Dr Phil Hickey
On January 10, 2017, I put up a post titled The Biological Evidence for “Mental Illness”. It was published simultaneously on Mad in America. The post was a response to an earlier comment from Carolina Partners in Mental Healthcare PLLC, which included the assertion “mental illnesses have a long history of biological evidence.” In my January 10 article, I challenged this assertion and pointed out that no such evidence existed. The article generated some comments, most of which were favorable. There was one comment, however, from Michael, who asserted:
“Your rebuttal that there are no scientific studies to these cases can be dismissed with a quick google search.”
In my response to Michael, I asked him to cite me some references to support this assertion. On January 15, Michael wrote back citing three studies: the first on the neurobiology of depression; the second on the neurobiology of “schizophrenia”; and the third on the neurobiology of “bipolar disorder”.
I examined these studies, and started to draft a response to Michael, but as I was writing, I realized that the subject matter warranted a wider audience and needed to be put up as a post. This is not because the studies cited are particularly compelling. As we shall see below, they are not. But rather, because what has happened here is something that occurs routinely in these debates. Psychiatry proponents claim there is evidence to support their position that “mental illnesses” are caused by biological malfunctions – but when pressed for references, they either don’t respond at all, or they dish up the kind of references cited by Michael.
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Showing posts with label Dr Philip Hickey. Show all posts
Showing posts with label Dr Philip Hickey. Show all posts
Monday, January 30, 2017
Thursday, January 26, 2017
Mental Health First Aid: Another Psychiatric Expansionist Tool
Dr Phil Hickey
On December 25, 2016, the Baltimore Sun published an excellent article titled Drug companies prey on children, by Patrick D. Hahn, PhD. Dr. Hahn is an affiliate professor of biology at Loyola University, Maryland. Here are some quotes:
Please take a look at Dr. Hahn’s article, and pass it on. Mental
Health First Aid is not a good thing. Rather, it is just another
psychiatric expansionist tool.
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Thank You Dr Hickey
And bookmark Dr Hickey's URL.
On December 25, 2016, the Baltimore Sun published an excellent article titled Drug companies prey on children, by Patrick D. Hahn, PhD. Dr. Hahn is an affiliate professor of biology at Loyola University, Maryland. Here are some quotes:
“I recently attended Youth Mental Health First Aid Training at a local public school. It was an eye-opening experience.”
“Youth Mental Health First Aid Training,
sponsored by the National Council for Behavioral Health, is intended to
enable teachers, parents and others in contact with young people to
identify potential ‘mental illnesses’ in order to facilitate early
detection and treatment by our mental health care system. My fellow
attendees were surprisingly open about their own experiences with that
system. One mentioned that her son became manic after being diagnosed
for ADHD. Another said that both she and her roommate became bipolar
after being diagnosed for depression. Neither our facilitators nor
anyone else present pointed out that mania and bipolar disorder are
toxic effects of medications commonly prescribed for ADHD and
depression.”
“Our training manual didn’t say anything
about this either, although it did claim that depression is caused by a
deficiency of serotonin — a fable that by now has become as discredited
as the phlogiston theory of chemistry. It also stated that mental health
interventions are ‘evidence-based’ and ‘scientifically tested’ —
neglecting to mention that much of that evidence is put forth by drug
companies who have a fiduciary duty to do everything they can to
maximize sales of their products.”
“So is all this a scheme to push more drugs to more kids? The 2013/2014 annual report
for the National Council for Behavioral Health, titled ‘A Legacy of
Excellence and Impact,’ gives us a hint. It lists the organization’s
supporters as including the Pharmaceutical Research and Manufacturers of
America (PhRMA) along with no fewer than 12 different drug companies.
Would these folks be ponying up the cash if they weren’t confident this
program would increase sales? And do the parents and teachers who attend
the council’s training program — no doubt with the best intentions in
the world — realize that they are essentially sitting through an
eight-hour infomercial bought and paid for by the drugmakers?”
“One out of 13 American children between the ages of 6 and 17 has taken a psychotropic medication within the last six months, according to the Centers for Disease Control. Meanwhile, youth suicide rates are at their peak
going back at least as far back as 1999, while the number of children
receiving disability benefits for mental illness is at an all-time high.”
Continue Reading.
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And bookmark Dr Hickey's URL.
Tuesday, January 10, 2017
The Biological Evidence For "Mental Illness"
Behaviorism and Mental Health
by Phil Hickey on January 10, 2017
On January 2, 2017, I published a short post titled Carrie Fisher Dead at Age 60 on Behaviorism and Mental Health. The article was published simultaneously on Mad in America.
On January 4, a response from Carolina Partners was entered into the comments string on both sites.
Carolina Partners in Mental Healthcare, PLLC, is a large psychiatric group practice based in North Carolina. According to their website, they comprise 14 psychiatrists, 7 psychologists, 34 Advanced Practice Nurse Practitioners/Physicians Assistants, and 43 Therapists and Counselors. They have 27 North Carolina locations.
Partners’ comment consists essentially of unsubstantiated assertions, non sequiturs, and appeals to psychiatric authority. As such, it is fairly typical of the kind of “rebuttals” that psychiatry’s adherents routinely direct towards those of us on this side of the issue. For this reason, and also because it comes from, and presumably represents the views of, an extremely large psychiatric practice, it warrants a close look.
I will discuss each paragraph in turn.
“We strongly disagree with this article, which neglects a lot of important information and uses selective hearing to distort what Carrie Fisher was about and also to distort the evidence for mental illness as a real disorder.”
My Carrie Fisher article was brief (566 words), and was intended as a counterpoint to the very widespread obituaries that lionized her as a champion of “bipolar disorder”. The essential point of my article was that Ms. Fisher had been a victim of psychiatry, and like a great many such victims, died prematurely. Obviously I neglected a lot of important information. I could have gone into great length as to the recklessness of psychiatry assigning the bipolar label, with all its implications of helplessness, disempowerment, and “chemical imbalance” to a young woman who by her own account was, at the time, using any drugs she could get her hands on. But I felt that a brief and respectful statement of the facts was all that was needed.
. . . . . . . . . . . . . . . .
“Mental illnesses have a long history of biological evidence. For example, researchers have demonstrated that people with depression have an overactive area of the brain, called Brodmann area 25. Schizophrenia has been linked to specific genes, as PTSD and autism have been linked to specific brain abnormalities. Suicide has been linked to a decreased concentration of serotonin in the brain. OCD has been linked to increased activity in the basal ganglia region of the brain.”
Brodmann area 25 (BA25)
Partners did not provide a specific reference in support of this contention, but my best guess is that the reference is Mayberg, HS, et al (1999) Reciprocal Limbic-Cortical Function and Negative Mood: Converging PET Findings in Depression and Normal Sadness (Am J Psychiatry 1999; 156:675–682). Here’s the study’s primary conclusion:
“Reciprocal changes involving subgenual cingulate [which includes Brodmann area 25] and right prefrontal cortex occur with both transient and chronic changes in negative mood.”
What this means essentially is that negative mood, whether transient or enduring, is correlated with changes in both the subgenual cingulate (Brodmann area 25) and the right pre-frontal cortex, and that when the depression is relieved, the changes are reversed.
This, of course, is an interesting finding, but provides no evidence that depression, mild or severe, transient or enduring, is caused by a biological pathology.
The reality is that all human activity is triggered by brain activity. Every thought, every feeling, every action has its origins in the brain. I cannot lift a finger, blink an eye, scratch my head, or recall my childhood home without a characteristic brain function initiating and maintaining the action in question. Without stimuli from the brain, my heart will stop beating, my respiratory apparatus will shut down, and I will die, unless these functions are maintained by machines.
So there is absolutely no surprise in the discovery that sadness and despondency have similar neural triggers and maintainers. It would be amazing if they didn’t. But – and this is the critical point – this does not warrant the conclusion that sadness which crosses arbitrary and vaguely-defined thresholds of severity, duration, and frequency is best conceptualized as an illness caused by pathological or excessive activity in BA 25.
Depression is a normal state. It is the normal human reaction to significant loss and/or living in sub-optimal conditions/circumstances. It is also an adaptive mechanism, the purpose of which is to encourage us to take action to restore the loss and/or improve the conditions.
All consciously-felt human drives stem from unpleasant feelings. Thirst drives us to seek water; hunger, food; hypothermia, warmth; hyperthermia, coolness; danger, safety, etc. Sadness and despondency are no exceptions. They drive us to seek change, and have been serving the species well since prehistoric times.
But – as is the case with all the above examples – when a drive is not acted upon, for whatever reason, the unpleasant feelings worsen. Just as unrequited hunger and thirst increase in strength, so the depression drive when not requited deepens.
The reality is that most people deal with depression in appropriate, naturalistic, and time-honored ways. If the source of the depression is the loss of a job, they start job-hunting. If the source is an abusive relationship, they seek ways to exit or remediate the situation. If the source is a shortage of money, they seek ways to budget more sensibly, or increase their earnings; etc.
Depression, either mild or severe, transient or lasting, is not a pathological condition. It is the natural, appropriate, and adaptive response when a feeling-capable organism confronts an adverse event or circumstance. And the only sensible and effective way to ameliorate depression is to deal appropriately and constructively with the depressing situation. Misguided tampering with the person’s feeling apparatus is analogous to deliberately damaging a person’s hearing because he is upset by the noise pollution in his neighborhood, or damaging his eyesight because of complaints about litter in the street.
Our feeling apparatus is as valuable and adaptive as our other senses. But psychiatry routinely numbs, and in many cases permanently damages, this apparatus to sell drugs and to promote the fiction that they are real doctors. Their justification for this blatantly destructive activity hinges on the false notion that depression becomes a diagnosable illness when its severity crosses arbitrary and vaguely-defined thresholds. But deep despondency is no more an illness than mild despondency. The latter is the appropriate and adaptive response to minor losses and adversity. The former is the appropriate and natural response to more profound or more enduring adversity. Though, of course, what constitutes profound adversity will vary enormously from person to person. An individual, for instance, raised to the expectation of stable and permanent employment may be truly heartbroken at the loss of a job. Another individual, raised to the notion that there’s always another job “around the corner” will, other things being equal, be less affected. And so on.
In this regard, it’s noteworthy that Partners’ comment refers to overactivity in BA 25. The use of the prefix over implies pathology, but in reality there is no yardstick to determine what would be a correct amount of activity for BA 25. All that can be said, on the basis of Mayberg et al’s findings, and subsequent BA 25 research, is that when a person is sad, there is more activity than when he is happy. So the use of the term “overactivity” is deceptive – sneaking in the notion of pathology without any genuine or valid reasons to consider it so. The “reasoning” here is:
– depression is an illness
– depression is correlated with high activity in BA 25
– therefore high activity in BA 25 is pathological
In other words, the contention of pathology rests on the assumption that depression is an illness. To turn around and use this falsely inferred pathology to prove that depression is an illness is obviously fallacious. It is also typical of the kind of circular reasoning that permeates psychiatric contentions. In reality, there is nothing in Mayberg et al or in subsequent research that warrants the conclusion that the increased activity in BA 25 is pathological or excessive.
. . . . . . . . . . . . . . . .
Schizophrenia linked to specific genes
This assertion, that schizophrenia is linked to specific genes, is frequently adduced in these debates, as evidence that “schizophrenia” is a real illness with a biological pathology. Here again, Partners do not provide any references in support of this assertion, but there have been a number of studies in the past fifteen years or so that have found links of this kind. However, in all cases, the correlations have been small. In other words, there are always a great many individuals who have been assigned the “schizophrenia” label, but who do not have the gene variant in question; and there are a great many who have the gene variant, but who do not acquire the label “schizophrenia”. To date, no genetic test has been found helpful in confirming or refuting a “diagnosis of schizophrenia”.
An additional problem arises here, in that the assertion that “schizophrenia has been linked to specific genes” is often interpreted as meaning that “schizophrenia” is a genetic disease, which it emphatically is not. To illustrate this, let’s look briefly at a real genetic illness: polycystic kidney disease (PKD). This is a well established genetic illness caused by cysts in the kidneys. The cysts progressively block the flow of blood through the kidneys, causing tissue death.
Most cases of PKD are caused by the defective gene (PKD-1). In polycystic kidney disease, the pathology occurs because the PKD-1 gene causes the nephrons to be made from cyst wall epithelium rather than nephron epithelium. And cyst wall epithelium produces fluid which accumulates in, and ultimately destroys, the nephrons and the kidney.
So the gene determines the structure of the nephron wall. This is the primary genetic effect. This structure causes the wall to produce fluid. As the nephrons become increasingly blocked, the kidneys produce less urine. So, reduced urination is a secondary effect of the gene PKD-1. Symptoms of PKD don’t usually emerge until adulthood, but about 25% of children with PKD1 experience pain and other symptoms. So a child growing up with polycystic kidney disease may feel sick much of the time. Such a child, other things being equal, is likely to be fussier and more distressed than other children, and it is entirely possible that one could find a weak correlational link between gene PKD-1 and childhood fussiness, though, of course, any search for such a correlation will be confounded by the obvious fact that children can be habitually fussy for other reasons. The fussiness would be a tertiary effect of the gene PKD1.
And from there the causal chain could continue in various ever-weakening directions. For instance, the child might become somewhat sad and despondent. Or it could be that the child received extra attention and comforting from his parents and was fairly content, and so on. Ultimately the outcome is impossible to predict with any kind of precision, and the best we can expect from genes vs. subsequent behavior studies are weak, tenuous correlations.
Cleft palate is another example of a pathology that is caused by a gene defect; actually a gene deletion. This condition results in a characteristically strained and nasal speech quality which can be quite stigmatizing. The nasal speech is a secondary effect of the gene deletion.
Children with this kind of speech are sometimes mocked and bullied by their peers. The child might react to this kind of stigmatizing by speaking as little as possible, by withdrawing socially, or in various other ways. These reactions would be considered tertiary effects of the defect. And so on. As with the PKD, each step in the chain takes us further from the genetic defect, and the statistical associations grow proportionally weaker, and it would be stretching the matter to say that the lack of speech was caused by the gene deletion. Nor would one conclude that the child’s social withdrawal was a symptom of a genetic disease. And this is true even though the link between the deletion and the cleft palate is clear-cut and direct.
In the same way, it is simply not tenable to claim that “schizophrenic” behaviors (e.g. disorganized speech) are symptoms of a genetic disease. This is particularly the case in that correlations between the “diagnosis” and genetic anomalies are typically very small. The effects of any minor genetic anomalies that might exist have had ample opportunity to be shaped by social and environmental factors, and these are more credible causal constructs.
“Schizophrenia” is not a unified condition. Rather, it is a loose collection of vaguely defined behaviors. For this reason, any genetic research done on this condition will inevitably result in conflicting and confusing results. It’s like looking for genetic similarities in all the people who play bridge, or read romance novels, visit libraries, play football, or whatever. If the sample sizes are large enough, and in genetic research sample sizes are often enormous, one could probably find small effects in all or most of these areas, but no one would conclude from this that these are genetically determined activities, much less illnesses.
A person’s ability to learn depends on two general factors: a) the structure of his brain, as determined by his DNA, and b) his experiences since birth.
One can’t learn to play the piano, for instance, unless one has appropriate neural apparatus, and fingers, both of which require appropriate DNA. But even a person with good genetic endowment in these regards, will never learn to play unless he is exposed to certain environmental factors. He must, at the very least, encounter a piano. In the same way, a person whose genetic endowment might be relatively marginal might become an excellent pianist, if he were to receive persistent environmental encouragement and support.
Similar reasoning can be applied to the behavior of not-being-“schizophrenic.” This behavior involves navigating the pitfalls of late adolescence/early adulthood, and establishing functional habits in interpersonal, occupational, and other important life areas. Obviously it requires appropriate neural apparatus, hence the weak correlations with genetic material, but equally clearly it calls for a nurturing childhood environment, with opportunities for emotional growth and acquisition of social, occupational, and other skills.
Given all of this, it’s not surprising that researchers are finding correlations between DNA variations and a “diagnosis” of schizophrenia, but given the number of links in the causal chain and the multiplicity of possible pathways at each link, it is also not surprising that the correlations are always found to be weak, and of little or no practical consequence.
