The spurious chemical imbalance theory of depression is arguably the most destructive thing that psychiatry has ever done. Worldwide, millions of individuals are taking antidepressants, often with a cocktail of other drugs, because they have been told the blatant falsehood that they need the pills to combat a brain illness–a “real illness just like diabetes.”
Many of these individuals were told the additional lie that they needed to take the pills for life and are now addicted to the products.
At the present time, some psychiatrists and psychiatric facilities are backing away from the hoax. Most of these recantations take the form: “We didn’t mean it literally. The chemical imbalance thing was just a metaphor.”
But what needs to be stressed is that the impetus for these diluted recantations came, not from psychiatry, but rather from the anti-psychiatry movement. It was the thousands of protesting voices that finally persuaded psychiatry that some backing off was needed, particularly as no proof of the theory had ever been uncovered.
The response from psychiatry, however, has not been commensurate with the damage done. What we need to see are full page ads in all major newspapers and cyber news outlets acknowledging that the chemical imbalance theory was a hoax; that it induced millions of people worldwide to take these drugs; and that it was developed and propagated to increase psychiatry’s prestige and earnings. But that’s not what we are seeing.
Instead, the general response from psychiatry continues to be one of denial, minimization, and excuse-making. The very eminent and learned Ronald Pies, MD, is the master of denial in this area, but minimizers and self-excusers abound. We are told that “patients” needed a simple formula for understanding their problems. They didn’t. They needed the truth. We are told that “patients” needed a biological explanation to reduce stigma and alleviate their feelings of guilt. They didn’t. They needed valid explanations. Besides, biological explanations actually increase stigma (here, here, here, and here).
The essential point is that as the drugs began to come on stream in the 50’s, 60’s and 70’s, psychiatry needed illnesses–real illnesses with clear-cut biological etiologies–to cash in on the pharma-generated bonanza. Real illnesses were not to hand, so they invented their various chemical imbalance theories and promoted them as fact with all the vigor and energy that they could muster. Since then, psychiatrists have produced a truly overwhelming volume of research all aimed at proving the theory correct, but with no success. The simplistic shortage-of-serotonin-in-the-brain nonsense remains stubbornly unproven. As mentioned above, psychiatrists have backed off the more blatant expressions of this theory, but, remarkably, the “treatments” remain the same: “Take these pills every day and come back in three months for more.”
All of which is very interesting. But of even more interest is the recent development of a new approach to validating–or rather attempting to validate–“psychiatric illness.”
The New Approach
In JAMA Psychiatry, October 2019, Kenneth Kendler, MD, published an essay titled From Many to One to Many-the Search for Causes of Psychiatric Illness. Dr. Kendler’s essential thesis is as follows. Prior to about 1850, “causes of illness were anecdotally recorded from individual cases, resulting in long and diverse lists for all disorders.” In the second half of the nineteenth century, “single causes were found for many infectious diseases.” Causal thinking shifted from multicausal approaches to monocausal theories of etiology. Dr. Kendler writes, “Indeed proving monocausal etiology became a way to establish the legitimacy of a disorder.” In the mid 20th century, general medicine “shifted to a chronic disease model in which paradigmatic disorders, such as cancer and cardiovascular disease, were shown to be highly multicausal.” Psychiatry, however, continued to pursue monocausal theories in their attempt to legitimize their activity. “Despite ample evidence to the contrary, monocausal thinking continues to influence our field, for example, in the popular but improbable view that we can, with a few key advances, move easily from descriptive to etiologically based diagnoses.”
Dr. Kendler works for Virginia Commonwealth University. He is a Distinguished Professor of Psychiatry, Professor of Human Genetics, and Director of the Virginia Institute of Psychiatric and Behavioral Genetics. He served on the DSM-III-R Work Group, on the DSM-IV Task Force, and on the DSM-5 Work Group for mood disorders.
Dr. Kendler’s Essay
Dr. Kendler’s essay highlights two main themes: firstly, that psychiatry is not blameworthy in the promotion of spurious and monocausal etiologies; and secondly, that even though the quest has failed dismally, this is not a problem because a multicausal approach is better anyway.
