On April 30, 2019, the very eminent and learned psychiatrist Ronald Pies, MD, published a piece in Psychiatric Times titled Debunking the Two Chemical Imbalance Myths, Again.
Here’s the opening paragraph:
“Like the legendary Count Dracula, who could be killed only by driving a stake through his heart, some myths seem almost immortal. For more than eight years now, I have tried to drive a stake through the heart of two myths regarding the so-called ‘chemical imbalance theory’1-3—but with only limited success, as a recent piece in The New Yorker brought home to me.4″
THE TWO MYTHS
Dr, Pies tells us that the first myth holds that “…mental illnesses (psychiatric disorders) in general are caused by ‘a chemical imbalance’ in the brain—the so-called ‘chemical imbalance theory’ (CIT)”. The second myth holds “…that ‘Psychiatry’ as a profession endorsed the first myth, deliberately and knowingly ‘lying’ to countless, unsuspecting patients.”
Then:
“Ironically, anti-psychiatry groups are quite right in heaping scorn on the ‘chemical imbalance theory’ of mental illness, but not for the reasons they usually give. (I hasten to add that debunking the CIT is not to deny that biological factors play an important role in serious mental illness, including but not limited to major depression, bipolar disorder, and schizophrenia—see below).”
And:
“The fact is, there could never have been a scientifically based ‘chemical imbalance theory’ of mental illness, because a genuine theory requires an integrated network of well-supported, interlinked hypotheses. And yes, the frequently ignored distinction between a theory and a hypothesis is crucial. It is the key to understanding why claims by antipsychiatry bloggers regarding the CIT nearly always crash and burn.”
WHEN IS A THEORY NOT A THEORY?
When Dr. Pies says so.
In just about everything Dr. Pies has written on this topic, he belabors the point that the chemical imbalance theory of depression and other “mental illnesses” is not really a theory in the formal scientific sense of the term.
This, of course, is wonderfully interesting, and serves to support the notion, which I’ve long promoted, that Dr. Pies is extraordinarily learned and erudite. But it adds nothing to the discussion, and serves only to distract from the real issue.
Besides, the word theory, which has been in use since about 1600, has a wide range of uses. Here’s what my 2009 Merriam Webster’s Dictionary gives:
“1: the analysis of a set of facts in their relation to one another 2: abstract thought: SPECULATION 3: the general or abstract principles of a body of fact, a science, or an art <music ~> 4a: a belief, policy, or procedure proposed or followed as the basis of action <her method is based on the ~ that all children want to learn> b: an ideal or hypothetical set of facts, principles, or circumstances – often used in the phrase in theory <in ~ we have always advocated freedom for all> 5: a plausible or scientifically acceptable general principle or body of principles offered to explain phenomena <the wave ~ of light> 6a: a hypothesis assumed for the sake of argument or investigation b: an unproved assumption: CONJECTURE c: a body of theorems presenting a concise systematic view of a subject <~ of equations> syn see HYPOTHESIS”
Similarly wide ranges of meaning can be found in Random House (1992) and New World (1988) dictionaries. The former includes “…a guess or conjecture,” and the latter “…a speculative idea or plan as to how something might be done.” So, when we anti-psychiatry bloggers refer to psychiatry’s chemical imbalance theory, we are, despite Dr. Pies’ tedious assertions to the contrary, well within the dictionary definition of the term.
But that’s neither here nor there. As I mentioned earlier, Dr. Pies’ carping at us for using what he, as self-appointed arbiter of such matters, considers the wrong term, is a distraction. It’s a bit like a person accused of embezzlement arguing that it wasn’t embezzlement, it was fraud.
It doesn’t matter a rodent’s posterior whether we call it a theory, a hypothesis, a guess, or a conjecture, the fact is that it was a lie, and psychiatry did promote it, knowing that it was groundless. In addition, it was, and still is, widely accepted, and it did induce millions of people who would not otherwise have taken the drugs or the shocks to do so. So, for psychiatrists and for their pharma allies, it was a very profitable lie.
DID PSYCHIATRY PROMOTE THE CHEMICAL IMBALANCE THEORY?
