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 of 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.
. . . . .
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?
Mad in America hosts blogs by a diverse group of writers. These posts are designed to serve as a public forum for a discussion—broadly speaking—of psychiatry and its treatments. The opinions expressed are the writers’ own.
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