Here are some pertinent quotes from Dr. Kendler’s paper, interspersed with my thoughts and observations.
“The second epidemiologic phase, termed infectious disease, had as its paradigm ‘the germ theory,’ lasted roughly from 1850 to 1950, and was dominated by monocausal etiologic theories in which the relationship between putative etiologic agents and specific diseases was one to one (although most investigators recognized such modifying factors as ‘host resistance’). The third epidemiological phase, termed chronic disease, had a dominant ‘black box’ paradigm. It incorporated a multifactorial disease model for what was termed chronic noncommunicable diseases (eg, diabetes, heart disease, certain forms of cancer, and hypertension), diseases often associated with particular lifestyles that could not be explained by a single salient causal factor. In this paradigm, the goal of epidemiology was to determine the magnitude and causal nature of the associations between a wide range of putative risk factors and these chronic noncommunicable diseases. This phase began around 1950 and has lasted until current times.” (p 1087)
The essential point that Dr. Kendler is making here is that there is a fundamental distinction between these two phases. But is this really so? Let us compare scarlet fever, a “classic” monocausal infectious disease, with diabetes, which is the first example Dr. Kendler gives of a multicausal chronic disease.
Scarlet fever is caused by a streptococcal infection of the throat, while diabetes is widely considered to arise from many causes, or risk factors, as they are sometimes called. These include inheritance, lifestyle factors, and diet. However, the essential cause of diabetes is an inability of the pancreas to produce enough insulin to adequately process and utilize the sugar in the blood stream. This in turn stems from a damaged or compromised pancreas, ingestion of more sugar than the pancreas can cope with, or other causes. When considered in this light, diabetes is a monocausal illness, even though there are multiple pathways to the final cause.
Applying the same logic in reverse, one can make a case that scarlet fever is multicausal. Firstly, the individual’s throat has to be exposed to the streptococcal infection. Secondly, the germ has to survive the initial immune system response. Thirdly, as hand-washing is one of the major protections against contracting this illness, anything that militates against frequent hand-washing could be considered a cause, e.g., living in crowded unsanitary conditions.
In addition, the time period leading up to the contraction of an illness can be analyzed and re-analyzed almost indefinitely. Any incident or event in that time frame has the potential to be considered a contributing cause. Let us say, for instance, that a child contracted scarlet fever at a birthday party given by one of his friends. We could legitimately say that the invitation caused the illness; or that the child’s acceptance of the invitation was the cause. Or let us become even more imaginative and say that the child in question was rather shy and didn’t want to go to the party, but was prevailed upon by his parents to do so, in the belief that it would “do him good.” So the illness was caused inadvertently by the parents! And so on.
Back to Dr. Kendler’s essay.
“During the second half of the 20th century, the approach to disease causation of major parts of psychiatry was out of step with the rest of medicine and medical epidemiology. Instead of multicausal models, the rising and soon to be dominant field of biological psychiatry pursued monocausal models for their major disorders.” (p 1088)
The reader will have no difficulty seeing where this is going. Psychiatrists were chasing single causes, for their so-called illnesses, when they should have been looking for many causes. So the great failure of psychiatry to deliver the promised causes wasn’t a failure at all. They were simply looking for the wrong kind of explanation. But–and this is the point that Dr. Kendler glosses over–it wasn’t a benign error. Psychiatry needed clear-cut biological explanations in order to take advantage of the drugs and to establish themselves as bona fide doctors. In this regard they routinely prioritized their own guild interests over the welfare of their clients.