I thought that I had laid this question to rest in my post Psychiatry DID Promote the Chemical Imbalance Theory (June 2014), but here comes Dr. Pies again.
“Scientifically speaking, there never was a network of validated hypotheses capable of sustaining a full-blown, global ‘chemical imbalance theory’ of mental illness in general. Moreover—and here we come back to Myth #2—psychiatry as a profession and medical specialty never endorsed such a bogus ‘theory,’ when judged by its professional organizations; its peer-reviewed publications; its standard textbooks5 or its official pronouncements. Furthermore, the whole notion of some looming, monolithic “Psychiatry” is absurd on its face, as my colleague, Dr George Dawson,6 has cogently argued.”
There are three critical points in the “Scientifically speaking…” paragraph quoted above. Firstly, it is important not to get hung up on the term “chemical imbalance”. This phrase was pushed strongly by psychiatry in the 80’s. But the essential issue is psychiatry’s unfounded insistence that the loose clusters of vaguely-defined thoughts, feelings, and behaviors which they call mental illnesses are real illnesses, caused by real physiological pathology. The phrase “chemical imbalance” and synonymous variations are still widely used, but psychiatry’s simplistic and spurious biological explanations have been promoted in many forms and guises. Secondly, Dr. Pies is attempting, once again, to restrict the debate by declaring, arbitrarily, that only statements from professional organizations, peer reviewed journals, standard textbooks, or official pronouncements are admissible. In reality, the philosophy and perspectives of a profession are more reliably identified in the practices and statements of its individual members than in its official pronouncements. Thirdly, Dr. Pies uses the caricature of some “looming, monolithic ‘Psychiatry'” to undermine the perfectly valid notion that one can make meaningful statements about a profession generally, even though there may be individual dissidents within the ranks, and even within the leadership.
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Here’s another quote from the “Debunking” article:
“To be sure: what many psychiatrists in the 1980s and 1990s did promote was some version of the biogenic amine (or catecholamine) hypothesis of mood disorders, focusing mainly on the neurotransmitters norepinephrine and serotonin. (Schizophrenia was conventionally explained by the now outdated ‘dopamine hypothesis.’). And, in truth, the significance of serotonin was considerably over-emphasized—owing to what Roger S. McIntyre, MD has facetiously called, ‘Psychiatry’s High School Crush.’7 Furthermore, the ‘SSRIs’ were accorded a rock-star status as effective antidepressants that they did not deserve. Most troubling from the standpoint of misleading the general public, pharmaceutical companies heavily promoted the ‘chemical imbalance’ trope in their direct-to-consumer advertising.8 But to be clear: there was no concerted attempt by ‘Psychiatry’ as a profession to promote a causal or etiological theory of mental illness in general, based solely on ‘chemical imbalances.’ Neither did the originators of the biogenic amine hypothesis—psychiatrists Joseph J. Schildkraut and Seymour S. Kety—promote such a view in the 1960s.9 Indeed, in 1965, Dr Schildkraut stated,
‘A rigorous extrapolation from pharmacological studies to pathophysiology clearly cannot be made. Clinical studies relevant to the catecholamine hypothesis are limited and the findings are inconclusive. It is not possible, therefore, to confirm definitively or to reject the catecholamine hypothesis on the basis of data currently available.’9“
There’s a lot in here, so let’s open it up. Firstly, it is noteworthy that Dr. Pies is admitting that many psychiatrists in the 1980s and 1990s did promote the “biogenic amine (or catecholamine) hypothesis” of depression and elation. Secondly, this theory did not originate with Drs. Schildkraut and Kety, as Dr. Pies asserts. Rather, the idea was first suggested in 1958 by two groups of researchers acting, as far as I know, independently. The first group was Guy Everett, PhD, James Toman, PhD, and several assistants from Chicago. The second group was John Saunders, MD, Nathan Kline, MD, Maurice Vaisberg, MD, et al from Rockland State Hospital, Orangeburg, New York.