Nor is it surprising that the correlations between being labeled “schizophrenic” and various psychosocial factors are by contrast generally strong. Having a schizophrenia label is correlated with childhood social adversity, childhood abuse and maltreatment, poverty, and a family history of migration.
. . . . . . . . . . . . . . . .
Generally similar considerations apply to Partners contentions with regards to “PTSD”, “autism”, suicide, and “OCD”, but space precludes a detailed discussion here.
. . . . . . . . . . . . . . . .
“Eric Kandel, MD, a Nobel Prize laureate and professor of brain science at Columbia University, says, ‘All mental processes are brain processes, and therefore all disorders of mental functioning are biological diseases…The brain is the organ of the mind. Where else could [mental illness] be if not in the brain?'”
Dr. Kandel (now 87 years old) is an eminent neuroscience researcher at Columbia University. There’s an extensive biography in Wikipedia. His early research focused on the neurophysiology of memory. He has received numerous awards, including the Nobel Prize in Physiology/Medicine (2000), and is widely published. His record of research achievements is enormous, and his knowledge and expertise are vast, but in the statement quoted by Partners, and, incidentally, by other psychiatry adherents, he is simply wrong.
Let’s take a closer look. Logically, the Kandel quote can be stated symbolically as: A is identical to B; therefore malfunctions or aberrations in A are malfunctions or aberrations in B.
On the face of it, this seems sound, and indeed, it is a valid inference in some situations. For instance, the furnace in a person’s home is the primary heating appliance; therefore, malfunctions in the furnace are malfunctions in the primary heating appliance. Indeed, in a simple example of this sort, the statement is tautological. We are simply substituting the synonyms furnace and primary heating appliance, and the inference contains no new information or insights. But the inference is fallacious in more complex matters.
Let’s concede, for the sake of discussion, that the premise of the Kandel quote is true, i.e., that all mental processes are brain processes. The term mental processes embraces a wide range of activities, including sensations, perceptions, thoughts, choices, positive feelings, negative feelings, hopes, beliefs, speaking, singing, general behavior, etc.
The term “disorders of mental functioning” is harder to define, but, again for the purposes of discussion, let’s accept the APA’s catalog as definitive in this regard. Let’s accept that anything listed in the DSM is a “disorder of mental functioning”.
It’s immediately obvious that some of the DSM entries are indeed the result of brain malfunctioning. In the text these are referred to as disorders due to a general medical condition or to the effects of a substance. But in the great majority of DSM labels, no such biological cause is identified, and so the conclusion in the Kandel quote would appear to call for some kind of evidence or proof. However, in the Kandel quote, the conclusion is not presented as something that has been, or even needs to be, proven. Rather, it is presented as a logical conclusion inherent in, and stemming directly from, the premise. And it is from this perspective that the Kandel quote needs to be evaluated.
To pursue this, let’s consider the example of “oppositional defiant disorder”. This is a disorder of mental functioning as defined above, because it is listed in the DSM. And according to Dr. Kandel’s “logic”, it is also therefore a “biological disease”. The “symptoms” of oppositional defiant disorder as listed in DSM-5 are:
Often loses temper.
Is often touchy or easily annoyed.
Is often angry and resentful.
Often argues with authority figures or, for children and adolescents, with adults.
Often actively defies or refuses to comply with requests from authority figures or with rules.
Often deliberately annoys others.
Often blames others for his or her mistakes or misbehavior.
Has been spiteful or vindictive at least twice within the past 6 months. (p 462)
Obviously for any of these behaviors to occur, there has to be corresponding neural activity. But there is no necessity that the neural activity is diseased or malfunctioning in any way. A child learning from his environment, developing his behavioral repertoire in accordance with the ordinary principles or learning, could acquire any or all of these behavioral habits without any malfunctioning in his neural apparatus. We acquire counterproductive habits as readily, and by essentially the same processes, as we acquire productive ones. In general, if a child discovers that he can acquire power and control in his environment by throwing temper tantrums, he will, other things being equal, acquire the habit of throwing temper tantrums. Similarly, if arguing with parents and other authority figures yields positive results, there is a good chance that this also will become habitual. And this is not because there is anything wrong with the child’s brain. Rather, it’s because his brain is functioning correctly. He is internalizing as habits those decisions and actions that pay off. It is often observed in child-raising practice that if you’re not training your children, they’re training you.
Similar observations can be made about the other seven “symptoms” of oppositional defiant disorder, and indeed all the DSM labels. A person with a perfectly normal-functioning brain can acquire the habits in question if the circumstances are conducive to this learning.
So to return to the question in the Kandel quote: “Where else could [mental illness] be if not in the brain?”, the answer is clear: In the self-serving and unwarranted perception of psychiatrists. Mental illness is the distorting lens through which psychiatrists view all problems of thinking, feeling, and behaving. It is the device they use to legitimize their drug-pushing and to maintain the fiction that they are practicing medicine.
. . . . . . . . . . . . . . . .
“You’re right that mental illness is also affected by social and environmental conditions–by a person’s disposition, or upbringing, or current environment. It’s also true that mental illness is affected by drug use (both prescribed and not prescribed). So are other medical conditions, such as heart disease and cancer.”
I’m not sure where Partners are coming from here, because I never made any such statement. In my view, which I have stated clearly on numerous occasions, “mental illness” is a psychiatric invention, self-servingly created to promote the spurious notion that all problematic thoughts, feelings, and/or behaviors are illnesses. And not just illnesses in some vague allegorical sense, but real illnesses “just like diabetes”, which need to be treated by medically trained psychiatrists with mood-altering drugs and high voltage electric shocks to the brain.
Partners’ vague concessions concerning environment, child-rearing, and drug effects is a fairly standard psychiatric sop, but doesn’t mitigate their earlier contentions on the “long history of biological evidence” and their uncritical endorsement of the logically spurious Kandel quote.
. . . . . . . . . . . . . . . .
“And it’s true that mental illness is often difficult to diagnose because of
1) the current limitations of the field of research. Thomas R. Insel, MD, director of the National Institute of Mental Health, for example, talks about how the diagnosis and treatment of mental illness today is where cardiology was 100 years ago, concluding that we need to continue scientific research of mental illnesses. (There’s a longer quote on this below.)”
And (from later in the comment)
“Longer aforementioned quote:
Take cardiology, Insel says. A century ago, doctors had little knowledge of the biological basis of heart disease. They could merely observe a patient’s physical presentation and listen to the patient’s subjective complaints. Today they can measure cholesterol levels, examine the heart’s electrical impulses with EKG, and take detailed CT images of blood vessels and arteries to deliver a precise diagnosis. As a result, Insel says, mortality from heart attacks has dropped dramatically in recent decades. ‘In most areas of medicine, we now have a whole toolkit to help us know what’s going on, from the behavioral level to the molecular level. That has really led to enormous changes in most areas of medicine,’ he says.
Insel believes the diagnosis and treatment of mental illness is today where cardiology was 100 years ago. And like cardiology of yesteryear, the field is poised for dramatic transformation, he says. ‘We are really at the cusp of a revolution in the way we think about the brain and behavior, partly because of technological breakthroughs. We’re finally able to answer some of the fundamental questions.'”
It is at least forty years since I started hearing about psychiatry’s great biological breakthroughs that were just around the proverbial corner, and the promise, if my readers will pardon the pun, is getting a little old.
What’s noteworthy, however, is that in other disciplines, where there is hope or expectation of breakthroughs, the proponents of these endeavors generally wait until the evidence is in, before implementing practices based on these hopes. In fact, to the best of my knowledge, psychiatry is the only profession whose entire work, indeed, whose entire conceptual framework, is based on “evidence” and “breakthroughs” that are not yet to hand.
Note also the truly exquisite contrast between Partners’ earlier and confident contention that “mental illnesses have a long history of biological evidence” with the assertion here that the “diagnosis” and “treatment” of “mental illness” today is where cardiology was 100 year ago.
Incidentally, Dr. Insel, former Director of the NIMH, also said:
“While DSM has been described as a ‘Bible’ for the field, it is, at best, a dictionary, creating a set of labels and defining each. The strength of each of the editions of DSM has been ‘reliability’ – each edition has ensured that clinicians use the same terms in the same ways. The weakness is its lack of validity. Unlike our definitions of ischemic heart disease, lymphoma, or AIDS, the DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure. In the rest of medicine, this would be equivalent to creating diagnostic systems based on the nature of chest pain or the quality of fever. Indeed, symptom-based diagnosis, once common in other areas of medicine, has been largely replaced in the past half century as we have understood that symptoms alone rarely indicate the best choice of treatment.” (Transforming Diagnosis, 2013)
And let us be quite clear. “Lack of validity” in this context means that the “diagnoses” don’t actually correspond to any disease entities in the real world. Note also that Dr. Insel didn’t say poor validity, or low validity. He said lack of validity – meaning none.
. . . . . . . . . . . . . . . .
Back to the Carolina Partners comment:
“2) mental illness symptoms often overlap with symptoms caused by other illnesses, for example, someone with cancer may also become depressed after diagnosis. Or someone’s fatigue may be caused by a vitamin deficiency, rather than by depression.
While considering all these factors, it is still completely inaccurate to state that there is no biological foundation for mental illnesses. They are not ‘make-believe’ diseases, but rather are caused by a variety of factors, including biological ones. As we understand more about mental illness through research we will (as we have with cardiology, for example) gain more precise vehicles for measuring and understanding the biological implications of these disorders.”
This is a little rambling, but let’s see if we can unravel it.
“… someone with cancer may also become depressed after diagnosis.”
This is true. In fact, I would say that most people who contract serious illness become somewhat sad and despondent. But this in no way establishes the notion that the sadness should be considered an additional illness.
“…someone’s fatigue may be caused by a vitamin deficiency, rather than by depression.”
This quote contains one of psychiatry’s core fallacies: that the various “mental illnesses” are the causes of their respective symptoms (as is the case in real illness). To illustrate the fallacy, consider the hypothetical conversation:
Client’s wife: Why is my husband so tired all the time?
Psychiatrist: Because he has an illness called major depressive disorder.
Client’s wife: How do you know he has this illness?
Psychiatrist: Because he is tired all the time.
Psychiatry defines major depression (the so-called illness) by the presence of five “symptoms” from a list of nine, one of which is fatigue, and then routinely adduces the “illness” to explain the symptoms. In reality, the “symptoms” are entailed in the definition of the “illness”, and the explanation is entirely spurious. There are many valid reasons why a person might feel fatigued, but none of these is because he “has a mental illness”. Mental illnesses are merely labels with no explanatory significance. And because of the inherent vagueness in the criteria, they’re not even good labels.
“…it is still completely inaccurate to state that there is no biological foundation for mental illnesses.”
As stressed above, there is a biological foundation to everything we do – every thought, every feeling, every eye blink, every action. But – and this is the point that seems to evade psychiatry – there is no good reason to believe that the various problems catalogued in the DSM are underlain by pathological biological processes. And there are lots of very good reasons to believe that they are not.
“They are not ‘make-believe’ diseases, but rather are caused by a variety of factors, including biological ones.”
I don’t think I’ve ever used the term “make-believe” to describe psychiatric “illnesses”, though I do routinely describe psychiatric labels as invented. The two terms are not synonymous. What psychiatry calls mental illnesses are actually nothing more than loose collections of vaguely-defined problems of thinking, feeling, and/or behaving. In most cases the “diagnosis” is polythetic (five out of nine, four out of six, etc.), so the labels aren’t coherent entities of any sort, let alone illnesses.
But the problems set out in the so-called symptom lists are real problems. That’s not the issue. I refer to these labels as inventions, because of psychiatry’s assertion that the loose clusters of problems are real diseases. In reality, they are not genuine diseases; they are inventions. They are not discovered in nature, but rather are voted into existence by APA committees.
“As we understand more about mental illness through research we will (as we have with cardiology, for example) gain more precise vehicles for measuring and understanding the biological implications of these disorders.”
But meanwhile psychiatry has made up its mind. Within psychiatric dogma, all significant human problems of thinking, feeling, and behaving are illnesses that need to be “treated” with drugs and electric shocks.
. . . . . . . . . . . . . . . . .
FINALLY
All of this is interesting, and I suppose it’s important to refute the more or less steady stream of unsubstantiated assertions, fallacious reasoning, and spin that flows from the psychiatric strongholds.
But meanwhile the carnage continues. There is abundant prima facie evidence that psychiatric drugs are causally implicated in the suicide/murders that have become almost daily occurrences here in the US. My challenge to organized psychiatry is simple: call publicly for an independent, definitive study to explore this relationship. And my challenge to rank and file psychiatrists is equally simple: pressure the APA to call for such a study. If what you are doing is unqualifiedly wholesome, safe, and effective, then what do you have to fear?
Thank You Dr Hickey.
by Phil Hickey on January 10, 2017
On January 2, 2017, I published a short post titled Carrie Fisher Dead at Age 60 on Behaviorism and Mental Health. The article was published simultaneously on Mad in America.
On January 4, a response from Carolina Partners was entered into the comments string on both sites.
Carolina Partners in Mental Healthcare, PLLC, is a large psychiatric group practice based in North Carolina. According to their website, they comprise 14 psychiatrists, 7 psychologists, 34 Advanced Practice Nurse Practitioners/Physicians Assistants, and 43 Therapists and Counselors. They have 27 North Carolina locations.
Partners’ comment consists essentially of unsubstantiated assertions, non sequiturs, and appeals to psychiatric authority. As such, it is fairly typical of the kind of “rebuttals” that psychiatry’s adherents routinely direct towards those of us on this side of the issue. For this reason, and also because it comes from, and presumably represents the views of, an extremely large psychiatric practice, it warrants a close look.
I will discuss each paragraph in turn.
“We strongly disagree with this article, which neglects a lot of important information and uses selective hearing to distort what Carrie Fisher was about and also to distort the evidence for mental illness as a real disorder.”
My Carrie Fisher article was brief (566 words), and was intended as a counterpoint to the very widespread obituaries that lionized her as a champion of “bipolar disorder”. The essential point of my article was that Ms. Fisher had been a victim of psychiatry, and like a great many such victims, died prematurely. Obviously I neglected a lot of important information. I could have gone into great length as to the recklessness of psychiatry assigning the bipolar label, with all its implications of helplessness, disempowerment, and “chemical imbalance” to a young woman who by her own account was, at the time, using any drugs she could get her hands on. But I felt that a brief and respectful statement of the facts was all that was needed.
. . . . . . . . . . . . . . . .
“Mental illnesses have a long history of biological evidence. For example, researchers have demonstrated that people with depression have an overactive area of the brain, called Brodmann area 25. Schizophrenia has been linked to specific genes, as PTSD and autism have been linked to specific brain abnormalities. Suicide has been linked to a decreased concentration of serotonin in the brain. OCD has been linked to increased activity in the basal ganglia region of the brain.”
Brodmann area 25 (BA25)
Partners did not provide a specific reference in support of this contention, but my best guess is that the reference is Mayberg, HS, et al (1999) Reciprocal Limbic-Cortical Function and Negative Mood: Converging PET Findings in Depression and Normal Sadness (Am J Psychiatry 1999; 156:675–682). Here’s the study’s primary conclusion:
“Reciprocal changes involving subgenual cingulate [which includes Brodmann area 25] and right prefrontal cortex occur with both transient and chronic changes in negative mood.”
What this means essentially is that negative mood, whether transient or enduring, is correlated with changes in both the subgenual cingulate (Brodmann area 25) and the right pre-frontal cortex, and that when the depression is relieved, the changes are reversed.
This, of course, is an interesting finding, but provides no evidence that depression, mild or severe, transient or enduring, is caused by a biological pathology.
The reality is that all human activity is triggered by brain activity. Every thought, every feeling, every action has its origins in the brain. I cannot lift a finger, blink an eye, scratch my head, or recall my childhood home without a characteristic brain function initiating and maintaining the action in question. Without stimuli from the brain, my heart will stop beating, my respiratory apparatus will shut down, and I will die, unless these functions are maintained by machines.