“In the early to mid-1960s, through histofluorescence stains, the cell bodies and neuronal pathways of the 3 monoamine neurotransmitters were identified: dopamine, norepinephrine, and serotonin. This further spurred the development of 3 long-lived monocausal neurochemical theories for psychiatric illness. All were proposed in the mid-to-late 1960s: the ‘catecholamine hypothesis of affective disorders,’ the ‘dopamine hypothesis of schizophrenia,’ and the ‘serotonin hypothesis of depression.’ Although based on a range of evidence, the primary support for these theories was reasoning backward from therapeutic mechanisms to etiology. That is, for Parkinson disease the logic was sound: clarification of cause leading to a proposed treatment. By contrast, psychiatry followed the more problematic approach of extrapolating backward from a proposed mechanism of treatment to the cause of the disease. Although the original articles proposing these theories were couched in qualifications, as a psychiatry resident in the late 1970s, I was taught these theories as monocausal explanations. Schizophrenia was caused by excess dopamine transmission. Decades later, I would commonly see patients who would say some version of ‘my psychiatrist said I have a chemical imbalance in my brain’ and then proceed to summarize one or more of these theories. It is now widely accepted that these theories, claiming a dominant causal pathway to illness, are false although debate continues regarding the dopamine hypothesis.” (p 1088) [Emphases added]
There’s a lot in this quote. Firstly, note the phrase “Although based on a range of evidence.” In fact the “evidence” supporting these chemical imbalance theories was flawed, i.e. it was not evidence at all. Secondly, note the sentence “By contrast, psychiatry followed the more problematic approach of extrapolating backward from a proposed mechanism of treatment to the cause of the disease.” [Emphasis added] This was not a “more problematic” approach; it was a bogus approach; a hoax. And if the psychiatrists who promoted these theories couldn’t see the deception, then they had no business presenting themselves as a helping profession. It became–and perhaps still is–routine for mental health workers who drew attention in case conferences to critical psychosocial realities to be told by the psychiatrists that “first we have to treat the depression”, which invariably meant drugs or electric shocks.
“Although the original articles proposing these theories were couched in qualifications, as a psychiatry resident in the late 1970s, I was taught these theories as monocausal explanations.” (p 1088)
Dr. Kendler did his psychiatry residence at Yale University, during which, he tells us, he was taught the various chemical imbalance theories, presumably as valid, factual explanations. This seems straightforward enough, and presents no surprises. But there is some ambiguity. If I were to say that my father taught me how to ride a bike, I am actually making two statements. Firstly, I am asserting that my father expended some time and effort in this process, and secondly, that his efforts were successful. In his essay, however, Dr. Kendler leaves this issue vague. Did he believe the hoax, and did he in turn foist it on his customers? It is obvious that Dr. Kendler is a very bright person and, given the fact that “the original articles proposing these theories were couched in qualifications,” it is reasonable to believe that he did see through the whole sordid deception. So what did he say to the trusting victims who parroted back the bogus theories to him? Did he tell them the truth? Or did he play along?
It is not my intention to pressure Dr. Kendler on this matter. Economics can make cowards of us all. But if he genuinely wants to promote honesty and integrity in this area, it would be helpful if he were to write an exposé of sorts concerning the pressures he experienced in these matters during his psychiatric residency at Yale. Such an endeavor would be unlikely to endear him to his colleagues, but would shed light on a facet of psychiatry that has for too long been kept hidden, and might even encourage other psychiatrists to follow suit.
“Psychiatry has had a long-term love affair with monocausal theories of illness dating at least from the late 19th century, heavily influenced by our success at the identification and effective eradication of GPI [general paresis of the insane]. In the latter half of the 20th century, with both neurochemical and molecular genetic theories of illness, our enthusiasm for monocausal theories outran our common sense. Emerging from decades of psychoanalytic dominance, we were deeply committed to reestablishing our medical legitimacy. What better way to show that we treated ‘real’ diseases than to show that they were monocausal?” (p 1089)
There is a distinct exculpatory tone to this passage. Instead of acknowledging that psychiatrists were systematically deceiving their customers for their own benefit, Dr. Kendler tells us that it was just “a long-term love affair,” in which their “enthusiasm for monocausal theories outran [their] common sense.”
Indeed, as mentioned earlier, this exculpatory stance is one of the dominant themes of the essay. Here are some additional quotes:
“Our long yearning for monocausal theories of etiology drives, at least in part, our heartfelt calls for the abandonment of our descriptive nosologic systems in favor of an etiologic model.” (p 1089)
There have not been “heartfelt calls” or “long yearning” from psychiatry on this matter. Rather, they simply declared the matter resolved, and promoted the chemical imbalance theories as fact. I have written extensively on this subject here.