Each group presented a paper at the scientific sessions of the Society of Biological Psychiatry, San Francisco, May, 1958. The proceedings were published under the title “Biological Psychiatry”, by Grune & Stratton (1959), edited by Jules H. Masserman, MD, who at the time was president of the society. The Everett and Toman proposal can be found in Chapter 6: “Mode of Action of Rauwolfia Alkaloids and Motor Activity”. Here are two quotes:
“The fact that essentially similar reversal of deserpidine effects with desoxyephedrine or DOPA was also observed in rats and monkeys leads to speculation regarding the same mechanisms in man. One may speculate on the possible role of centrally active amines present in the brain in the normal activity and general responsiveness of an individual. An excess of these might result in irritability, restlessness and aggressiveness. In the opposite direction, a deficiency of these substances would result in depressions and general lassitude.” (p 80)
and
“It would be presumptuous to expect that so simple a scheme would account for all the variations of motor behavior and reactivity of man in health and disease, but the evidence thus far obtained in animals has been highly reproducible and suggests that we may indeed be dealing with a biochemical area of major importance in the understanding of animal and human behavior.” (p 80)
It is interesting that the cautionary note expressed in the second quote above is promptly eclipsed by the expression of optimism that the theory may have “…major importance in the understanding of animal and human behavior.”
The Saunders, Kline, et al proposal can be found in the same volume, Chapter 24: “Psychic Energizers” (p 306). In the 1950’s, the term “psychic energizers” was commonly used for what today would be called antidepressants. Here’s the pertinent quote:
“The search for compounds other than iproniazid to act as psychic energizers continues. Our efforts to elucidate and evaluate compounds as psychic energizers emphasize that there are distinct differences between energizers and stimulants, probably even greater than between sedatives and ataractics. The mechanism of action of this clinical difference is of utmost importance since the etiology of this disease of affect, depression, may be related, to a disturbance of metabolic equilibrium of several amines.11, 12” (p 309) [Emphasis added]
Note that there are two references (11 and 12) cited in support of this proposal. Reference 11 was not entirely clear, but reference 12 is a gem. It’s Saunders, JC: Psychiatric Research Reports, No. 8, December 1957, Discussion, p 184. Here’s the quote:
“It has been said that if there is a twist in the mind of man there is a twist in the molecule. I would like to refute that statement. I believe there is a difference in the biochemical balance or equilibrium and not in the molecule per se.”
Incidentally, or perhaps not, Dr. Everett, at the time of publication, was Group Leader in Neuropharmacology, Abbott Laboratories, North Chicago, Illinois (Biological Psychiatry, same volume, p xi); Dr. Toman was an Associate Professor of Physiology and Pharmacology, Chicago Medical School, Chicago, Illinois (same volume, p xiii); and Abbott Laboratories was working on an antidepressant – CS 293 (Same volume, p 306)
The Saunders et al team were based at Rockland State Hospital, New York, and had been conducting trials on several experimental compounds:
“A number of experimental compounds are presently in clinical trial at Rockland State Hospital to evaluate their usefulness as psychoactivating (psychoanaleptic) agents. These preparations are: Warner-Chilcott, W-1544; Lakeside, JB-516; Hoffmann-La Roche, Ro 4-1018; Geigy, imipramine (G 22355); Bristol, phenyltoloxamine (PRN) and methonalide (BLM 188); Riker, Deaner (deanol, DMAE); and Abbott, CS 293.” (Same volume, p 306)
I apologize for laboring this matter, but the critical point is that the chemical imbalance theory of depression/elation was first proposed at about the same time by two groups of psychiatric researchers, both of whom were working closely with pharmaceutical companies in the development of antidepressants, and both of whom were members of the Society of Biological Psychiatry. Incidentally, the Society of Biological Psychiatry was founded in 1946, and is still very active today.
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Back to Dr. Pies’ “Debunking” article:
“Schizophrenia was conventionally explained by the now outdated ‘dopamine hypothesis.'”
Even by Dr. Pies’ standards for exonerating psychiatry, this is an extraordinary statement. The essence of the dopamine hypothesis was that people “with schizophrenia” had too much dopamine activity in their brains, and that this could be corrected with neuroleptic drugs. It is a chemical imbalance theory, and despite a great deal of highly motivated, and lavishly funded, research on the part of psychiatry, there has never been any convincing evidence for its validity. Nevertheless, it was promoted by psychiatrists and their pharma allies in their attempts to legitimize the use of major tranquilizers and to persuade their customers to take them.