So there is absolutely no surprise in the discovery that sadness and despondency have similar neural triggers and maintainers. It would be amazing if they didn’t. But – and this is the critical point – this does not warrant the conclusion that sadness which crosses arbitrary and vaguely-defined thresholds of severity, duration, and frequency is best conceptualized as an illness caused by pathological or excessive activity in BA 25.
Depression is a normal state. It is the normal human reaction to significant loss and/or living in sub-optimal conditions/circumstances. It is also an adaptive mechanism, the purpose of which is to encourage us to take action to restore the loss and/or improve the conditions.
All consciously-felt human drives stem from unpleasant feelings. Thirst drives us to seek water; hunger, food; hypothermia, warmth; hyperthermia, coolness; danger, safety, etc. Sadness and despondency are no exceptions. They drive us to seek change, and have been serving the species well since prehistoric times.
But – as is the case with all the above examples – when a drive is not acted upon, for whatever reason, the unpleasant feelings worsen. Just as unrequited hunger and thirst increase in strength, so the depression drive when not requited deepens.
The reality is that most people deal with depression in appropriate, naturalistic, and time-honored ways. If the source of the depression is the loss of a job, they start job-hunting. If the source is an abusive relationship, they seek ways to exit or remediate the situation. If the source is a shortage of money, they seek ways to budget more sensibly, or increase their earnings; etc.
Depression, either mild or severe, transient or lasting, is not a pathological condition. It is the natural, appropriate, and adaptive response when a feeling-capable organism confronts an adverse event or circumstance. And the only sensible and effective way to ameliorate depression is to deal appropriately and constructively with the depressing situation. Misguided tampering with the person’s feeling apparatus is analogous to deliberately damaging a person’s hearing because he is upset by the noise pollution in his neighborhood, or damaging his eyesight because of complaints about litter in the street.
Our feeling apparatus is as valuable and adaptive as our other senses. But psychiatry routinely numbs, and in many cases permanently damages, this apparatus to sell drugs and to promote the fiction that they are real doctors. Their justification for this blatantly destructive activity hinges on the false notion that depression becomes a diagnosable illness when its severity crosses arbitrary and vaguely-defined thresholds. But deep despondency is no more an illness than mild despondency. The latter is the appropriate and adaptive response to minor losses and adversity. The former is the appropriate and natural response to more profound or more enduring adversity. Though, of course, what constitutes profound adversity will vary enormously from person to person. An individual, for instance, raised to the expectation of stable and permanent employment may be truly heartbroken at the loss of a job. Another individual, raised to the notion that there’s always another job “around the corner” will, other things being equal, be less affected. And so on.
In this regard, it’s noteworthy that Partners’ comment refers to overactivity in BA 25. The use of the prefix over implies pathology, but in reality there is no yardstick to determine what would be a correct amount of activity for BA 25. All that can be said, on the basis of Mayberg et al’s findings, and subsequent BA 25 research, is that when a person is sad, there is more activity than when he is happy. So the use of the term “overactivity” is deceptive – sneaking in the notion of pathology without any genuine or valid reasons to consider it so. The “reasoning” here is:
– depression is an illness
– depression is correlated with high activity in BA 25
– therefore high activity in BA 25 is pathological
In other words, the contention of pathology rests on the assumption that depression is an illness. To turn around and use this falsely inferred pathology to prove that depression is an illness is obviously fallacious. It is also typical of the kind of circular reasoning that permeates psychiatric contentions. In reality, there is nothing in Mayberg et al or in subsequent research that warrants the conclusion that the increased activity in BA 25 is pathological or excessive.
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Schizophrenia linked to specific genes
This assertion, that schizophrenia is linked to specific genes, is frequently adduced in these debates, as evidence that “schizophrenia” is a real illness with a biological pathology. Here again, Partners do not provide any references in support of this assertion, but there have been a number of studies in the past fifteen years or so that have found links of this kind. However, in all cases, the correlations have been small. In other words, there are always a great many individuals who have been assigned the “schizophrenia” label, but who do not have the gene variant in question; and there are a great many who have the gene variant, but who do not acquire the label “schizophrenia”. To date, no genetic test has been found helpful in confirming or refuting a “diagnosis of schizophrenia”.
An additional problem arises here, in that the assertion that “schizophrenia has been linked to specific genes” is often interpreted as meaning that “schizophrenia” is a genetic disease, which it emphatically is not. To illustrate this, let’s look briefly at a real genetic illness: polycystic kidney disease (PKD). This is a well established genetic illness caused by cysts in the kidneys. The cysts progressively block the flow of blood through the kidneys, causing tissue death.
Most cases of PKD are caused by the defective gene (PKD-1). In polycystic kidney disease, the pathology occurs because the PKD-1 gene causes the nephrons to be made from cyst wall epithelium rather than nephron epithelium. And cyst wall epithelium produces fluid which accumulates in, and ultimately destroys, the nephrons and the kidney.
So the gene determines the structure of the nephron wall. This is the primary genetic effect. This structure causes the wall to produce fluid. As the nephrons become increasingly blocked, the kidneys produce less urine. So, reduced urination is a secondary effect of the gene PKD-1. Symptoms of PKD don’t usually emerge until adulthood, but about 25% of children with PKD1 experience pain and other symptoms. So a child growing up with polycystic kidney disease may feel sick much of the time. Such a child, other things being equal, is likely to be fussier and more distressed than other children, and it is entirely possible that one could find a weak correlational link between gene PKD-1 and childhood fussiness, though, of course, any search for such a correlation will be confounded by the obvious fact that children can be habitually fussy for other reasons. The fussiness would be a tertiary effect of the gene PKD1.
And from there the causal chain could continue in various ever-weakening directions. For instance, the child might become somewhat sad and despondent. Or it could be that the child received extra attention and comforting from his parents and was fairly content, and so on. Ultimately the outcome is impossible to predict with any kind of precision, and the best we can expect from genes vs. subsequent behavior studies are weak, tenuous correlations.
Cleft palate is another example of a pathology that is caused by a gene defect; actually a gene deletion. This condition results in a characteristically strained and nasal speech quality which can be quite stigmatizing. The nasal speech is a secondary effect of the gene deletion.
Children with this kind of speech are sometimes mocked and bullied by their peers. The child might react to this kind of stigmatizing by speaking as little as possible, by withdrawing socially, or in various other ways. These reactions would be considered tertiary effects of the defect. And so on. As with the PKD, each step in the chain takes us further from the genetic defect, and the statistical associations grow proportionally weaker, and it would be stretching the matter to say that the lack of speech was caused by the gene deletion. Nor would one conclude that the child’s social withdrawal was a symptom of a genetic disease. And this is true even though the link between the deletion and the cleft palate is clear-cut and direct.
In the same way, it is simply not tenable to claim that “schizophrenic” behaviors (e.g. disorganized speech) are symptoms of a genetic disease. This is particularly the case in that correlations between the “diagnosis” and genetic anomalies are typically very small. The effects of any minor genetic anomalies that might exist have had ample opportunity to be shaped by social and environmental factors, and these are more credible causal constructs.
“Schizophrenia” is not a unified condition. Rather, it is a loose collection of vaguely defined behaviors. For this reason, any genetic research done on this condition will inevitably result in conflicting and confusing results. It’s like looking for genetic similarities in all the people who play bridge, or read romance novels, visit libraries, play football, or whatever. If the sample sizes are large enough, and in genetic research sample sizes are often enormous, one could probably find small effects in all or most of these areas, but no one would conclude from this that these are genetically determined activities, much less illnesses.
A person’s ability to learn depends on two general factors: a) the structure of his brain, as determined by his DNA, and b) his experiences since birth.
One can’t learn to play the piano, for instance, unless one has appropriate neural apparatus, and fingers, both of which require appropriate DNA. But even a person with good genetic endowment in these regards, will never learn to play unless he is exposed to certain environmental factors. He must, at the very least, encounter a piano. In the same way, a person whose genetic endowment might be relatively marginal might become an excellent pianist, if he were to receive persistent environmental encouragement and support.
Similar reasoning can be applied to the behavior of not-being-“schizophrenic.” This behavior involves navigating the pitfalls of late adolescence/early adulthood, and establishing functional habits in interpersonal, occupational, and other important life areas. Obviously it requires appropriate neural apparatus, hence the weak correlations with genetic material, but equally clearly it calls for a nurturing childhood environment, with opportunities for emotional growth and acquisition of social, occupational, and other skills.
Given all of this, it’s not surprising that researchers are finding correlations between DNA variations and a “diagnosis” of schizophrenia, but given the number of links in the causal chain and the multiplicity of possible pathways at each link, it is also not surprising that the correlations are always found to be weak, and of little or no practical consequence.
Nor is it surprising that the correlations between being labeled “schizophrenic” and various psychosocial factors are by contrast generally strong. Having a schizophrenia label is correlated with childhood social adversity, childhood abuse and maltreatment, poverty, and a family history of migration.
. . . . . . . . . . . . . . . .
Generally similar considerations apply to Partners contentions with regards to “PTSD”, “autism”, suicide, and “OCD”, but space precludes a detailed discussion here.
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“Eric Kandel, MD, a Nobel Prize laureate and professor of brain science at Columbia University, says, ‘All mental processes are brain processes, and therefore all disorders of mental functioning are biological diseases…The brain is the organ of the mind. Where else could [mental illness] be if not in the brain?'”
Dr. Kandel (now 87 years old) is an eminent neuroscience researcher at Columbia University. There’s an extensive biography in Wikipedia. His early research focused on the neurophysiology of memory. He has received numerous awards, including the Nobel Prize in Physiology/Medicine (2000), and is widely published. His record of research achievements is enormous, and his knowledge and expertise are vast, but in the statement quoted by Partners, and, incidentally, by other psychiatry adherents, he is simply wrong.
Let’s take a closer look. Logically, the Kandel quote can be stated symbolically as: A is identical to B; therefore malfunctions or aberrations in A are malfunctions or aberrations in B.
On the face of it, this seems sound, and indeed, it is a valid inference in some situations. For instance, the furnace in a person’s home is the primary heating appliance; therefore, malfunctions in the furnace are malfunctions in the primary heating appliance. Indeed, in a simple example of this sort, the statement is tautological. We are simply substituting the synonyms furnace and primary heating appliance, and the inference contains no new information or insights. But the inference is fallacious in more complex matters.
Let’s concede, for the sake of discussion, that the premise of the Kandel quote is true, i.e., that all mental processes are brain processes. The term mental processes embraces a wide range of activities, including sensations, perceptions, thoughts, choices, positive feelings, negative feelings, hopes, beliefs, speaking, singing, general behavior, etc.
The term “disorders of mental functioning” is harder to define, but, again for the purposes of discussion, let’s accept the APA’s catalog as definitive in this regard. Let’s accept that anything listed in the DSM is a “disorder of mental functioning”.
It’s immediately obvious that some of the DSM entries are indeed the result of brain malfunctioning. In the text these are referred to as disorders due to a general medical condition or to the effects of a substance. But in the great majority of DSM labels, no such biological cause is identified, and so the conclusion in the Kandel quote would appear to call for some kind of evidence or proof. However, in the Kandel quote, the conclusion is not presented as something that has been, or even needs to be, proven. Rather, it is presented as a logical conclusion inherent in, and stemming directly from, the premise. And it is from this perspective that the Kandel quote needs to be evaluated.
To pursue this, let’s consider the example of “oppositional defiant disorder”. This is a disorder of mental functioning as defined above, because it is listed in the DSM. And according to Dr. Kandel’s “logic”, it is also therefore a “biological disease”. The “symptoms” of oppositional defiant disorder as listed in DSM-5 are:
Often loses temper.
Is often touchy or easily annoyed.
Is often angry and resentful.
Often argues with authority figures or, for children and adolescents, with adults.
Often actively defies or refuses to comply with requests from authority figures or with rules.
Often deliberately annoys others.
Often blames others for his or her mistakes or misbehavior.
Has been spiteful or vindictive at least twice within the past 6 months. (p 462)
Obviously for any of these behaviors to occur, there has to be corresponding neural activity. But there is no necessity that the neural activity is diseased or malfunctioning in any way. A child learning from his environment, developing his behavioral repertoire in accordance with the ordinary principles or learning, could acquire any or all of these behavioral habits without any malfunctioning in his neural apparatus. We acquire counterproductive habits as readily, and by essentially the same processes, as we acquire productive ones. In general, if a child discovers that he can acquire power and control in his environment by throwing temper tantrums, he will, other things being equal, acquire the habit of throwing temper tantrums. Similarly, if arguing with parents and other authority figures yields positive results, there is a good chance that this also will become habitual. And this is not because there is anything wrong with the child’s brain. Rather, it’s because his brain is functioning correctly. He is internalizing as habits those decisions and actions that pay off. It is often observed in child-raising practice that if you’re not training your children, they’re training you.
Similar observations can be made about the other seven “symptoms” of oppositional defiant disorder, and indeed all the DSM labels. A person with a perfectly normal-functioning brain can acquire the habits in question if the circumstances are conducive to this learning.
So to return to the question in the Kandel quote: “Where else could [mental illness] be if not in the brain?”, the answer is clear: In the self-serving and unwarranted perception of psychiatrists. Mental illness is the distorting lens through which psychiatrists view all problems of thinking, feeling, and behaving. It is the device they use to legitimize their drug-pushing and to maintain the fiction that they are practicing medicine.
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“You’re right that mental illness is also affected by social and environmental conditions–by a person’s disposition, or upbringing, or current environment. It’s also true that mental illness is affected by drug use (both prescribed and not prescribed). So are other medical conditions, such as heart disease and cancer.”
I’m not sure where Partners are coming from here, because I never made any such statement. In my view, which I have stated clearly on numerous occasions, “mental illness” is a psychiatric invention, self-servingly created to promote the spurious notion that all problematic thoughts, feelings, and/or behaviors are illnesses. And not just illnesses in some vague allegorical sense, but real illnesses “just like diabetes”, which need to be treated by medically trained psychiatrists with mood-altering drugs and high voltage electric shocks to the brain.
Partners’ vague concessions concerning environment, child-rearing, and drug effects is a fairly standard psychiatric sop, but doesn’t mitigate their earlier contentions on the “long history of biological evidence” and their uncritical endorsement of the logically spurious Kandel quote.
. . . . . . . . . . . . . . . .
“And it’s true that mental illness is often difficult to diagnose because of
1) the current limitations of the field of research. Thomas R. Insel, MD, director of the National Institute of Mental Health, for example, talks about how the diagnosis and treatment of mental illness today is where cardiology was 100 years ago, concluding that we need to continue scientific research of mental illnesses. (There’s a longer quote on this below.)”
And (from later in the comment)
“Longer aforementioned quote:
Take cardiology, Insel says. A century ago, doctors had little knowledge of the biological basis of heart disease. They could merely observe a patient’s physical presentation and listen to the patient’s subjective complaints. Today they can measure cholesterol levels, examine the heart’s electrical impulses with EKG, and take detailed CT images of blood vessels and arteries to deliver a precise diagnosis. As a result, Insel says, mortality from heart attacks has dropped dramatically in recent decades. ‘In most areas of medicine, we now have a whole toolkit to help us know what’s going on, from the behavioral level to the molecular level. That has really led to enormous changes in most areas of medicine,’ he says.
Insel believes the diagnosis and treatment of mental illness is today where cardiology was 100 years ago. And like cardiology of yesteryear, the field is poised for dramatic transformation, he says. ‘We are really at the cusp of a revolution in the way we think about the brain and behavior, partly because of technological breakthroughs. We’re finally able to answer some of the fundamental questions.'”
It is at least forty years since I started hearing about psychiatry’s great biological breakthroughs that were just around the proverbial corner, and the promise, if my readers will pardon the pun, is getting a little old.
What’s noteworthy, however, is that in other disciplines, where there is hope or expectation of breakthroughs, the proponents of these endeavors generally wait until the evidence is in, before implementing practices based on these hopes. In fact, to the best of my knowledge, psychiatry is the only profession whose entire work, indeed, whose entire conceptual framework, is based on “evidence” and “breakthroughs” that are not yet to hand.
Note also the truly exquisite contrast between Partners’ earlier and confident contention that “mental illnesses have a long history of biological evidence” with the assertion here that the “diagnosis” and “treatment” of “mental illness” today is where cardiology was 100 year ago.