“This search has 2 prominent phases, both fueled by new scientific developments. The first was neurochemical. The stage was set in 1957 by Montagu’s discovery of dopamine in brain tissue quickly followed, in 1960, by the dramatic finds from Ehringer and Hornykiewicz of the decreased content of dopamine in the postmortem brains of patients with Parkinson disease. Here was a major neurologic disorder fitting apparently into a monocausal neurochemical theory. What could be more exciting for the then young and ambitious field of biological psychiatry?” (p 1088) [Emphasis added]
So the systematic, self-serving, and widespread deception perpetrated by psychiatry stemmed from their excitement! How eminently understandable.
“The second wave of monocausal theories in psychiatry was genetic. Despite much evidence from family studies that major psychiatric disorders did not segregate in pedigrees as expected for a mendelian condition, the first successful linkage study of Huntington disease in 1983 elicited intense excitement in psychiatric genetics and launched a large number of linkage studies, especially of schizophrenia and bipolar illness.” (p 1088) [Emphasis added]
Even more excitement!
“Yet the ghost of GPI—of monocausal psychiatric disorders—lurks in our memory. To this day, it influences our nosologic thinking. It makes us too willing to adopt a monocausal perspective in our clinical work and in our explanations of psychiatric disorders to patients. Monocausal thinking continues to support hard reductionist approaches that seek the cause of our major disorders and is one of several factors inhibiting collaborative psychiatric research work across scientific levels.” (pp 1089-1090)
So it is the “ghost” of GPI lurking in psychiatrists’ collective memories that inhibits them from acknowledging the non-medical nature of depression, painful memories, paranoid thinking, distractibility, etc…
“Despite the wide acceptance of the chronic noncommunicable disease model in modern medicine, there remains in our culture a sense that disorders with many causes have reduced legitimacy. Therefore, both clinicians and their patients would feel more secure if a large indisputable cause were found for their disorders. This, however, is a social and not a scientific problem.” (p 1089-1090) [Emphasis added]
So a monocausal breakthrough would make “clinicians and their patients” feel more secure. So, telling a bereaved woman that her sadness is the expected and reasonable response to the death of her spouse will make her feel less secure than telling her the gross falsehood that there is something wrong with her brain. Or telling a battered wife that her sadness is the understandable response to the violence would make her feel less secure than telling her it stems from a brain disease. This is exculpation taken to a new level. We lie to our customers because it makes them feel more secure.
Dr. Kendler’s Conclusions
Dr. Kendler closes his essay on an upbeat, exhortative note.
“The stigma of psychiatric illness and the low status of the psychiatric profession need to be addressed at both social and political levels and will not likely be solved through the discovery of major single causes for our illnesses. The legitimacy of the discipline of psychiatry does not rest on our ability to find single major causes of our disorders.” (p 1090)
How does one address the stigma associated with “psychiatric disorders” and the low status of the psychiatric profession at social and political levels? PR campaigns? Lobbying politicians to pass psychiatry-friendly laws? These things are happening already, but the routine prescribing of pills and electric shocks continues to be psychiatry’s only stock in trade, and the self-centered promotion of biological psychiatry continues to dominate the field.
“Rather than grieving for the loss of our visions of another GPI around the corner, we can positively embrace the etiologic complexity of our disorders.” (p 1090)
Actually they are not psychiatrists’ “disorders.” Rather, they are the “disorders” that psychiatrists self-servingly foist on their hapless clients.
“If the common, morbid dysfunctions of the human cardiovascular, immune, hormonal, musculoskeletal, and gastrointestinal systems, which cause most of the morbidity in our country, are highly multifactorial, could we realistically expect anything else from the parallel dysfunctions of our mind/brain system?” (p 1090)
In other words, psychiatric “illnesses” have as much ontological reality as diabetes, heart disease, cancers, hypertension, etc. Dr. Kendler encourages his colleagues not to grieve the abandonment of the quest, but rather to “positively embrace the etiological complexity” of psychiatric “illnesses.”
