards the fact that drug companies are marketing directly to consumers, and they’re not doing it from an evidence-based point of view (ie, presenting information from clinical trials proving the effectiveness of the drug). It’s all about symbolism, emotion, and the sub-conscious.
Dettore and Piergrossi point to the brand Invega for a Johnson & Johnson anti-psychotic.
The word Vega, the brightest star in the constellation Lyra, is imbedded in it. Any imagery related to the stars or space carries a positive connotation.
“It almost offers the patient hope through the name,” Piergrossi said.
(from this recent news article; emphasis added)
So let’s have a look at a few common drug names. What kind of beast was this drug intended to be? How is it meant to propel itself directly into our hearts and minds? AND, how do the emotions and symbolism invoked compare to the actual evidence surrounding the effectiveness of the drug?
Pro – Positive, affirmative. Additionally, we have the “p” sound, which conveys “effectiveness.”
Zac – “speed.”
Given that research has shown that antidepressants are only marginally (at best) more effective than placebo, and usually take about 3-5 weeks to begin “working,” this name is a bit misleading.
May I suggest TRIAPLACEBOFIRST instead?
SER – the “s” sound is soothing, and this seems to imply “serenity.”
QUEL – calm, quell.
Despite the calming sound of its name, research has shown that acute akathisia (maddening restless energy which can cause pacing, twitching, and even violence) is a common side effect of Seroquel.
Perhaps the name JUMPOUTTAURSKIN would better convey this “side effect”/main effect of the drug?
Anyone else out there have a suggestion for a better name for a particular “beast?” I’m anxious to hear your ideas… Language change is a powerful force, a way to re-define and reframe. It can work for you.