Incidentally, Dr. Insel, former Director of the NIMH, also said:
“While DSM has been described as a ‘Bible’ for the field, it is, at best, a dictionary, creating a set of labels and defining each. The strength of each of the editions of DSM has been ‘reliability’ – each edition has ensured that clinicians use the same terms in the same ways. The weakness is its lack of validity. Unlike our definitions of ischemic heart disease, lymphoma, or AIDS, the DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure. In the rest of medicine, this would be equivalent to creating diagnostic systems based on the nature of chest pain or the quality of fever. Indeed, symptom-based diagnosis, once common in other areas of medicine, has been largely replaced in the past half century as we have understood that symptoms alone rarely indicate the best choice of treatment.” (Transforming Diagnosis, 2013)
And let us be quite clear. “Lack of validity” in this context means that the “diagnoses” don’t actually correspond to any disease entities in the real world. Note also that Dr. Insel didn’t say poor validity, or low validity. He said lack of validity – meaning none.
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Back to the Carolina Partners comment:
“2) mental illness symptoms often overlap with symptoms caused by other illnesses, for example, someone with cancer may also become depressed after diagnosis. Or someone’s fatigue may be caused by a vitamin deficiency, rather than by depression.
While considering all these factors, it is still completely inaccurate to state that there is no biological foundation for mental illnesses. They are not ‘make-believe’ diseases, but rather are caused by a variety of factors, including biological ones. As we understand more about mental illness through research we will (as we have with cardiology, for example) gain more precise vehicles for measuring and understanding the biological implications of these disorders.”
This is a little rambling, but let’s see if we can unravel it.
“… someone with cancer may also become depressed after diagnosis.”
This is true. In fact, I would say that most people who contract serious illness become somewhat sad and despondent. But this in no way establishes the notion that the sadness should be considered an additional illness.
“…someone’s fatigue may be caused by a vitamin deficiency, rather than by depression.”
This quote contains one of psychiatry’s core fallacies: that the various “mental illnesses” are the causes of their respective symptoms (as is the case in real illness). To illustrate the fallacy, consider the hypothetical conversation:
Client’s wife: Why is my husband so tired all the time?
Psychiatrist: Because he has an illness called major depressive disorder.
Client’s wife: How do you know he has this illness?
Psychiatrist: Because he is tired all the time.
Psychiatry defines major depression (the so-called illness) by the presence of five “symptoms” from a list of nine, one of which is fatigue, and then routinely adduces the “illness” to explain the symptoms. In reality, the “symptoms” are entailed in the definition of the “illness”, and the explanation is entirely spurious. There are many valid reasons why a person might feel fatigued, but none of these is because he “has a mental illness”. Mental illnesses are merely labels with no explanatory significance. And because of the inherent vagueness in the criteria, they’re not even good labels.
“…it is still completely inaccurate to state that there is no biological foundation for mental illnesses.”
As stressed above, there is a biological foundation to everything we do – every thought, every feeling, every eye blink, every action. But – and this is the point that seems to evade psychiatry – there is no good reason to believe that the various problems catalogued in the DSM are underlain by pathological biological processes. And there are lots of very good reasons to believe that they are not.
“They are not ‘make-believe’ diseases, but rather are caused by a variety of factors, including biological ones.”
I don’t think I’ve ever used the term “make-believe” to describe psychiatric “illnesses”, though I do routinely describe psychiatric labels as invented. The two terms are not synonymous. What psychiatry calls mental illnesses are actually nothing more than loose collections of vaguely-defined problems of thinking, feeling, and/or behaving. In most cases the “diagnosis” is polythetic (five out of nine, four out of six, etc.), so the labels aren’t coherent entities of any sort, let alone illnesses.
But the problems set out in the so-called symptom lists are real problems. That’s not the issue. I refer to these labels as inventions, because of psychiatry’s assertion that the loose clusters of problems are real diseases. In reality, they are not genuine diseases; they are inventions. They are not discovered in nature, but rather are voted into existence by APA committees.
“As we understand more about mental illness through research we will (as we have with cardiology, for example) gain more precise vehicles for measuring and understanding the biological implications of these disorders.”
But meanwhile psychiatry has made up its mind. Within psychiatric dogma, all significant human problems of thinking, feeling, and behaving are illnesses that need to be “treated” with drugs and electric shocks.
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FINALLY
All of this is interesting, and I suppose it’s important to refute the more or less steady stream of unsubstantiated assertions, fallacious reasoning, and spin that flows from the psychiatric strongholds.
But meanwhile the carnage continues. There is abundant prima facie evidence that psychiatric drugs are causally implicated in the suicide/murders that have become almost daily occurrences here in the US. My challenge to organized psychiatry is simple: call publicly for an independent, definitive study to explore this relationship. And my challenge to rank and file psychiatrists is equally simple: pressure the APA to call for such a study. If what you are doing is unqualifiedly wholesome, safe, and effective, then what do you have to fear?
Thank You Dr Hickey.
Monday, November 14, 2016
Senator McCain Introduces Bill Calling For VA Study RE: Psychiatric Drugs Causing Suicides
madinamerica
Neuroleptic Drugs, Akathisia, and Suicide and Violence
Thirty-three years ago, in August 1983, an article titled Suicide Associated with Akathisia and Depot Fluphenazine Treatment appeared in the Journal of Clinical Psychopharmacology. The authors were Katherine Shear, MD, Allen Frances, MD, and Peter Weiden, MD.
Here are some quotes, interspersed with my comments/observations:
"Akathisia is a common and distressing side effect of neuroleptic medication that can be difficult to recognize and treat. Several previous reports mention maladaptive behavioral consequences, such as poor compliance with prescribed medication and aggressive or self-destructive outbursts. We are reporting suicides in two young Hispanic men who had developed severe akathisia after treatment with depot fluphenazine. Depression with suicidal behavior has been observed following fluphenazine injection, but suicide associated with akathisia has not been previously noted."
Fluphenazine is a neuroleptic drug of the phenothiazine class that was introduced in 1959. It is marketed as Prolixin and other brand names, and according to Wikipedia, is on the WHO's "List of Essential Medicines, most important medications needed in a basic health system."
The "treatment" used in each case was a depot injection of fluphenazine. This is a long-lasting injection, typically 30 days, in which the drug is lodged in a dermal or muscular mass from which it is slowly drawn into the blood stream. (Hence depot: a place where goods are stored for later distribution.)
Depot injections have some obvious convenience value, but in psychiatry are usually used to ensure compliance. Their major downside is that if the person has an adverse reaction to the drug, there's no way to remove the stored chemicals from his body.
The authors may be correct in stating that this is the first published report of suicide associated with akathisia, but it is not the first report of suicide associated with fluphenazine. Seventeen years earlier, Dorothy West, MD, had published the following letter in the British Journal of Psychiatry, 117 (1970), 718-9:
Dangers of Fluphenazine
Dear Sir,
A new drug is being widely used in the treatment of mental illness. It is long-acting and used by injection – its name is fluphenazine (Moditen). Is this the thalidomide of the 70's? I would like to have the opinion of other doctors. Whilst it is still new maybe we are lulled into a false sense of security, but are we justified in using a drug, which may take up to six weeks to eradicate from the tissues, without being sure of its safety? Its side effects alone are legion. A study of 13 papers gives the following:
Common side-effects reported are – lethargy, drowsiness, dizziness, muscular inco-ordination, paraesthesia, hypotension, blurring of vision, dryness of mouth, malaise, feelings of tension, confusion, nausea, vomiting, and aches and pains.
Parkinsonism is extremely common. Incidence in reports varies from 100 per cent to 24 per cent with many reports around 50 per cent. Depression is quite common and tends to be severe – 5 suicides reported and two suicide attempts. Other reported side-effects include psychotic relapse and glaucoma.
Dorothy West
. . . . .
Back to the Shear, Frances, and Weiden paper:
CASE NO. 1
"A 23-year-old single unemployed Hispanic man had been socially withdrawn, blunted in affect, and thought disordered since his early teenage years. He was intermittently delusional with auditory hallucinations which responded to phenothiazines. He was treated in a day hospital after one of multiple hospitalizations; depot fluphenazine was used because of medication noncompliance. He received two injections of 25 mg of fluphenazine decanoate separated by 1 week, with noticeable improvement in his psychotic symptoms. He also developed akathisia and was prescribed trihexyphenadyl, 2 mg twice a day, which he probably did not take. There was no improvement in his akathisia and no anticholinergic side effects. He soon stopped attending the day hospital and a family member called a week later to say that the man had killed himself by jumping off the roof of their building. He had given no indication of being suicidal and his family believed the increased 'nervousness' had driven him to this desperate measure. The patient had no previous history of suicidal behavior and did not drink alcohol or use drugs."
So, we have a young man who has been socially withdrawn and joyless since his early teens. Not surprisingly his perceptions and thinking patterns deviated from the conventional. For reasons unknown he came within the orbit of psychiatry, and had had extensive contact with the psychiatric system. He was given two depot injections of fluphenazine one week apart. His "psychotic symptoms" improved, but he developed akathisia. He was prescribed an anticholinergic agent to combat the akathisia, but apparently this was ineffective, or as the authors suggest, he didn't take it. In any event, a week later he killed himself by jumping from the roof of a building.
We don't know if the fluphenazine was administered involuntarily, but we do know that he had taken phenothiazine in the past and had been noncompliant. So it is reasonable to assume that there was some adverse effect. Did the day hospital psychiatrists explore the reason for this "noncompliance"? In any event, given the outcome, the phrase "depot fluphenazine was used because of medication noncompliance" is a haunting and compelling testament to psychiatric arrogance. This anonymous young man was clearly prone to acute akathisia, and his "noncompliance" was a sensible and correct response to the neuro-poisoning he was receiving from psychiatrists. He stopped attending the day hospital (again, understandably),but he had no way to get the drug out of his body. The trihexyphenidyl is an anticholinergic agent and might have mitigated the akathisia. Or perhaps he took it and it was not effective, as is frequently the case.
CASE NO. 2
"A 36-year-old non-English speaking Hispanic man was seen once in our walk-in clinic because of severe restlessness and leg cramps. Intermittent somatic symptoms and nervousness began shortly after he arrived in the United States 8 months earlier. When the symptoms worsened, he began a series of visits to hospital emergency rooms and private psychiatrists. Three weeks before the walk-in visit a Spanish-speaking psychiatrist diagnosed paranoid schizophrenia and administered depot fluphenazine. Following this injection, the patient developed a dystonic reaction and then began to complain continuously of leg cramps and restlessness. In the ensuing weeks he received numerous drugs from emergency room or private physicians, some given by injection and some by prescription. He brought bottles of thiothixene, chlorazepate, amitriptyline, meprobamate, and lorazepam to the clinic. He was agitated, paced, and begged for help. He denied symptoms of depression or suicidal ideation. He claimed he was devoted to his wife and 9-year-old daughter, but he felt his unbearable symptoms would never go away. He made good contact in a translated interview and showed no thought disorder, hallucinations, or delusions. Thorough medical examination was negative except for the parkinsonian symptoms. He had no prior history of psychiatric treatment and the family history was negative for depression, nervousness, and significant psychiatric or medical illness. Since the diagnosis was uncertain, plans were made to discontinue all medication and a follow-up appointment was scheduled. The next day he killed himself without warning by jumping in front of a subway train."
The 36-year-old man had come to the US eight months earlier, and had begun to experience "somatic symptoms and nervousness". This seems hardly surprising in someone who is having to adapt to a new environment, but we are provided no details with regards to his psychosocial context, other than the fact that he had a wife and 9-year-old daughter, and that he didn't speak English. What we do know is that he visited "emergency rooms and private psychiatrists" to help with "somatic symptoms and nervousness". One of the psychiatrists "diagnosed paranoid schizophrenia", and gave him a depot injection of fluphenazine. He developed severe akathisia, and continued to visit emergency rooms and private psychiatrists in an attempt to gain some relief. During this period he received "numerous drugs" from these sources, some by injection, some by prescription. At this point he came to the authors' walk-in clinic.
"He was agitated, paced, and begged for help."
and
"He denied symptoms of depression or suicidal ideation. He claimed he was devoted to his wife and 9-year-old daughter, but he felt his unbearable symptoms would never go away."
Plans were made to discontinue all the drugs, which the authors euphemistically refer to as medications, but it was too little, too late. He jumped to his death in front of a train the next day.
So, we have a healthy young man, devoted to his wife and daughter, who seeks medical help for what were probably stress-related "somatic complaints and nervousness". Psychiatrists throw a bewildering array of drugs at him, including a depot injection of fluphenazine, which results in his death. And the only reason we know about this forgotten victim of psychiatry is because the authors wrote up and published the case. How many other thousands have died from the same kind of irresponsible drug-pushing; from the same arrogant conviction that for every human problem, psychiatry has a "safe and effective" pill?
. . . . .
Here are some more quotes from the Shear et al article:
"Akathisia is an intensely unpleasant feeling characterized by muscle discomfort, inability to sit still, continuous agitation, restlessness, and fidgety feelings. Sleep may be disturbed by an inability to lie down. Some patients say they feel like jumping out of their skin"
"The estimated incidence of akathisia with neuroleptic use ranges from 20 to 45%. Several studies using depot fluphenazine report an incidence around 35%."
"Akathisia is a distressing symptom which may be difficult to diagnose and treat. Restlessness may be mistaken for anxiety and clinicians may err by raising neuroleptic dosage."
"Sometimes the only effective treatment is withdrawal of the neuroleptic. Although we cannot be sure that akathisia caused the deaths of our patients, akathitic symptoms seemed to be immediate precipitants of suicidal behavior. We urge clinicians to be alert to the discomfort of akathisia and to treat it aggressively. If treatment with anticholinergics or γ-aminobutyric acid agonists fails or symptoms are especially severe, hospitalization may be indicated."
It is clear that the authors are leaning heavily towards the conclusion that neuroleptic-induced akathisia was the immediate precipitant of both suicides.
OTHER SIMILAR REPORTS
Several similar reports have appeared in the literature for decades. Here are some examples, with relevant quotes:
Van Putten, T., MD, The Many Faces of Akathisia, Comprehensive Psychiatry, 1975, 16(1):
"AKATHISIA, a common side effect of neuroleptic therapy, is an emotional state and 'refers not to any type or pattern of movement, but rather to a subjective need or desire to move.'"
"A 44-year-old woman with hebephrenic schizophrenia started to bang her head against the wall three days after an injection of 25 mg of fluphenazine enanthate. Her only utterance was: 'I just want to get rid of this whole body.'"
"Akathisia is often associated with strong affects of fright, terror, anger or rage, anxiety, and vague somatic complaints."
"On this regime, she usually developed an episode of akathisia during the week following her injection. She described several such episodes as follows: 'I just get these attacks of tension. I don't feel right. My stomach feels strange. It's like I'm churning inside. I feel hostile and I hate (with intense affect) everybody."
"Patients have described the inner restlessness and agitation of akathisia in many other ways, such as: 'My nerves are just jumping' I feel like I'm wired to the ceiling; I just feel impatient and nasty. I can't concentrate; it's like I got ants in my pants; my nerves are raw; I just feel on edge; I feel just nasty; I feel like jumping out of my skin; if this feeling continues, I would rather be dead. I can't describe the feelings; I'm quivery from the waist up; I want to climb the walls; I feel all revved up; it's like I got diaper rash inside.'"
"Patients with severe akathisia, however, cannot sit quietly for more than a few seconds at a time, and at times the 'impatience musculaire' can result in running, agitated dancing, or rocking."
"Akathisia is tolerated very poorly by hostile paranoid patients in that they tend to misinterpret the inner agitation of akathisia as further proof that they are being poisoned or controlled by outside malevolent forces."
Note the presumably unintended irony in the word misinterpret. In reality, they are being poisoned and controlled by outside forces!
. . . . .