But what does “etiologic complexity” actually mean in this context, and why is it so important to Dr. Kendler?
Dr. Kendler uses various terms to describe “etiologic complexity.” For instance, he describes the illnesses in question as “multifactorial,” “chronic noncommunicable,” “often associated with particular life styles,” “multicausal,” etc.
Dr. Kendler has been working on this general theme for quite some time. In 2012 he published an article in Molecular Psychiatry called Levels of explanation in psychiatric and substance use disorders: implications for the development of an etiologically based nosology (2012: 17, 11-21). Here are two quotes from the abstract:
“The soft medical model for psychiatric illness, which was operationalized in DSM-III, defines psychiatric disorders as syndromes with shared symptoms, signs, course of illness and response to treatment. Many in our field want to move to a hard medical model based on etiological mechanisms.” (p 11)
“…a move toward an etiologically based diagnostic system cannot assume that one level of explanation will stand out as the obvious candidate on which to base the nosology. This leaves two options. Either a hard medical model will be implemented that will require a consensus about a preferred level of explanation which must reflect value judgments as well as science. To take this approach, we need to agree on what we most want from our explanations. Alternatively, we will need to move away from the traditional hard medical model that requires that we ground our diagnoses in single biological essences, and focus instead on fuzzy, cross-level mechanisms, which may more realistically capture the true nature of psychiatric disorders.” (p 11)
There’s a lot here. Firstly, there is what many readers might consider a contradiction in the first sentence: “The soft medical model for psychiatric illness, which was operationalized in DSM-III, defines psychiatric disorders as syndromes…” [Emphases added] But syndromes are not illnesses. Here’s how DSM-III defines a syndrome:
“A grouping of symptoms that occur together and that constitute a recognizable condition. The term ‘syndrome’ is less specific than ‘disorder’ or ‘disease.’ The term ‘disease’ generally implies a specific etiology or pathophysiological process. In DSM-III most of the disorders are, in fact, syndromes.” (p 368)
And elsewhere in the text (p 6), the term mental disorders is defined as “a clinically significant behavioral or psychological syndrome.” However, even before DSM-III was published (in 1980), it was widely accepted and promoted by psychiatrists that many psychiatric “disorders,” including depression, were genuine bona fide illnesses. (In my entire career I have encountered only one psychiatrist who acknowledged that psychiatric disorders were “syndromes, not real illnesses”.) This massive deception has been discussed at great length in various venues and need not be labored here. But what is noteworthy is Dr. Kendler’s next sentence: “Many in our field want to move to a hard medical model based on etiological mechanisms.” But in fact almost all psychiatrists have already made this move and have been promoting the chemical imbalance hoax for decades. Many psychiatrists who are now retired practiced nothing but bio-bio-bio psychiatry for their entire careers.
Obviously Dr. Kendler is aware of this. So, what point is he making?
“…a move toward an etiologically based diagnostic system cannot assume that one level of explanation will stand out as the obvious candidate on which to base the nosology.” (p 11)
In other words: if psychiatrists continue down their present road trying to use science to prove their various disease theories, they are just as likely to discover that “major depression,” “schizophrenia,” “PTSD,” etc., stem from psychosocial and economic causes rather than from their cherished brain diseases. In effect Dr. Kendler is saying: abandon the search or we run the risk of losing everything. “(We) cannot assume that one level of explanation will stand out as the obvious candidate on which to base the nosology.” In other words, we cannot assume that biological explanations will emerge as the dominant perspective. Dr. Kendler warns his colleagues, “we need to agree on what we most want from our explanations.” What does he mean by this? Read on.