And to describe this self-serving mendacity on the part of his colleagues, Dr. Pies uses the passive voice construction: “…was conventionally explained…”. So it wasn’t a case of self-serving deception on the part of psychiatrists, but rather a nebulous, disembodied convention that led people so widely astray. Furthermore, the assertion that the dopamine hypothesis is “now outdated”, implies that formerly it had some validity. In reality, there was never any evidence for this chemical imbalance theory, and its dissemination by psychiatry over several decades is nothing less than a hoax. I have discussed this matter in more detail in an earlier post.
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And then it gets even worse:
“And, in truth, the significance of serotonin was considerably over-emphasized—owing to what Roger S. McIntyre, MD has facetiously called, ‘Psychiatry’s High School Crush.’7“
For decades psychiatry pushed these false, destructive, disempowering, and stigmatizing chemical imbalance theories on their trusting customers, often with disastrous results, and here’s Dr. Pies excusing the whole shabby enterprise as a high school crush! So an entire, monolithic, so-called medical profession was operating at the cognitive and emotional level of a love-smitten teenager. And by Dr. Pies’ assessment, that excuses the deception and the damage!
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“Furthermore, the ‘SSRIs’ were accorded a rock-star status as effective antidepressants that they did not deserve.”
Again, the poor immature psychiatrists, infatuated as they were, could not resist dancing to the tune of their rhinestone-festooned products and their pharma cheerleaders. The poor little babes in the woods, stalked and exploited by colorful pills and their manufacturers! For three decades, psychiatry has been promoting these products as safe and effective, and has dismissed anti-psychiatry’s contentions to the contrary as unfounded. Now here’s Dr. Pies back-handedly conceding that we were correct all along, but dismissing the deception as rock-star idolatry!
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“Most troubling from the standpoint of misleading the general public, pharmaceutical companies heavily promoted the ‘chemical imbalance’ trope in their direct-to-consumer advertising.8“
It was psychiatrists who originated, developed, and promoted the chemical imbalance theory. They did not present it as a trope, but rather as neurochemical fact, even though the evidence for the theory was not to hand, and abundant contrary evidence was readily available. The correct word for this kind of presentation is hoax. Psychiatrists gambled their entire professional status on the hope that evidence for the theory would materialize, and they could become real doctors, treating real illnesses with real medicine.
Against these obvious and well-known historical realities, the eminent Dr. Pies is trying to persuade us that the chemical imbalance theory was just a trope – something not meant to be taken literally – and blaming the dissemination of this hoax on pharma.
Certainly pharma helped in the process, but at any time in the past fifty years psychiatry could have stopped the deception in its tracks. But the hoax suited psychiatry’s purpose, and they promoted it, and in many cases still promote it, with all the resources at their disposal.
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“Neither did the originators of the biogenic amine hypothesis—psychiatrists Joseph J. Schildkraut and Seymour S. Kety—promote such a view in the 1960s.9 Indeed, in 1965, Dr Schildkraut stated,
‘A rigorous extrapolation from pharmacological studies to pathophysiology clearly cannot be made. Clinical studies relevant to the catecholamine hypothesis are limited and the findings are inconclusive. It is not possible, therefore, to confirm definitively or to reject the catecholamine hypothesis on the basis of data currently available.’9“
Actually, as I mentioned earlier, the originators of the biogenic amine theory of depression were Guy Everett and James Toman (1959) and John Saunders, et al (1959). But Drs. Schildkraut and Kety did give the theory an enormous push. And the paragraph that Dr. Pies cites (“A rigorous extrapolation…”) can indeed be found in the Conclusion section of Dr. Schildkraut’s 1965 paper: The Catecholamine Hypothesis of Affective Disorders: A review of supporting evidence. And the paragraph does point out that definitive evidence for the theory is not “currently available”.