Keckich, W., MD: Neuroleptics: Violence as a Manifestation of Akathisia, JAMA, 1978, Nov 10 (240) 20, 2185:
"NEUROLEPTIC medications (eg, phenothiazines, butyrophenones) are used in medicine to control psychotic symptoms and concomitant agitated and violent behavior. They also are used to control anxiety and agitation whenever minor tranquilizers (eg, benzodiazepines) would be inappropriate. Development of akathisia as a parkinsonian side effect is confirmed in the use of these drugs. Akathisia is a condition that gives rise to the subjective desire to be in constant motion, with a feeling of inner agitation and muscle tension. The patient cannot sit still and paces constantly"
"One week later the patient reported that he was more agitated at night. Since it was not known at the time that akathisia was beginning, haloperidol treatment was increased to 4 mg at bedtime to decrease the agitation. Four days later, after his evening dose of 4 mg of haloperidol, he became uncontrollably agitated, could not sit still, and paced for several hours. He complained of tightness in his muscles, rigidity, a jumpy feeling inside, and violent urges to assault anyone near him. This culminated in an assault on his dog with an intent to kill. He became frightened over his loss of control and came to the emergency room. He was given 50 mg of thioridazine hydrochloride, which brought the hostility under control but did not remove it.
He subsequently discontinued the treatment with imipramine and haloperidol. The following morning he reported that the muscle tightness, jumpy feelings, and hostility were decreased but still present. Three days after drug treatment was discontinued all of the symptoms had ceased, and he was at his baseline of difficulty once again. The half-life of haloperidol is approximately 24 hours, and this symptom relief coincided with expected excretion of the drug.
In retrospect it was apparent that he had experienced increasing akathitic side effects from the haloperidol medication, which accounted for his increasing night-time agitation and culminated in a stimulation of violent and aggressive activity."
. . . . .
Schulte, JL, MD, Homicide and Suicide Associated with Akathisia and Haloperidol, American Journal of Forensic Psychiatry, Jan 1985, 6(2):
"The following five cases are reported to bring attention to the potential for severe violence, as a result of akathisia, following such administration of a neuroleptic for acute psychiatric symptoms. Particular emphasis is directed to an experience of sensory dissociation associated with the uncomfortable physical reactions, resulting in extreme acts of physical violence."
CASE NO. 1
"A 23-year-old married, Salvadorian-born male, with a four-day history of progressive paranoia and disorganized behavior, had been taken by the police department to a hospital at the request of his parents. The physician insisted he receive an injection of haloperidol in the emergency room while awaiting admission to the psychiatric unit where he had previously been a patient on a number of occasions.
He tried to resist but felt he had no option with the staff and police surrounding him. He felt he was being unnecessarily delayed in being admitted to the inpatient unit. In addition, he felt he had been lied to, in that apparently he had been told he was going to see his wife who had deserted him approximately 48 hours earlier. He then escaped from the emergency room and the authorities, ran several miles to a park, tried to get a policeman to help him, escaped again and totally disrobed. Within the next 45-minute period of time, he assaulted one woman who was walking her dog and attempted to rape her. When pulled off by the husband, he proceeded down the street, broke down the front door of a house where an 81-year-old lady was sleeping. He severely beat her with his fists, 'to a pulp', by his own description. Following which he found knives and stabbed her repeatedly, resulting in her death. Then, after being confronted in the street by a policeman who sprayed him with Mace, he returned through the house, exiting the back door where he ran into another woman with her child. He repeatedly stabbed the woman in front of the child, whereupon he moved on to the next person he encountered, a woman whom he severely assaulted and stabbed to the extent that an eye was lost and an opening into the anus was created resulting in major surgery and serious residual problems, including a colostomy. He was then finally captured and subdued by eight policemen and hospitalized.
He had ten previous psychiatric hospitalizations between 1975 and the present. All of these hospitalizations have been only a matter of hours to several days. He would always be placed on medication and released, following which he would stop taking the medication and go along until another upheaval would occur.
He had a history of problems with anger and acute paranoid beliefs leading to hyperactive behavior and one incident in which it was reported he tried to choke one of his brothers.
His description of his mental status at the time of his offense is quite striking. He describes himself as feeling almost like a spectator in a movie. He makes a point of describing how he had lost all sense of caring about anything or anyone in life. Additionally, he describes a feeling of loss of physical sensation, including feeling nothing when maced by the police. He felt enormous energy with a feeling of needing to rid himself of it.
He gives the history of having been picked up by the police on a traffic violation in 1979 and placed in jail for the first time in his life. He became angry and was given a series of haloperidol injections, becoming progressively more agitated and unmanageable to the point he was rolled up in a mattress and handcuffed in order to be transported to a psychiatric inpatient unit. In 1980, during another hospitalization, he was, despite his protests, changed from chlorpromazine to haloperidol and within hours became totally unmanageable, requiring six individuals to subdue him and place him in seclusion and restraint." [Emphasis added]
It is noteworthy that this individual asked not to be changed from chlorpromazine to haloperidol, but his request was ignored.
Eight years later, Herrera et al confirmed in a controlled study that an increase in violent behavior was more likely with haloperidol than with chlorpromazine. Apparently, the individual had some intuitive awareness of this from previous experience, but as is often the case, the psychiatrists discounted his protests and gave him the haloperidol anyway.
Here are two quotes from the Herrera et al study:
"We found in a controlled study that some patients have a marked increase in violence when treated with moderately high-dose haloperidol."
"…these patients did not show an increase in violence during a placebo period, nor did they have a history of violent behavior."
Back to the Schulte JL article:
CASE NO. 2
"A 30-year-old man with a history of mental illness dating back seven years, with hospitalizations in three other states, was admitted to the hospital on six counts of burglary. His diagnosis was paranoid schizophrenia, and he had been found not guilty by reason of insanity by the courts. The admission note by the psychiatrist stated, 'He is somewhat paranoid, but says he has side effects from most tranquilizers.' On the third day of hospitalization, he was referred to the psychiatrist by nurses because of difficulty getting to sleep. No evidence of aggressiveness or self-injurious behavior was charted that day in the nurses' notes. The psychiatrist prescribed haloperidol, 5mg. three times a day, which was begun the next day, with three doses administered with Cogentin, 2mg twice a day. Nurses' notes that day stated, 'He was very anxious about being in the hospital and threatened to kill himself if he gets up the nerve.' At 10:45 p.m., notes stated, 'He has regressed during this shift in all assessment areas. His hygiene is poor, and he is irresponsible, e.g., lying on the floor without shoes or socks.' He refused medication initially at 5 p. m., and stated that phenothiazines, 'fuck me up.' He finally took the medication but then stated angrily, 'Now I'll really get crazy.' He ranted loudly and profanely for 30 minutes. He took his 9 p.m. medication and started his haranguing again, only louder and more threatening. 'l'll kill all of you mother-fuckers before I leave here,' He was found in his room at 6:50 a.m., having hung himself with a bed sheet. A letter from his attorney to the hospital had stated that 'medications caused him problems (l should perhaps state that by medications I mean psychotropic drugs).'" [Emphasis added]
CASE NO. 3
"A 52-year-old male first came to psychiatric attention eleven years earlier following an assault on his wife. He had delusions of cancer, a belief he would die and felt sexually inadequate.
He had been unsuccessfully treated with Lithium and antidepressants, as well as various tranquilizers. He had continually been an inpatient or in board and care facilities, and three and one-half months earlier, he had his medications changed to 10mg. of Haloperidol in the a.m. and 40mg. of Haloperidol at hour of sleep, with 2mg.of Artane twice daily. Each month he stated he complained to his psychiatrist of severe restlessness. He stated he had to roll over and over in bed at night and usually would be unable to get to sleep until 3 or 4 a.m. During the day, he would try to lie down but couldn't because of his severe uncomfortableness. He described after being turned down again by the psychiatrist, he became despondent and angry, lost hope and decided if he could not ever even sleep like the rest of his boarding home mates that life wasn't worthwhile. He secured a knife and repeatedly stabbed himself in the abdomen, was rushed to the hospital and barely survived. He remarked he could never even feel the knife when stabbing himself." [Emphasis added]
. . . . .
Van Putten, T. MD and Marder, SR, MD, Behavioral Toxicity of Antipsychotic Drugs, J Clin Psychiatry, September 1987, 48: 9 (Suppl):
"The subjective restlessness of akathisia is usually accompanied by telltale foot movements: rocking from foot to foot while standing or walking on the spot. Akathisia is strongly associated with depression and dysphoric responses to neuroleptics and has even been linked to suicidal and homicidal behavior in extreme cases."
"The aforementioned case literature reads convincingly: it is reasonable to conclude that akathisia, in the extreme case, can drive people to suicide or homicide."
. . . . .
Crowner, ML, Douyon, R, et al, Akathisia and violence Psychopharmacology Bulletin, 1990: 26(1): 115-7:
"Akathisia is a common side effect of neuroleptic drugs that may present with behavioral disturbances. There have been preliminary reports on the association between violence and akathisia. We report the first observational study of this relationship. Patients studied were from a special unit for violent patients. A closed-circuit television camera was installed in each of the corners in its dayroom. Incidents of assault plus the 5 minutes preceding each assault were recorded on videotape. Participants and bystanders were rated for the motor component of akathisia. For each of nine incidents, we compared the akathisia scores for participants and for bystanders. Both victims and assailants were akathisic before about half of all incidents; bystanders rarely were. The classification of the movements we rated and the implications for further studies are discussed."
The extraordinary irony here is that the individuals in this study "were from a special unit for violent patients," but in fact the drug used to control this behavior was actually precipitating more violence!
. . . . .
Galynker, I, MD, PhD and Nazarian, D, MD, letter to the editor, Journal of Clinical Psychiatry, 1997, 58: 31-32:
"Case Report. Mr. A, a 47-year-old white man with a diagnosis of bipolar mood disorder, was brought to the emergency room because he was screaming in the streets. Mr. A had over 30 past psychiatric admissions associated with agitation and violence and was often discharged against medical advice. He was nearly always noncompliant with his antipsychotic medications, claiming that they made him 'jump and lose my temper.' Prior to the present admission, Mr. A's daily medications included haloperidol 20 mg, lithium carbonate 1500 mg, divalproex sodium 500 mg, and benztropine 1 mg. At admission, the patient was grandiose, had loud and pressured speech, and admitted he was not taking haloperidol. He was given haloperidol 15 mg q.h.s. and benztropine 1 mg q.a.m. Within 24 hours he started pacing; became restless, agitated, and violent; complained of feeling 'jumpy'; and attacked a staff member. On Day 5 of his hospitalization, haloperidol and benztropine were discontinued; chlorpromazine was started, and the dose was increased to 950 mg/day. Mr. A, although sedated, remained threatening and violent. On Day 13, chlorpromazine was discontinued, and haloperidol was restarted at a higher dose of 15 mg p.o. b.i.d. Mr. A again complained of 'jumpiness' and punched a television cabinet, causing a self-inflicted fracture. On hospital Day 17, owing to an error, haloperidol was discontinued. The patient became calmer, less irritable, displayed no angry outbursts, and required no further room restrictions. After 5 days, when the error was discovered, haloperidol was restarted at a lower daily dose of 10 mg. Within 3 days, the patient became violent and required room restriction. Haloperidol was then discontinued, the patient's agitation and violence resolved, and a week later he was discharged. His daily medications were lithium carbonate 1500 mg (serum level = 0.9mEq/L; this dose had not been changed during his hospitalization), lorazepam 1 mg, and divalproex sodium 500 mg. On these mediations, he remained well 6 months postdischarge, his longest period as an outpatient."
In their commentary, the authors point out:
"The fact that the jumpiness occurred with haloperidol and not with chlorpromazine is another factor indicative that Mr. A has exhibited akathisia rather than nonspecific activation of mania; this is because akathisia is more common with higher potency as compared with low-potency neuroleptics."
and, with more candor than one customarily finds in psychiatry:
"One can also speculate that Mr. A's rocky clinical history was related to aggressive behavior perpetuated by antipsychotic administration."
And it is worth remembering that Mr. A's "rocky clinical history" entailed "over 30 past psychiatric admissions associated with agitation and violence".
. . . . .
So, since at least the early 80's, individual psychiatrists have been drawing attention to the fact that neuroleptic drugs induce akathisia in many cases, and that in some cases this can precipitate suicide and/or homicide.
Akathisia & Antidepressants
Although it is well known that neuroleptic drugs cause akathisia, the link between antidepressants and this condition is less widely appreciated. The Wikipedia article on akathisia contains this:
"Antidepressants can also induce the appearance of akathisia, due to increased serotonin signalling within the CNS."
. . . . .
Hamilton, MS, MD, Obler, LA, Akathisia, suicidality, and fluoxetine, J Clin Psychiatry, 1992, Nov 53(11), 401-406, write:
"The propose[d] link between fluoxetine and suicidal ideation is explained by fluoxetine-induced akathisia and other dysphoric extrapyramidal reactions."
and
"The literature suggests that fluoxetine-induced extrapyramidal reactions may be a mediator of de novo suicidal ideation."
Fluoxetine is an SSRI, marketed as Prozac, Sarafem, and other names.
. . . . .
Wirshing, WC, MD, Van Putten, T, MD, Rosenberg, J, MD, et al, Fluoxetine, Akathisia, and Suicidality: Is There a Causal Connection?, Arch Gen Psychiatry, 1992, 49(7), 580-581, write:
"We have now had experience with five such patients. All were women. None had a history of significant suicidal behavior; all described their distress as an intense and novel somatic-emotional state; all reported an urge to pace that paralleled the intensity of the distress; all experienced suicidal thoughts at the peak of their restless agitation; and all experienced a remission of their agitation, restlessness, pacing urge, and suicidality after the fluoxetine was discontinued. We describe herein five cases of what we think might be fluoxetine-induced akathisia accounting for suicidal ideation."
Eikelenboom-Schieveld, SJM, Lucire, Y, MD, Fogleman, J, PhD, The relevance of cytochrome P450 polymorphism in forensic medicine and akathisia-related violence and suicide, Journal of Forensic and legal Medicine, 2016, 41. 65-71, wrote:
"Antidepressants have been reported as causing suicide and homicide and share the class attribute of frequently producing akathisia, a state of severe restlessness associated with thoughts of death and violence."
and
"In this paper, we report our investigation into adverse drug reactions/interactions in three persons who committed homicide, two also intending suicide, while on antidepressants prescribed for stressful life events"
and
"Three persons committed homicide, two of which intended to commit suicide. None had been aggressive or mentally ill before getting medication. None had known that they needed to take medication regularly or how to stop taking it safely. None improved on medication, and no prescriber recognized their complaints as adverse drug reactions or was aware of impending danger. Interviews elicited accounts of restlessness, akathisia, confusion, delirium, euphoria, extreme anxiety, obsessive preoccupation with aggression, and incomplete recall of events. Weird impulses to kill were acted on without warning. On recovery, all recognized their actions to be out of character, and their beliefs and behaviours horrified them."
. . . . .
Whitehead, PD, Causality and Collateral Estoppel: Process and Content of Recent SSRI Litigation, 2003, J Am Acad Psychiatry Law 31:377–82, wrote:
"In Tobin v. SmithKline Beecham Pharmaceuticals a jury in the U.S. District Court for the District of Wyoming found that the medication Paxil 'can cause some individuals to commit homicide and/or suicide,' and that it was a legal cause of the deaths in this case."
. . . . .
Breggin, PR, MD, Suicidality, violence and mania caused by selective serotonin reuptake inhibitors (SSRIs): A review and analysis. International Journal of Risk & Safety in Medicine, 2004, 16, 31-49, wrote:
"Evidence from many sources confirms that selective serotonin reuptake inhibitors (SSRIs) commonly cause or exacerbate a wide range of abnormal mental and behavioral conditions. These adverse drug reactions include the following overlapping clinical phenomena: a stimulant profile that ranges from mild agitation to manic psychoses, agitated depression, obsessive preoccupations that are alien or uncharacteristic of the individual, and akathisia. Each of these reactions can worsen the individual’s mental condition and can result in suicidality, violence, and other forms of extreme abnormal behavior. Evidence for these reactions is found in clinical reports, controlled clinical trials, and epidemiological studies in children and adults. Recognition of these adverse drug reactions and withdrawal from the offending drugs can prevent misdiagnosis and the worsening of potentially severe iatrogenic disorders. These findings also have forensic application in criminal, malpractice, and product liability cases."
and
"There are many reports and studies confirming that SSRI antidepressants can cause violence, suicide, mania and other forms of psychotic and bizarre behavior."
. . . . .
Although there is a great deal of prima facie evidence and many case reports detailing the neuroleptic/antidepressant link to suicide and violence, there has not to my knowledge been a definitive large-scale study by American psychiatry of the link between psychiatric drugs and the murder/suicides that are occurring with increased frequency.
And the great question is: why not? Why is this urgent, life-threatening issue not afforded the highest priority by the APA, NIMH, and university psychiatry departments? Is their self-serving need to protect psychiatry from the consequences of its errors eclipsing their ethical integrity and their sense of responsibility?
DSM & Akathisia
In this regard, it's interesting to see how psychiatric drug-induced akathisia has been handled in the various editions of DSM.
DSM-III-R (1987) makes no specific reference to neuroleptic or antidepressant-induced akathisia. There are, however, a number of statements in the chapter on "schizophrenia" which clearly (and deceptively) ascribe symptoms of akathisia and tardive dyskinesia to "schizophrenia" itself. For instance:
"In addition, odd mannerisms, grimacing, or waxy flexibility may be present [in schizophrenia]. (p 190)
"Almost any symptom can occur as an associated feature [of schizophrenia]. The person may appear perplexed, disheveled, or eccentrically groomed or dressed. Abnormalities of psychomotor activity—e.g., pacing, rocking, or apathetic immobility—are common." (p 190) [Emphasis added]
In reality, most of the pacing, grimacing, and rocking exhibited by people labeled schizophrenic is a direct result of neuroleptic drug poisoning, and not an associated feature of the so-called illness itself.
"Dysphoric mood is common [with schizophrenia], and may take the form of depression, anxiety, anger, or a mixture of these." (p 190)
Anxiety and anger are also direct effects of neuroleptic poisoning for many people.
"Although violent acts performed by people with this disorder often attract public attention, whether their frequency is actually greater than in the general population is not known. What is known is that the life expectancy of people with Schizophrenia is shorter than that of the general population because of an increased suicide rate and death from a variety of other causes." (p 191)
As is clear from the material quoted earlier, suicide is frequently a result of akathisia. The phrase "death from a variety of other causes" is unclear.
. . . . .
DSM-IV (1994) was markedly more honest in acknowledging the existence of neuroleptic-induced akathisia. In fact, this was included as an actual diagnosis in the fourth edition. It was coded as 333.99, and 2½ pages (744-746) were devoted to its description. Here are some quotes:
"In its most severe form, the individual may be unable to maintain any position for more than a few seconds." (p 744)
"The subjective distress resulting from akathisia is significant and can lead to noncompliance with neuroleptic treatment. Akathisia may be associated with dysphoria, irritability, aggression, or suicide attempts. Worsening of psychotic symptoms or behavioral dyscontrol may lead to an increase in neuroleptic medication dose, which may exacerbate the problem. Akathisia can develop very rapidly after initiating or increasing neuroleptic medication. The development of akathisia appears to be dose dependent and to be more frequently associated with particular neuroleptic medications. Acute akathisia tends to persist for as long as neuroleptic medications are continued, although the intensity may fluctuate over time. The reported prevalence of akathisia among individuals receiving neuroleptic medication has varied widely (20%-75%)." (p 745) [Emphasis added]
Note the reference in the third line above to "irritability, aggression, or suicide attempts". In fact, as the material quoted earlier makes clear, neuroleptic-induced akathisia has been causally-linked to actual homicides and suicides. This understatement was clearly deliberate, as Allen Frances, MD, architect of DSM-IV, was also one of the authors of the Shear et al paper quoted earlier, which linked neuroleptic-induced akathisia to actual completed suicides.
"Neuroleptic-Induced Acute Akathisia may be clinically indistinguishable from syndromes of restlessness due to certain neurological or other general medical conditions, to nonneuroleptic substances, and to agitation presenting as part of a mental disorder (e.g., a Manic Episode)." (p 745)
In other words, people who are experiencing neuroleptic-induced acute akathisia are at risk of being assigned a "diagnosis" of "bipolar disorder"!
"Serotonin-specific reuptake inhibitor antidepressant medications may produce akathisia that appears to be identical in phenomenology and treatment response to Neuroleptic-Induced Acute Akathisia. Akathisia due to nonneuroleptic medication can be diagnosed as Medication-Induced Movement Disorder Not Otherwise Specified." (p 745) [Bold face in original]
and
"Individuals with Depressive Episodes, Manic Episodes, Generalized Anxiety Disorder, Schizophrenia and other Psychotic Disorders, Attention-Deficit/Hyperactivity Disorder, dementia, delirium, Substance Intoxication, (e.g., with cocaine), or Substance Withdrawal (.e.g., from an opioid) may also display agitation that is difficult to distinguish from akathisia." (p 745-746) [Bold face in original]
Which prompts one to wonder how many people who have been assigned these so-called diagnoses were actually suffering from one of the toxic effects of neuroleptic drugs or SSRI's. It is also entirely plausible, as DSM-IV suggests, that many of these individuals would have been "treated" with even higher doses of neuroleptics!
. . . . .
The entry in DSM-IV-TR (2000) is identical to that in DSM-IV except for the following addition:
"Although the atypical [newer] neuroleptic medications are less likely to cause akathisia than the typical [older] neuroleptics, nonetheless, these medications do cause akathisia in some individuals." (p 801)
. . . . .
DSM-5 is remarkably less frank concerning psychiatric drug-induced akathisia than was DSM-IV. The name Neuroleptic-Induced Acute Akathisia was changed to Medication-Induced Acute Akathisia and the entry is given a total of four-and-a-half lines of text:
"333.99 (G25.71) Medication-Induced Acute Akathisia
Subjective complaints of restlessness, often accompanied by observed excessive movements (e.g., fidgety movements of the legs, rocking from foot to foot, pacing, inability to sit or stand still), developing within a few weeks of starting or raising the dosage of a medication (such as a neuroleptic) or after reducing the dosage of a medication used to treat extrapyramidal symptoms." (p 711) [Bold face in original]
There is no reference to the fact that, as earlier psychiatric authors had stated, the condition can be so unbearable as to drive people to suicide and even homicide.
There is, however, an interesting admission in a separate, also brief, entry:
"333.72 (G24.09) Tardive Dystonia
333.99 (G25.71) Tardive Akathisia
Tardive syndrome involving other types of movement problems, such as dystonia or akathisia, which are distinguished by their late emergence in the course of treatment and their potential persistence for months to years, even in the face of neuroleptic discontinuation or dosage reduction." (p 712) [Bold face in original]
In other words, neuroleptic-induced akathisia can persist for years, even if the person stops taking the drugs! But even granting this admission, it is clear that DSM-5 is markedly down-playing the significance and seriousness of neuroleptic-induced akathisia. And it is also clear from elsewhere in the text that the agenda here is to protect the reputation of the neuroleptic drugs:
"The term neuroleptic is becoming outdated because it highlights the propensity of antipsychotic medications to cause abnormal movements, and it is being replaced with the term antipsychotic in many contexts." (p 709)
Note the deceptive use of the passive voice ("is becoming outdated"). In reality, psychiatrists are consciously and deliberately phasing out the term "neuroleptic" in an attempt to conceal, or at least not draw attention to, the severe and potentially life-threatening neurotoxic effects of these drugs.
But the more important question is why has the APA eliminated the DSM-IV category "neuroleptic-induced akathisia" that ran to 2 ½ pages, and replaced it with the more general "medication-induced acute akathisia", which runs to 4 ½ lines? Why has this dangerous and relatively widespread adverse effect been so downplayed? On page 809 of the DSM-5 text there is a section called Highlights of Changes from DSM-IV to DSM-5, but there is no explanation for the change there. There is a note in this section referring the reader to "An expanded description of nearly all changes…" on the APA website. The link leads to an article titled "Highlights of Changes from DSM-IV-TR to DSM-5". But the article contains no reference to the change in question.
So we don't know the APA's justification for suppressing information about this potentially devastating adverse effect. But we do know that neuroleptic drugs are being prescribed for an increasing range of problems, and are even being prescribed to toddlers for temper tantrums and to nursing home residents for "management problems". Some have even acquired "block-buster" sales status. It is clearly in pharma's interests to suppress this information and it is consistent with psychiatry's hand-in-glove relationship with pharma that they should oblige their generous benefactors in this way. Remember, 69% of the DSM-5 workforce were in the pay of pharma while working on the revision.
Despite the early, and very clear, statements from individual psychiatrists linking psychiatric drugs to murder/suicides, the psychiatric leadership has consistently failed to address this link. Instead, they deceptively attribute these incidents to a lack of psychiatric "treatment", and they call for legal enforcement of even more drugging.
Finally
On June 9, 2016, Maria Oquendo, MD, President of the APA, wrote a post in support of the Senate's so-called Mental Health Reform Bill. The post was standard psychiatric propaganda, including the inane 21% annual and 50% lifetime prevalence of "mental illness". The reality is that if one can invent illnesses at will and arbitrarily reduce the "diagnostic" thresholds of these "illnesses", one can produce any prevalence numbers one chooses.
The post also drew attention to the fact that there were 41,000 suicides in the US in 2013, and asserted that "…we continue to fail people with mental illness every day."
In other words, more psychiatric treatment would reduce the suicide rate. But meanwhile, we have no data on how many of these individuals were in the throes of neuroleptic or antidepressant-induced akathisia. And as long as psychiatry and pharma are controlling the research agenda, such information will be systematically repressed.
As I've stated many times, psychiatry is intellectually and morally bankrupt. They are adamantly resistant to anything resembling critical self-appraisal, and there are no depths of deception and spin to which they will not go, to suppress the reality and the consequences of their drug-pushing depredations. Neuroleptic and antidepressant drugs induce some individuals to take their own lives and/or the lives of others. Neuroleptic and antidepressant drugs are almost certainly the proximate causes of many of the mass shootings that have plagued our country for almost twenty years. How much longer can psychiatry sustain this dreadful, self-serving deception?
And, Incidentally
Senator John McCain and Congressman David Jolly have introduced bills in their respective chambers that if enacted will require the Veterans Administration to conduct a comprehensive study of the link between psychiatric drugs and veterans' suicides. It will be an enormous step forward if these bills become law. It is also an interesting reflection that these bills were initiated by politicians, and not by psychiatrists, who present themselves as caring professionals acting in the best interests of their so-called patients.
If you live in the US, please encourage your representatives to support the McCain and Jolly bills (S 3410 and H 4640).
Thank You Dr Hickey, MIA and Sen McCain.
Neuroleptic Drugs, Akathisia, and Suicide and Violence
Thirty-three years ago, in August 1983, an article titled Suicide Associated with Akathisia and Depot Fluphenazine Treatment appeared in the Journal of Clinical Psychopharmacology. The authors were Katherine Shear, MD, Allen Frances, MD, and Peter Weiden, MD.
Here are some quotes, interspersed with my comments/observations:
"Akathisia is a common and distressing side effect of neuroleptic medication that can be difficult to recognize and treat. Several previous reports mention maladaptive behavioral consequences, such as poor compliance with prescribed medication and aggressive or self-destructive outbursts. We are reporting suicides in two young Hispanic men who had developed severe akathisia after treatment with depot fluphenazine. Depression with suicidal behavior has been observed following fluphenazine injection, but suicide associated with akathisia has not been previously noted."
Fluphenazine is a neuroleptic drug of the phenothiazine class that was introduced in 1959. It is marketed as Prolixin and other brand names, and according to Wikipedia, is on the WHO's "List of Essential Medicines, most important medications needed in a basic health system."
The "treatment" used in each case was a depot injection of fluphenazine. This is a long-lasting injection, typically 30 days, in which the drug is lodged in a dermal or muscular mass from which it is slowly drawn into the blood stream. (Hence depot: a place where goods are stored for later distribution.)
Depot injections have some obvious convenience value, but in psychiatry are usually used to ensure compliance. Their major downside is that if the person has an adverse reaction to the drug, there's no way to remove the stored chemicals from his body.
The authors may be correct in stating that this is the first published report of suicide associated with akathisia, but it is not the first report of suicide associated with fluphenazine. Seventeen years earlier, Dorothy West, MD, had published the following letter in the British Journal of Psychiatry, 117 (1970), 718-9:
Dangers of Fluphenazine
Dear Sir,
A new drug is being widely used in the treatment of mental illness. It is long-acting and used by injection – its name is fluphenazine (Moditen). Is this the thalidomide of the 70's? I would like to have the opinion of other doctors. Whilst it is still new maybe we are lulled into a false sense of security, but are we justified in using a drug, which may take up to six weeks to eradicate from the tissues, without being sure of its safety? Its side effects alone are legion. A study of 13 papers gives the following:
Common side-effects reported are – lethargy, drowsiness, dizziness, muscular inco-ordination, paraesthesia, hypotension, blurring of vision, dryness of mouth, malaise, feelings of tension, confusion, nausea, vomiting, and aches and pains.
Parkinsonism is extremely common. Incidence in reports varies from 100 per cent to 24 per cent with many reports around 50 per cent. Depression is quite common and tends to be severe – 5 suicides reported and two suicide attempts. Other reported side-effects include psychotic relapse and glaucoma.
Dorothy West
. . . . .
Back to the Shear, Frances, and Weiden paper:
CASE NO. 1
"A 23-year-old single unemployed Hispanic man had been socially withdrawn, blunted in affect, and thought disordered since his early teenage years. He was intermittently delusional with auditory hallucinations which responded to phenothiazines. He was treated in a day hospital after one of multiple hospitalizations; depot fluphenazine was used because of medication noncompliance. He received two injections of 25 mg of fluphenazine decanoate separated by 1 week, with noticeable improvement in his psychotic symptoms. He also developed akathisia and was prescribed trihexyphenadyl, 2 mg twice a day, which he probably did not take. There was no improvement in his akathisia and no anticholinergic side effects. He soon stopped attending the day hospital and a family member called a week later to say that the man had killed himself by jumping off the roof of their building. He had given no indication of being suicidal and his family believed the increased 'nervousness' had driven him to this desperate measure. The patient had no previous history of suicidal behavior and did not drink alcohol or use drugs."
So, we have a young man who has been socially withdrawn and joyless since his early teens. Not surprisingly his perceptions and thinking patterns deviated from the conventional. For reasons unknown he came within the orbit of psychiatry, and had had extensive contact with the psychiatric system. He was given two depot injections of fluphenazine one week apart. His "psychotic symptoms" improved, but he developed akathisia. He was prescribed an anticholinergic agent to combat the akathisia, but apparently this was ineffective, or as the authors suggest, he didn't take it. In any event, a week later he killed himself by jumping from the roof of a building.
We don't know if the fluphenazine was administered involuntarily, but we do know that he had taken phenothiazine in the past and had been noncompliant. So it is reasonable to assume that there was some adverse effect. Did the day hospital psychiatrists explore the reason for this "noncompliance"? In any event, given the outcome, the phrase "depot fluphenazine was used because of medication noncompliance" is a haunting and compelling testament to psychiatric arrogance. This anonymous young man was clearly prone to acute akathisia, and his "noncompliance" was a sensible and correct response to the neuro-poisoning he was receiving from psychiatrists. He stopped attending the day hospital (again, understandably),but he had no way to get the drug out of his body. The trihexyphenidyl is an anticholinergic agent and might have mitigated the akathisia. Or perhaps he took it and it was not effective, as is frequently the case.