However, most of the Conclusion section appears more supportive of the catecholamine theory. For instance:
“Thus, although lacking direct experimental confirmation, the catecholamine hypothesis currently seems to be the strongest and most useful pathophysiological hypothesis of affective disorders. It must be stressed, however, that this hypothesis is undoubtedly, at best, a reductionistic over-simplification of a very complex biological state and that the simultaneous effects of the indoleamines, other biogenic amines, hormones and ionic changes will ultimately have to be included in any comprehensive formulation of the biochemistry of the affective disorders. In our present state of knowledge, however, the catecholamine hypothesis is of considerable heuristic value, providing the investigator and the clinician with a frame of reference integrating much of our experience with those psychopharmacological agents which produce alterations in human affective states.” (p 517)
And here’s a quote from the Summary Section of the article:
“The ‘catecholamine hypothesis of affective disorders’ proposes that some, if not all, depressions are associated with an absolute or relative decrease in catecholamines, particularly norepinephrine, available at central adrenergic receptor sites. Elation, conversely, may be associated with an excess of such amines.” (p 518)
And, Dr. Schildkraut’s paper had an enormous impact in the promotion of the chemical imbalance theory of depression and elation. According to Google Scholar, his paper has been cited over 3930 times.
There is an article on Dr. Schildkraut in Encyclopaedia Britannica. Here’s a quote:
“Joseph Jacob Schildkraut…was a pioneering researcher in the field of biological psychiatry. He was widely known for his research paper ‘The Catecholamine Hypothesis of Affective Disorders,’ published in the American Journal of Psychiatry in 1965, which helped establish a biochemical basis for depression and other mood disorders.” [Emphasis added]
Seymour Kety died in 2000, and in 2003, the National Academy of Sciences published a biographical memoir written by Louis Sokoloff, MD, a neuroscientist at NIMH.
“Although no definitive evidence of a biochemical defect linked to schizophrenia was derived from these studies, they did serve to organize Seymour’s thinking about the subject and led to his publication of several critical and heuristic papers in Science that almost certainly laid the foundation for modern biological psychiatry.” [Emphasis added]
So whether Dr. Schildkraut promoted the chemical imbalance theory of depression, as I suggest, or did not, as Dr. Pies believes, is a topic that could be debated at length. Dr. Schildkraut did acknowledge “…the importance of psychological factors in the etiology of at least some depressions…”, and in a subsequent paper in the April ’67 issue of Science, he and his co-author Seymour Kety re-emphasized the importance of “…environmental or psychological…” factors in the etiology of depression. But their references to these factors are complicated. Here’s the quote:
“Confirmation of this hypothesis must ultimately depend upon direct demonstration of the biochemical abnormality in the naturally occurring illness. It should be emphasized, however, that the demonstration of such a biochemical abnormality would not necessarily imply a genetic or constitutional, rather than an environmental or psychological, etiology of depression. Whereas specific genetic factors may be of importance in the etiology of some, and possibly all, depressions, it is equally conceivable that early experiences of the infant or child may cause enduring biochemical changes and that these may predispose some individuals to depressions in adulthood.”
The key point here is the word “enduring” in the last sentence. Essentially what Drs. Schildkraut and Kety are saying is that early experiences may cause lasting neurochemical changes, which is obviously true. But they are also implying that these changes are pathological in nature, solely on the grounds that they might contribute to feelings of despondency or sadness in later life.
And that’s the flaw in the logic. The reality is that all experiences, whether good, bad, or indifferent, produce lasting changes in our brains. That’s how we learn and remember. Some such changes are indeed pathological (e.g., a serious head injury), but most are not. A major loss during childhood, for instance, will usually leave us with a feeling of sadness which might persist long into adulthood. And this enduring feeling of sadness is indeed a reflection of the neurological changes. But these changes, these neurological bases for memory and learning, and emotion, are no more pathological than the neurological bases for pleasant feelings such as joy and success. It is frequently asserted that children “get over” major losses that occur during childhood. Sometimes this is true. Some children retain the memory of the loss, but the feeling of sadness recedes with time. Other children retain the feeling of sadness, and the attendant pessimistic outlook, for years and even decades. But – and this is the crucial point – the presence of despondency, at any time of life, no more confirms the existence of neurological pathology than the seeing of a particularly horrific incident confirms pathology in the visual apparatus. Sadness is the natural, non-pathological response to loss and/or adverse circumstances.