CASE NO. 2
"A 36-year-old non-English speaking Hispanic man was seen once in our walk-in clinic because of severe restlessness and leg cramps. Intermittent somatic symptoms and nervousness began shortly after he arrived in the United States 8 months earlier. When the symptoms worsened, he began a series of visits to hospital emergency rooms and private psychiatrists. Three weeks before the walk-in visit a Spanish-speaking psychiatrist diagnosed paranoid schizophrenia and administered depot fluphenazine. Following this injection, the patient developed a dystonic reaction and then began to complain continuously of leg cramps and restlessness. In the ensuing weeks he received numerous drugs from emergency room or private physicians, some given by injection and some by prescription. He brought bottles of thiothixene, chlorazepate, amitriptyline, meprobamate, and lorazepam to the clinic. He was agitated, paced, and begged for help. He denied symptoms of depression or suicidal ideation. He claimed he was devoted to his wife and 9-year-old daughter, but he felt his unbearable symptoms would never go away. He made good contact in a translated interview and showed no thought disorder, hallucinations, or delusions. Thorough medical examination was negative except for the parkinsonian symptoms. He had no prior history of psychiatric treatment and the family history was negative for depression, nervousness, and significant psychiatric or medical illness. Since the diagnosis was uncertain, plans were made to discontinue all medication and a follow-up appointment was scheduled. The next day he killed himself without warning by jumping in front of a subway train."
The 36-year-old man had come to the US eight months earlier, and had begun to experience "somatic symptoms and nervousness". This seems hardly surprising in someone who is having to adapt to a new environment, but we are provided no details with regards to his psychosocial context, other than the fact that he had a wife and 9-year-old daughter, and that he didn't speak English. What we do know is that he visited "emergency rooms and private psychiatrists" to help with "somatic symptoms and nervousness". One of the psychiatrists "diagnosed paranoid schizophrenia", and gave him a depot injection of fluphenazine. He developed severe akathisia, and continued to visit emergency rooms and private psychiatrists in an attempt to gain some relief. During this period he received "numerous drugs" from these sources, some by injection, some by prescription. At this point he came to the authors' walk-in clinic.
"He was agitated, paced, and begged for help."
and
"He denied symptoms of depression or suicidal ideation. He claimed he was devoted to his wife and 9-year-old daughter, but he felt his unbearable symptoms would never go away."
Plans were made to discontinue all the drugs, which the authors euphemistically refer to as medications, but it was too little, too late. He jumped to his death in front of a train the next day.
So, we have a healthy young man, devoted to his wife and daughter, who seeks medical help for what were probably stress-related "somatic complaints and nervousness". Psychiatrists throw a bewildering array of drugs at him, including a depot injection of fluphenazine, which results in his death. And the only reason we know about this forgotten victim of psychiatry is because the authors wrote up and published the case. How many other thousands have died from the same kind of irresponsible drug-pushing; from the same arrogant conviction that for every human problem, psychiatry has a "safe and effective" pill?
. . . . .
Here are some more quotes from the Shear et al article:
"Akathisia is an intensely unpleasant feeling characterized by muscle discomfort, inability to sit still, continuous agitation, restlessness, and fidgety feelings. Sleep may be disturbed by an inability to lie down. Some patients say they feel like jumping out of their skin"
"The estimated incidence of akathisia with neuroleptic use ranges from 20 to 45%. Several studies using depot fluphenazine report an incidence around 35%."
"Akathisia is a distressing symptom which may be difficult to diagnose and treat. Restlessness may be mistaken for anxiety and clinicians may err by raising neuroleptic dosage."
"Sometimes the only effective treatment is withdrawal of the neuroleptic. Although we cannot be sure that akathisia caused the deaths of our patients, akathitic symptoms seemed to be immediate precipitants of suicidal behavior. We urge clinicians to be alert to the discomfort of akathisia and to treat it aggressively. If treatment with anticholinergics or γ-aminobutyric acid agonists fails or symptoms are especially severe, hospitalization may be indicated."
It is clear that the authors are leaning heavily towards the conclusion that neuroleptic-induced akathisia was the immediate precipitant of both suicides.
OTHER SIMILAR REPORTS
Several similar reports have appeared in the literature for decades. Here are some examples, with relevant quotes:
Van Putten, T., MD, The Many Faces of Akathisia, Comprehensive Psychiatry, 1975, 16(1):
"AKATHISIA, a common side effect of neuroleptic therapy, is an emotional state and 'refers not to any type or pattern of movement, but rather to a subjective need or desire to move.'"
"A 44-year-old woman with hebephrenic schizophrenia started to bang her head against the wall three days after an injection of 25 mg of fluphenazine enanthate. Her only utterance was: 'I just want to get rid of this whole body.'"
"Akathisia is often associated with strong affects of fright, terror, anger or rage, anxiety, and vague somatic complaints."
"On this regime, she usually developed an episode of akathisia during the week following her injection. She described several such episodes as follows: 'I just get these attacks of tension. I don't feel right. My stomach feels strange. It's like I'm churning inside. I feel hostile and I hate (with intense affect) everybody."
"Patients have described the inner restlessness and agitation of akathisia in many other ways, such as: 'My nerves are just jumping' I feel like I'm wired to the ceiling; I just feel impatient and nasty. I can't concentrate; it's like I got ants in my pants; my nerves are raw; I just feel on edge; I feel just nasty; I feel like jumping out of my skin; if this feeling continues, I would rather be dead. I can't describe the feelings; I'm quivery from the waist up; I want to climb the walls; I feel all revved up; it's like I got diaper rash inside.'"
"Patients with severe akathisia, however, cannot sit quietly for more than a few seconds at a time, and at times the 'impatience musculaire' can result in running, agitated dancing, or rocking."
"Akathisia is tolerated very poorly by hostile paranoid patients in that they tend to misinterpret the inner agitation of akathisia as further proof that they are being poisoned or controlled by outside malevolent forces."
Note the presumably unintended irony in the word misinterpret. In reality, they are being poisoned and controlled by outside forces!
. . . . .
Keckich, W., MD: Neuroleptics: Violence as a Manifestation of Akathisia, JAMA, 1978, Nov 10 (240) 20, 2185:
"NEUROLEPTIC medications (eg, phenothiazines, butyrophenones) are used in medicine to control psychotic symptoms and concomitant agitated and violent behavior. They also are used to control anxiety and agitation whenever minor tranquilizers (eg, benzodiazepines) would be inappropriate. Development of akathisia as a parkinsonian side effect is confirmed in the use of these drugs. Akathisia is a condition that gives rise to the subjective desire to be in constant motion, with a feeling of inner agitation and muscle tension. The patient cannot sit still and paces constantly"
"One week later the patient reported that he was more agitated at night. Since it was not known at the time that akathisia was beginning, haloperidol treatment was increased to 4 mg at bedtime to decrease the agitation. Four days later, after his evening dose of 4 mg of haloperidol, he became uncontrollably agitated, could not sit still, and paced for several hours. He complained of tightness in his muscles, rigidity, a jumpy feeling inside, and violent urges to assault anyone near him. This culminated in an assault on his dog with an intent to kill. He became frightened over his loss of control and came to the emergency room. He was given 50 mg of thioridazine hydrochloride, which brought the hostility under control but did not remove it.
He subsequently discontinued the treatment with imipramine and haloperidol. The following morning he reported that the muscle tightness, jumpy feelings, and hostility were decreased but still present. Three days after drug treatment was discontinued all of the symptoms had ceased, and he was at his baseline of difficulty once again. The half-life of haloperidol is approximately 24 hours, and this symptom relief coincided with expected excretion of the drug.
In retrospect it was apparent that he had experienced increasing akathitic side effects from the haloperidol medication, which accounted for his increasing night-time agitation and culminated in a stimulation of violent and aggressive activity."
. . . . .
Schulte, JL, MD, Homicide and Suicide Associated with Akathisia and Haloperidol, American Journal of Forensic Psychiatry, Jan 1985, 6(2):
"The following five cases are reported to bring attention to the potential for severe violence, as a result of akathisia, following such administration of a neuroleptic for acute psychiatric symptoms. Particular emphasis is directed to an experience of sensory dissociation associated with the uncomfortable physical reactions, resulting in extreme acts of physical violence."
CASE NO. 1
"A 23-year-old married, Salvadorian-born male, with a four-day history of progressive paranoia and disorganized behavior, had been taken by the police department to a hospital at the request of his parents. The physician insisted he receive an injection of haloperidol in the emergency room while awaiting admission to the psychiatric unit where he had previously been a patient on a number of occasions.
He tried to resist but felt he had no option with the staff and police surrounding him. He felt he was being unnecessarily delayed in being admitted to the inpatient unit. In addition, he felt he had been lied to, in that apparently he had been told he was going to see his wife who had deserted him approximately 48 hours earlier. He then escaped from the emergency room and the authorities, ran several miles to a park, tried to get a policeman to help him, escaped again and totally disrobed. Within the next 45-minute period of time, he assaulted one woman who was walking her dog and attempted to rape her. When pulled off by the husband, he proceeded down the street, broke down the front door of a house where an 81-year-old lady was sleeping. He severely beat her with his fists, 'to a pulp', by his own description. Following which he found knives and stabbed her repeatedly, resulting in her death. Then, after being confronted in the street by a policeman who sprayed him with Mace, he returned through the house, exiting the back door where he ran into another woman with her child. He repeatedly stabbed the woman in front of the child, whereupon he moved on to the next person he encountered, a woman whom he severely assaulted and stabbed to the extent that an eye was lost and an opening into the anus was created resulting in major surgery and serious residual problems, including a colostomy. He was then finally captured and subdued by eight policemen and hospitalized.
He had ten previous psychiatric hospitalizations between 1975 and the present. All of these hospitalizations have been only a matter of hours to several days. He would always be placed on medication and released, following which he would stop taking the medication and go along until another upheaval would occur.
He had a history of problems with anger and acute paranoid beliefs leading to hyperactive behavior and one incident in which it was reported he tried to choke one of his brothers.
His description of his mental status at the time of his offense is quite striking. He describes himself as feeling almost like a spectator in a movie. He makes a point of describing how he had lost all sense of caring about anything or anyone in life. Additionally, he describes a feeling of loss of physical sensation, including feeling nothing when maced by the police. He felt enormous energy with a feeling of needing to rid himself of it.
He gives the history of having been picked up by the police on a traffic violation in 1979 and placed in jail for the first time in his life. He became angry and was given a series of haloperidol injections, becoming progressively more agitated and unmanageable to the point he was rolled up in a mattress and handcuffed in order to be transported to a psychiatric inpatient unit. In 1980, during another hospitalization, he was, despite his protests, changed from chlorpromazine to haloperidol and within hours became totally unmanageable, requiring six individuals to subdue him and place him in seclusion and restraint." [Emphasis added]
It is noteworthy that this individual asked not to be changed from chlorpromazine to haloperidol, but his request was ignored.
Eight years later, Herrera et al confirmed in a controlled study that an increase in violent behavior was more likely with haloperidol than with chlorpromazine. Apparently, the individual had some intuitive awareness of this from previous experience, but as is often the case, the psychiatrists discounted his protests and gave him the haloperidol anyway.
Here are two quotes from the Herrera et al study:
"We found in a controlled study that some patients have a marked increase in violence when treated with moderately high-dose haloperidol."
"…these patients did not show an increase in violence during a placebo period, nor did they have a history of violent behavior."
Back to the Schulte JL article:
CASE NO. 2
"A 30-year-old man with a history of mental illness dating back seven years, with hospitalizations in three other states, was admitted to the hospital on six counts of burglary. His diagnosis was paranoid schizophrenia, and he had been found not guilty by reason of insanity by the courts. The admission note by the psychiatrist stated, 'He is somewhat paranoid, but says he has side effects from most tranquilizers.' On the third day of hospitalization, he was referred to the psychiatrist by nurses because of difficulty getting to sleep. No evidence of aggressiveness or self-injurious behavior was charted that day in the nurses' notes. The psychiatrist prescribed haloperidol, 5mg. three times a day, which was begun the next day, with three doses administered with Cogentin, 2mg twice a day. Nurses' notes that day stated, 'He was very anxious about being in the hospital and threatened to kill himself if he gets up the nerve.' At 10:45 p.m., notes stated, 'He has regressed during this shift in all assessment areas. His hygiene is poor, and he is irresponsible, e.g., lying on the floor without shoes or socks.' He refused medication initially at 5 p. m., and stated that phenothiazines, 'fuck me up.' He finally took the medication but then stated angrily, 'Now I'll really get crazy.' He ranted loudly and profanely for 30 minutes. He took his 9 p.m. medication and started his haranguing again, only louder and more threatening. 'l'll kill all of you mother-fuckers before I leave here,' He was found in his room at 6:50 a.m., having hung himself with a bed sheet. A letter from his attorney to the hospital had stated that 'medications caused him problems (l should perhaps state that by medications I mean psychotropic drugs).'" [Emphasis added]
CASE NO. 3
"A 52-year-old male first came to psychiatric attention eleven years earlier following an assault on his wife. He had delusions of cancer, a belief he would die and felt sexually inadequate.
He had been unsuccessfully treated with Lithium and antidepressants, as well as various tranquilizers. He had continually been an inpatient or in board and care facilities, and three and one-half months earlier, he had his medications changed to 10mg. of Haloperidol in the a.m. and 40mg. of Haloperidol at hour of sleep, with 2mg.of Artane twice daily. Each month he stated he complained to his psychiatrist of severe restlessness. He stated he had to roll over and over in bed at night and usually would be unable to get to sleep until 3 or 4 a.m. During the day, he would try to lie down but couldn't because of his severe uncomfortableness. He described after being turned down again by the psychiatrist, he became despondent and angry, lost hope and decided if he could not ever even sleep like the rest of his boarding home mates that life wasn't worthwhile. He secured a knife and repeatedly stabbed himself in the abdomen, was rushed to the hospital and barely survived. He remarked he could never even feel the knife when stabbing himself." [Emphasis added]
. . . . .
Van Putten, T. MD and Marder, SR, MD, Behavioral Toxicity of Antipsychotic Drugs, J Clin Psychiatry, September 1987, 48: 9 (Suppl):
"The subjective restlessness of akathisia is usually accompanied by telltale foot movements: rocking from foot to foot while standing or walking on the spot. Akathisia is strongly associated with depression and dysphoric responses to neuroleptics and has even been linked to suicidal and homicidal behavior in extreme cases."
"The aforementioned case literature reads convincingly: it is reasonable to conclude that akathisia, in the extreme case, can drive people to suicide or homicide."
. . . . .
Crowner, ML, Douyon, R, et al, Akathisia and violence Psychopharmacology Bulletin, 1990: 26(1): 115-7:
"Akathisia is a common side effect of neuroleptic drugs that may present with behavioral disturbances. There have been preliminary reports on the association between violence and akathisia. We report the first observational study of this relationship. Patients studied were from a special unit for violent patients. A closed-circuit television camera was installed in each of the corners in its dayroom. Incidents of assault plus the 5 minutes preceding each assault were recorded on videotape. Participants and bystanders were rated for the motor component of akathisia. For each of nine incidents, we compared the akathisia scores for participants and for bystanders. Both victims and assailants were akathisic before about half of all incidents; bystanders rarely were. The classification of the movements we rated and the implications for further studies are discussed."
The extraordinary irony here is that the individuals in this study "were from a special unit for violent patients," but in fact the drug used to control this behavior was actually precipitating more violence!
. . . . .
Galynker, I, MD, PhD and Nazarian, D, MD, letter to the editor, Journal of Clinical Psychiatry, 1997, 58: 31-32:
"Case Report. Mr. A, a 47-year-old white man with a diagnosis of bipolar mood disorder, was brought to the emergency room because he was screaming in the streets. Mr. A had over 30 past psychiatric admissions associated with agitation and violence and was often discharged against medical advice. He was nearly always noncompliant with his antipsychotic medications, claiming that they made him 'jump and lose my temper.' Prior to the present admission, Mr. A's daily medications included haloperidol 20 mg, lithium carbonate 1500 mg, divalproex sodium 500 mg, and benztropine 1 mg. At admission, the patient was grandiose, had loud and pressured speech, and admitted he was not taking haloperidol. He was given haloperidol 15 mg q.h.s. and benztropine 1 mg q.a.m. Within 24 hours he started pacing; became restless, agitated, and violent; complained of feeling 'jumpy'; and attacked a staff member. On Day 5 of his hospitalization, haloperidol and benztropine were discontinued; chlorpromazine was started, and the dose was increased to 950 mg/day. Mr. A, although sedated, remained threatening and violent. On Day 13, chlorpromazine was discontinued, and haloperidol was restarted at a higher dose of 15 mg p.o. b.i.d. Mr. A again complained of 'jumpiness' and punched a television cabinet, causing a self-inflicted fracture. On hospital Day 17, owing to an error, haloperidol was discontinued. The patient became calmer, less irritable, displayed no angry outbursts, and required no further room restrictions. After 5 days, when the error was discovered, haloperidol was restarted at a lower daily dose of 10 mg. Within 3 days, the patient became violent and required room restriction. Haloperidol was then discontinued, the patient's agitation and violence resolved, and a week later he was discharged. His daily medications were lithium carbonate 1500 mg (serum level = 0.9mEq/L; this dose had not been changed during his hospitalization), lorazepam 1 mg, and divalproex sodium 500 mg. On these mediations, he remained well 6 months postdischarge, his longest period as an outpatient."