A detailed discussion of these issues would take us very far afield, but what is beyond debate is the fact that the work of Dr. Schildkraut, a psychiatrist, and Dr. Kety, a psychiatric neuroscientist, gave the simplistic and false chemical imbalance theory of depression an enormous boost, and was widely received by psychiatry as an endorsement of this spurious and destructive perspective, and of the increased prescribing of psychiatric drugs.
Perhaps the most noteworthy point of the entire matter is that Dr. Schildkraut’s and Dr. Kety’s reservations in both the 1965 and 1967 papers were largely ignored by the psychiatric profession. In 2005 the APA published on their website a brochure called “Let’s Talk Facts About Depression.” The brochure was offered free for downloading, and paper versions were sold in bundles of fifty for $29.95 (here). The document has since been taken down, but can still be found in various locations by searching for the title.
“Antidepressants may be prescribed to correct imbalances in the levels of chemicals in the brain. These medications are not sedatives, ‘uppers’ or tranquilizers. Neither are they habit-forming.” (Let’s Talk Facts About Depression) [Emphasis added]
This is a very clear endorsement of the spurious chemical imbalance theory of depression, with nothing to suggest a metaphysical or otherwise non-literal intention. And, incidentally, the notion that antidepressants are not habit-forming is questionable at the very least.
In the same document, under the heading Conclusion, the APA asserts:
“Depression is never normal and always produces needless suffering.”
This is the kernel of the entire self-serving hoax, because depression is the natural and expectable reaction to loss and/or abiding adverse circumstances. Not only is depression normal in this sense, it is actually adaptive. It alerts friends and family to the fact that we are experiencing difficulties; it encourages us to share our concerns; and it provides an incentive to make appropriate changes. Depression becomes intractable when the individual is unable – for whatever reason – to take appropriate remedial action. Eating pills to suppress this adaptive mechanism is analogous to sticking a piece of duct tape over the “check engine” light on a car’s dashboard. The pills may block or obscure the message, but in many cases, the issues remain unresolved, and when/if the pills are stopped, the depression returns. Psychiatry, ever creative in the promotion of its own interests, calls this treatment-resistant depression, and here’s what the APA has to say about that:
“Psychiatrists usually recommend that patients continue to take medication for six or more months after symptoms have improved. After two or three episodes of major depression, long-term maintenance treatment may be suggested to decrease the risk of future episodes.” (Same document)
So, pills for life, with all the collateral damage, reduced expectations, disempowerment, and stigma that this entails, for a result that is only marginally better than placebo. And not one whit of energy or resources is expended in trying to help the customer identify or ameliorate the true source or sources of the despondency. In fact, the customer is told the grotesque lie that the true source of the despondency is a neurochemical imbalance that the pills correct!
ACADEMIC PSYCHIATRISTS
Back to Dr. Pies’ present “Debunking” paper:
“…psychiatry as a profession and medical specialty never endorsed such a bogus ‘theory,’ when judged by its professional organizations; its peer-reviewed publications; its standard textbooks5 or its official pronouncements.“
In an earlier article on this topic (2014) Dr. Pies had stated:
“…I am not aware of any concerted effort by academic psychiatrists, psychiatric textbooks, or official psychiatric organizations to promote a simplistic chemical imbalance hypothesis of mental illness.”
It is particularly interesting that in the more recent paper Dr. Pies has dropped academic psychiatrists from this list. Indeed, it could be described as a prudent move on his part, in that academic psychiatrists have probably been more ardent than any other group in the promotion of chemical imbalance theories and other bio-bio-bio perspectives that dominate psychiatric practice today.
In previous posts, I have cited examples of this kind of promotion on the part of academic psychiatrists, and could readily cite more examples here. But perhaps one further example will suffice
The March 1992 issue of the American Journal of Psychiatry published the following letter to the editor on page 420. The letter was written by Dr. Ronald Pies himself.
“Proposed Model for Self-Injurious Behavior
Sir: The excellent review of self-injurious behavior by Ronald M Winchel, M.D., and Michael Stanley, PhD.(1) makes clear that we have no unifying theory or model for self-injurious behavior. Rather, it is approached from a variety of perspectives, including the affected population, putative psycho-dynamic issues, and possible neurotransmitter abnormalities. I wish to propose a heuristic model in which two broad types of self-injurious behavior are distinguished.
In type I, onset is usually during early adulthood, and the self-injurious behavior entails one or more isolated but serious acts. The lesion is frequently ‘ablative’ (e.g., autocastration) and associated with either a circumscribed somatic delusion or a severe identity disturbance. Such self-injurious behavior is generally seen in schizophrenic or other psychotic patients. I hypothesize that a primary excess of dopaminergic function is the principal neurotransmitter abnormality in type I and that both D2 and D1 receptors are implicated (possibly with D2 dysfunction predominant). Dopamine agonists would tend to worsen this type of self-injurious behavior, which may respond to conventional antipsychotics.
In contrast, type II has its usual onset in childhood or adolescence, in association with a variety of neurodevelopmental and character disorders, for example, Tourette’s disorder, autism, attention deficit hyperactivity disorder, and Lesch-Nyhan syndrome. Some individuals with borderline personality disorder and ‘obsessive spectrum’ disorders also fit the type II pattern. Self-injury is usually chronic, repetitive, and ‘irritative’ rather than ablative. The lesion is usually not ‘symbolic’ (as in autocastration) but is associated with a more general relief of tension, anxiety, or anger. Clear secondary gain is sometimes involved, as when a patient with borderline personality disorder engages in low-lethality wrist cutting to delay discharge from the hospital. Although endogenous opiate dysregulation may be involved, I postulate two principal neurotransmitter abnormalities in type II self-injurious behavior: a primary dopamine deficiency which, over time, may lead to secondary dopamine receptor hyper-sensitivity and/or a dysregulation of serotonergic systems (1-4). D1 receptors –– possibly in nigrostriatal more than in mesolimbic tracts –– are involved preferentially. Treatment with either dopamine agonists or antagonists may be helpful, depending on the point of ‘transition’ between primary dopamine deficiency and dopamine receptor hypersensitivity. Serotonergic agents (e.g., fluoxetine, clomipramine) are also helpful in this type, particularly in patients with ‘obsessive spectrum’ symptoms such as trichotillomania (5).
I propose this dichotomy as a spur to the development of a unified theory of self-injurious behavior and not as the definitive statement on this complex condition.
REFERENCES
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- Winchel RM, Stanley M: Self-injurious behavior: a review of the behavior and biology of self-mutilation. Am J Psychiatry 1991; 148:306-317
- Goldstein M, Meller E: The role of central dopamine in movement disorders, in Receptors and Ligands in Neurological Disorders. Edited by Sen AK, Lee T. Cambridge, Cambridge University Press, 1988
- Breese GR, Criswell HE, Duncan GE, Mueller RA: Dopamine deficiency in self-injurious behavior. Psychopharmacol Bull 1989; 25: 353-357
- Ratey JR, Sovner R, Parks A, Rogentine K: Buspirone treatment of aggression and anxiety in mentally retarded patients: a multiple-baseline, placebo lead-in study. J Clin psychiatry 1991; 52: 159-162
- Pollard CA, Ibe IO, Krojanker DN, Kitchen AD, Bronson SS, Flynn TM: Clomipramine treatment of trichotillomania: a follow-up report on four cases. J Clin Psychiatry 1991; 52: 128-130
Ronald Pies, MD
Boston Mass.”
This letter is a very good example of a chemical imbalance theory (using the word “theory” in the dictionary-endorsed sense of guess or conjecture). Note the following components: 1. the dismissal of psychodynamic issues; 2. the promotion of unproven “neurotransmitter abnormalities” as explanations; 3. the suggestion that the “abnormalities” may be resolvable by means of psychiatric drugs; and 4. the expression of hope, that the theory will be improved (“unified”) at some time in the future, with no intimation that any psychosocial factors would need to be included. The brief reference to secondary gains is very much in the nature of an incidental aside.
In addition, the last sentence in the third paragraph is particularly interesting:
“Serotonergic agents (e.g., fluoxetine, clomipramine) are also helpful in this type, particularly in patients with ‘obsessive spectrum’ symptoms such as trichotillomania (5).”