In their commentary, the authors point out:
"The fact that the jumpiness occurred with haloperidol and not with chlorpromazine is another factor indicative that Mr. A has exhibited akathisia rather than nonspecific activation of mania; this is because akathisia is more common with higher potency as compared with low-potency neuroleptics."
and, with more candor than one customarily finds in psychiatry:
"One can also speculate that Mr. A's rocky clinical history was related to aggressive behavior perpetuated by antipsychotic administration."
And it is worth remembering that Mr. A's "rocky clinical history" entailed "over 30 past psychiatric admissions associated with agitation and violence".
. . . . .
So, since at least the early 80's, individual psychiatrists have been drawing attention to the fact that neuroleptic drugs induce akathisia in many cases, and that in some cases this can precipitate suicide and/or homicide.
Akathisia & Antidepressants
Although it is well known that neuroleptic drugs cause akathisia, the link between antidepressants and this condition is less widely appreciated. The Wikipedia article on akathisia contains this:
"Antidepressants can also induce the appearance of akathisia, due to increased serotonin signalling within the CNS."
. . . . .
Hamilton, MS, MD, Obler, LA, Akathisia, suicidality, and fluoxetine, J Clin Psychiatry, 1992, Nov 53(11), 401-406, write:
"The propose[d] link between fluoxetine and suicidal ideation is explained by fluoxetine-induced akathisia and other dysphoric extrapyramidal reactions."
and
"The literature suggests that fluoxetine-induced extrapyramidal reactions may be a mediator of de novo suicidal ideation."
Fluoxetine is an SSRI, marketed as Prozac, Sarafem, and other names.
. . . . .
Wirshing, WC, MD, Van Putten, T, MD, Rosenberg, J, MD, et al, Fluoxetine, Akathisia, and Suicidality: Is There a Causal Connection?, Arch Gen Psychiatry, 1992, 49(7), 580-581, write:
"We have now had experience with five such patients. All were women. None had a history of significant suicidal behavior; all described their distress as an intense and novel somatic-emotional state; all reported an urge to pace that paralleled the intensity of the distress; all experienced suicidal thoughts at the peak of their restless agitation; and all experienced a remission of their agitation, restlessness, pacing urge, and suicidality after the fluoxetine was discontinued. We describe herein five cases of what we think might be fluoxetine-induced akathisia accounting for suicidal ideation."
Eikelenboom-Schieveld, SJM, Lucire, Y, MD, Fogleman, J, PhD, The relevance of cytochrome P450 polymorphism in forensic medicine and akathisia-related violence and suicide, Journal of Forensic and legal Medicine, 2016, 41. 65-71, wrote:
"Antidepressants have been reported as causing suicide and homicide and share the class attribute of frequently producing akathisia, a state of severe restlessness associated with thoughts of death and violence."
and
"In this paper, we report our investigation into adverse drug reactions/interactions in three persons who committed homicide, two also intending suicide, while on antidepressants prescribed for stressful life events"
and
"Three persons committed homicide, two of which intended to commit suicide. None had been aggressive or mentally ill before getting medication. None had known that they needed to take medication regularly or how to stop taking it safely. None improved on medication, and no prescriber recognized their complaints as adverse drug reactions or was aware of impending danger. Interviews elicited accounts of restlessness, akathisia, confusion, delirium, euphoria, extreme anxiety, obsessive preoccupation with aggression, and incomplete recall of events. Weird impulses to kill were acted on without warning. On recovery, all recognized their actions to be out of character, and their beliefs and behaviours horrified them."
. . . . .
Whitehead, PD, Causality and Collateral Estoppel: Process and Content of Recent SSRI Litigation, 2003, J Am Acad Psychiatry Law 31:377–82, wrote:
"In Tobin v. SmithKline Beecham Pharmaceuticals a jury in the U.S. District Court for the District of Wyoming found that the medication Paxil 'can cause some individuals to commit homicide and/or suicide,' and that it was a legal cause of the deaths in this case."
. . . . .
Breggin, PR, MD, Suicidality, violence and mania caused by selective serotonin reuptake inhibitors (SSRIs): A review and analysis. International Journal of Risk & Safety in Medicine, 2004, 16, 31-49, wrote:
"Evidence from many sources confirms that selective serotonin reuptake inhibitors (SSRIs) commonly cause or exacerbate a wide range of abnormal mental and behavioral conditions. These adverse drug reactions include the following overlapping clinical phenomena: a stimulant profile that ranges from mild agitation to manic psychoses, agitated depression, obsessive preoccupations that are alien or uncharacteristic of the individual, and akathisia. Each of these reactions can worsen the individual’s mental condition and can result in suicidality, violence, and other forms of extreme abnormal behavior. Evidence for these reactions is found in clinical reports, controlled clinical trials, and epidemiological studies in children and adults. Recognition of these adverse drug reactions and withdrawal from the offending drugs can prevent misdiagnosis and the worsening of potentially severe iatrogenic disorders. These findings also have forensic application in criminal, malpractice, and product liability cases."
and
"There are many reports and studies confirming that SSRI antidepressants can cause violence, suicide, mania and other forms of psychotic and bizarre behavior."
. . . . .
Although there is a great deal of prima facie evidence and many case reports detailing the neuroleptic/antidepressant link to suicide and violence, there has not to my knowledge been a definitive large-scale study by American psychiatry of the link between psychiatric drugs and the murder/suicides that are occurring with increased frequency.
And the great question is: why not? Why is this urgent, life-threatening issue not afforded the highest priority by the APA, NIMH, and university psychiatry departments? Is their self-serving need to protect psychiatry from the consequences of its errors eclipsing their ethical integrity and their sense of responsibility?
DSM & Akathisia
In this regard, it's interesting to see how psychiatric drug-induced akathisia has been handled in the various editions of DSM.
DSM-III-R (1987) makes no specific reference to neuroleptic or antidepressant-induced akathisia. There are, however, a number of statements in the chapter on "schizophrenia" which clearly (and deceptively) ascribe symptoms of akathisia and tardive dyskinesia to "schizophrenia" itself. For instance:
"In addition, odd mannerisms, grimacing, or waxy flexibility may be present [in schizophrenia]. (p 190)
"Almost any symptom can occur as an associated feature [of schizophrenia]. The person may appear perplexed, disheveled, or eccentrically groomed or dressed. Abnormalities of psychomotor activity—e.g., pacing, rocking, or apathetic immobility—are common." (p 190) [Emphasis added]
In reality, most of the pacing, grimacing, and rocking exhibited by people labeled schizophrenic is a direct result of neuroleptic drug poisoning, and not an associated feature of the so-called illness itself.
"Dysphoric mood is common [with schizophrenia], and may take the form of depression, anxiety, anger, or a mixture of these." (p 190)
Anxiety and anger are also direct effects of neuroleptic poisoning for many people.
"Although violent acts performed by people with this disorder often attract public attention, whether their frequency is actually greater than in the general population is not known. What is known is that the life expectancy of people with Schizophrenia is shorter than that of the general population because of an increased suicide rate and death from a variety of other causes." (p 191)
As is clear from the material quoted earlier, suicide is frequently a result of akathisia. The phrase "death from a variety of other causes" is unclear.
. . . . .
DSM-IV (1994) was markedly more honest in acknowledging the existence of neuroleptic-induced akathisia. In fact, this was included as an actual diagnosis in the fourth edition. It was coded as 333.99, and 2½ pages (744-746) were devoted to its description. Here are some quotes:
"In its most severe form, the individual may be unable to maintain any position for more than a few seconds." (p 744)
"The subjective distress resulting from akathisia is significant and can lead to noncompliance with neuroleptic treatment. Akathisia may be associated with dysphoria, irritability, aggression, or suicide attempts. Worsening of psychotic symptoms or behavioral dyscontrol may lead to an increase in neuroleptic medication dose, which may exacerbate the problem. Akathisia can develop very rapidly after initiating or increasing neuroleptic medication. The development of akathisia appears to be dose dependent and to be more frequently associated with particular neuroleptic medications. Acute akathisia tends to persist for as long as neuroleptic medications are continued, although the intensity may fluctuate over time. The reported prevalence of akathisia among individuals receiving neuroleptic medication has varied widely (20%-75%)." (p 745) [Emphasis added]
Note the reference in the third line above to "irritability, aggression, or suicide attempts". In fact, as the material quoted earlier makes clear, neuroleptic-induced akathisia has been causally-linked to actual homicides and suicides. This understatement was clearly deliberate, as Allen Frances, MD, architect of DSM-IV, was also one of the authors of the Shear et al paper quoted earlier, which linked neuroleptic-induced akathisia to actual completed suicides.
"Neuroleptic-Induced Acute Akathisia may be clinically indistinguishable from syndromes of restlessness due to certain neurological or other general medical conditions, to nonneuroleptic substances, and to agitation presenting as part of a mental disorder (e.g., a Manic Episode)." (p 745)
In other words, people who are experiencing neuroleptic-induced acute akathisia are at risk of being assigned a "diagnosis" of "bipolar disorder"!
"Serotonin-specific reuptake inhibitor antidepressant medications may produce akathisia that appears to be identical in phenomenology and treatment response to Neuroleptic-Induced Acute Akathisia. Akathisia due to nonneuroleptic medication can be diagnosed as Medication-Induced Movement Disorder Not Otherwise Specified." (p 745) [Bold face in original]
and
"Individuals with Depressive Episodes, Manic Episodes, Generalized Anxiety Disorder, Schizophrenia and other Psychotic Disorders, Attention-Deficit/Hyperactivity Disorder, dementia, delirium, Substance Intoxication, (e.g., with cocaine), or Substance Withdrawal (.e.g., from an opioid) may also display agitation that is difficult to distinguish from akathisia." (p 745-746) [Bold face in original]
Which prompts one to wonder how many people who have been assigned these so-called diagnoses were actually suffering from one of the toxic effects of neuroleptic drugs or SSRI's. It is also entirely plausible, as DSM-IV suggests, that many of these individuals would have been "treated" with even higher doses of neuroleptics!
. . . . .
The entry in DSM-IV-TR (2000) is identical to that in DSM-IV except for the following addition:
"Although the atypical [newer] neuroleptic medications are less likely to cause akathisia than the typical [older] neuroleptics, nonetheless, these medications do cause akathisia in some individuals." (p 801)
. . . . .
DSM-5 is remarkably less frank concerning psychiatric drug-induced akathisia than was DSM-IV. The name Neuroleptic-Induced Acute Akathisia was changed to Medication-Induced Acute Akathisia and the entry is given a total of four-and-a-half lines of text:
"333.99 (G25.71) Medication-Induced Acute Akathisia
Subjective complaints of restlessness, often accompanied by observed excessive movements (e.g., fidgety movements of the legs, rocking from foot to foot, pacing, inability to sit or stand still), developing within a few weeks of starting or raising the dosage of a medication (such as a neuroleptic) or after reducing the dosage of a medication used to treat extrapyramidal symptoms." (p 711) [Bold face in original]
There is no reference to the fact that, as earlier psychiatric authors had stated, the condition can be so unbearable as to drive people to suicide and even homicide.
There is, however, an interesting admission in a separate, also brief, entry:
"333.72 (G24.09) Tardive Dystonia
333.99 (G25.71) Tardive Akathisia
Tardive syndrome involving other types of movement problems, such as dystonia or akathisia, which are distinguished by their late emergence in the course of treatment and their potential persistence for months to years, even in the face of neuroleptic discontinuation or dosage reduction." (p 712) [Bold face in original]
In other words, neuroleptic-induced akathisia can persist for years, even if the person stops taking the drugs! But even granting this admission, it is clear that DSM-5 is markedly down-playing the significance and seriousness of neuroleptic-induced akathisia. And it is also clear from elsewhere in the text that the agenda here is to protect the reputation of the neuroleptic drugs:
"The term neuroleptic is becoming outdated because it highlights the propensity of antipsychotic medications to cause abnormal movements, and it is being replaced with the term antipsychotic in many contexts." (p 709)
Note the deceptive use of the passive voice ("is becoming outdated"). In reality, psychiatrists are consciously and deliberately phasing out the term "neuroleptic" in an attempt to conceal, or at least not draw attention to, the severe and potentially life-threatening neurotoxic effects of these drugs.
But the more important question is why has the APA eliminated the DSM-IV category "neuroleptic-induced akathisia" that ran to 2 ½ pages, and replaced it with the more general "medication-induced acute akathisia", which runs to 4 ½ lines? Why has this dangerous and relatively widespread adverse effect been so downplayed? On page 809 of the DSM-5 text there is a section called Highlights of Changes from DSM-IV to DSM-5, but there is no explanation for the change there. There is a note in this section referring the reader to "An expanded description of nearly all changes…" on the APA website. The link leads to an article titled "Highlights of Changes from DSM-IV-TR to DSM-5". But the article contains no reference to the change in question.
So we don't know the APA's justification for suppressing information about this potentially devastating adverse effect. But we do know that neuroleptic drugs are being prescribed for an increasing range of problems, and are even being prescribed to toddlers for temper tantrums and to nursing home residents for "management problems". Some have even acquired "block-buster" sales status. It is clearly in pharma's interests to suppress this information and it is consistent with psychiatry's hand-in-glove relationship with pharma that they should oblige their generous benefactors in this way. Remember, 69% of the DSM-5 workforce were in the pay of pharma while working on the revision.
Despite the early, and very clear, statements from individual psychiatrists linking psychiatric drugs to murder/suicides, the psychiatric leadership has consistently failed to address this link. Instead, they deceptively attribute these incidents to a lack of psychiatric "treatment", and they call for legal enforcement of even more drugging.
Finally
On June 9, 2016, Maria Oquendo, MD, President of the APA, wrote a post in support of the Senate's so-called Mental Health Reform Bill. The post was standard psychiatric propaganda, including the inane 21% annual and 50% lifetime prevalence of "mental illness". The reality is that if one can invent illnesses at will and arbitrarily reduce the "diagnostic" thresholds of these "illnesses", one can produce any prevalence numbers one chooses.
The post also drew attention to the fact that there were 41,000 suicides in the US in 2013, and asserted that "…we continue to fail people with mental illness every day."
In other words, more psychiatric treatment would reduce the suicide rate. But meanwhile, we have no data on how many of these individuals were in the throes of neuroleptic or antidepressant-induced akathisia. And as long as psychiatry and pharma are controlling the research agenda, such information will be systematically repressed.
As I've stated many times, psychiatry is intellectually and morally bankrupt. They are adamantly resistant to anything resembling critical self-appraisal, and there are no depths of deception and spin to which they will not go, to suppress the reality and the consequences of their drug-pushing depredations. Neuroleptic and antidepressant drugs induce some individuals to take their own lives and/or the lives of others. Neuroleptic and antidepressant drugs are almost certainly the proximate causes of many of the mass shootings that have plagued our country for almost twenty years. How much longer can psychiatry sustain this dreadful, self-serving deception?
And, Incidentally
Senator John McCain and Congressman David Jolly have introduced bills in their respective chambers that if enacted will require the Veterans Administration to conduct a comprehensive study of the link between psychiatric drugs and veterans' suicides. It will be an enormous step forward if these bills become law. It is also an interesting reflection that these bills were initiated by politicians, and not by psychiatrists, who present themselves as caring professionals acting in the best interests of their so-called patients.
If you live in the US, please encourage your representatives to support the McCain and Jolly bills (S 3410 and H 4640).
Thank You Dr Hickey, MIA and Sen McCain.
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