Firstly, note the definitiveness of the assertion: Serotonergic agents (e.g. fluoxetine, clomipramine) are helpful in this type. Secondly, note the reference number 5 at the end of the sentence. Ordinarily, this would denote that reference 5 provides some proof or evidence for the assertion in question. From the reference list we can see that reference 5 is Pollard et al, 1991. But Pollard et al in fact offers no proof for Dr. Pies’ assertion. Indeed the opposite is the case. Here’s the abstract:
“Four consecutive patients treated for trichotillomania (hair pulling) with clomipramine reported initially dramatic reductions in symptoms. However, three of the four patients had relapsed completely at 3-month follow-up, although all four were still taking previously effective levels of the drug. The fourth patient relapsed for about 2 weeks but regained initial treatment benefits. Implications for the treatment of trichotillomania are discussed.” (p 128) [Emphasis added]
And here’s a quote from the Discussion section:
“These four cases provide preliminary evidence that the short-term beneficial effects of clomipramine may not be maintained in the treatment of trichotillomania. Interestingly, a similar pattern of initial benefit followed by relapse was evident in another trichotillomanic patient treated in our clinic with fluoxetine, another potent serotonin reuptake blocker (unpublished report, 1990). However, our present report should be interpreted with caution. More definitive conclusions must await reports on the long-term outcome of larger numbers of trichotillomanic patients treated with clomipramine.” (p 129) [Emphasis added]
and, surprise! surprise!
“At the time their hair pulling returned, each of the three relapsed patients was experiencing substantial emotional turmoil. Specifically, two patients had been involved in conflict with significant others and the third patient had returned to school, which she found anxiety provoking. Notably, these patients were not receiving concomitant psychological treatment. Resumption of hair pulling might have been prevented by adjunctive therapy that, for example, taught these patients how to manage anxiety more effectively, or how to deal with interpersonal relationships in a more productive fashion. Of course, it is also possible that some alternative pharmacologic intervention would have been helpful. Although further increases in the dosages of clomipramine were either rejected or ineffective, the addition of an anxiolytic or another medication might also have circumvented relapse.” (p 129)
Note the reluctance to accept the obvious explanations, and the almost desperate attempts to salvage the pharmacological approach.
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LIMITATIONS OF THE MEDICAL MODEL
An additional, and perhaps most important, consideration in this general area is the fact that the medical model, effective as it is in the treatment of real illness, is not helpful, and is usually counter-productive, in addressing problems of thinking, feeling, and/or behaving. The critical difference here is that real illnesses have a relatively large degree of homogeneity with regards to their origins, etiology, course, outcome, and appropriate treatment. Individual variations, though sometimes critical, are usually secondary. Pneumonia, for instance, is caused by germs in the lungs, and the treatment consists essentially of eliminating those germs. By contrast, the kinds of life problems that psychiatry purports to address do not have this homogeneous core. The sources of despondency are as varied as the individuals who experience it.
Whereas it makes perfect sense to ask how do people get pneumonia, it makes no sense to ask how do people get self-injurious behavior, or despondency, or temper tantrums. One gets pneumonia because the germs successfully establish a colony in the lung tissue. But people engage in self-injurious behavior, or become despondent, or rant and rage, for an extremely wide range of reasons, even though the presentations may seem superficially similar. In matters of thinking, feeling, and behaving, there are always multiple paths to the same place, and conversely, superficially similar antecedents can lead to very different outcomes. The notion that psychiatry can develop criteria for “diagnosing” depression, and guidelines for “treating” it, in the same way that real doctors do for real illnesses is a fundamental error. It is on their self-serving refusal to acknowledge these simple and obvious facts that psychiatry’s attempts to impose a medical model on problems of thinking, feeling, and behaving always have, and always will, founder, to the endless detriment of their customers.
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The subtitle of Dr. Pies’ Debunking article is:
“‘A little learning is a dangerous thing.’—Alexander Pope”
And indeed it is. But it is not nearly as dangerous as a psychiatrist with a head full of spurious diagnoses and a ready prescription pad.
Psychiatry is flawed at its very core, and is simply irremediable. The damage it has done, and continues to do, is profound and everywhere to be seen.