Here are some quotes from the body of the 2012 article:
“Let me sketch what we might find for MD [major depression]. Single gene effects for MD are even smaller and less well established than for AD [alcohol dependence]. Aggregate genetic effects are also somewhat weaker and are modified by a range of environmental exposures. Structural and functional magnetic resonance imaging studies have suggested a range of central nervous system abnormalities that correlate with MD but the specificity and strength of these associations, as well as their causal status, remain uncertain. A number of physiological abnormalities including endocrine and immune function have been reported in cases of MD but again, sensitivity and specificity have typically remained modest. Several aspects of personality are strongly correlated with risk for MD—especially neuroticism. This association is almost certainly causal but is nonspecific as high levels of neuroticism predispose to many internalizing disorders. Some cognitive processes may be more specific and here their causal role has been clearly demonstrated by many randomized controlled trials of cognitive behavior therapy. A range of early environmental risk factors have been well established for MD (for example, poor parenting and sexual abuse) and are generalizable across cultures but are quite nonspecific. Stressful life events can be quite strongly associated with risk for MD. Much, but not all, of this association is likely causal and some classes of events are moderately specific for MD. However, stressful life events are likely to be quite distal influences on risk pathways to MD and many such events predispose to other psychiatric disorders. Economic factors can impact on risk for MD via levels of unemployment and cultural factors can shape the expression and help-seeking behavior of those with depressive syndromes.” (p 16)
“Nature does not appear to have provided us one critical level of explanation for psychiatric illness that stands out from the background. For CF [cystic fibrosis], explanatory power is highly concentrated in the level of DNA base-pair variation. For psychiatric disorders, explanatory power is dispersed and diffuse.” (p 16)
So, genuine scientific investigation might show that depression, say, is as likely to stem from sad events in people’s lives as from any kind of brain disease.
“The current status of our science, and, most probably, the nature of psychiatric disorders themselves, does not yield up unambiguous choices for the best level at which to define psychiatric illness etiologically.” (p 16) [Emphasis added]
Or might even show that depression is much more likely to stem from sad events.
But, despite these obvious concessions to a bio-psycho-social-cultural-economic perspective, Dr. Kendler is careful not to jettison the baby with the bathwater. He still seeks to preserve the notion that psychiatric disorders are “real illnesses.”
“…a rejection of the hard medical model for psychiatric disorders should not be misunderstood as setting up a deep divide between etiologic models for psychiatric and medical disorders.” (p 16)
“If, as our review of the data suggest, there is no a priori way to pick a single level of explanation on which to base an etiological nosology, we could try to argue it out on pragmatic grounds. What do we most want as a field from our explanations?” (p 17)
What indeed? To date, psychiatry’s primary motivations have been enhanced prestige, expansion of scope, and increased earning power, all of which were well-served by the chemical imbalance hoax.
What Dr. Kendler is telling his colleagues here is that the hoax is exposed; that science will not give them what they seek; and that by continuing to promote a purely biological perspective they are running the risk of losing what they want most: the “reality” of “psychiatric illness.” In other words, the science is not going our way, so we need to ask ourselves what do we most want, and then promote concepts that will help us achieve this. Dr. Kendler’s wording is carefully chosen, but it seems to be that he is encouraging his colleagues to dispense with the formalities and neutrality of science and promote concepts that will retain psychiatry’s hegemony in the field: what we want most.
Towards the end of the article Dr. Kendler provides us with more descriptors of the psychiatric “diagnostic” system that he envisions for the future. These include “disorders (of)… complex, mutually reinforcing networks of causal mechanisms,” “disordered multi-level mechanisms,” and “higher-order disturbances in multi-level mechanisms.” [Emphases added]
Note the words “disorders,” “disordered,” and “disturbances.” Dr. Kendler, as in the 2019 paper, affords no recognition to the fact that the thoughts, feelings, and actions in question are not actually illnesses, and in many (perhaps most) cases are clearly adaptive.
Four years later (2016) Dr. Kendler published The Nature of Psychiatric Disorders (World Psychiatry, 2016: 15: 5-12). Here’s a quote from the abstract:
“Therefore, we should argue more confidently for the reality of broader constructs of psychiatric illness rather than our current diagnostic categories, which remain tentative. Finally, instead of thinking that our disorders are true because they correspond to clear entities in the world, we should consider a coherence theory of truth by which disorders become more true when they fit better into what else we know about the world. In our ongoing project to study and justify the nature of psychiatric disorders, we ought to be broadly pragmatic but not lose sight of an underlying commitment, despite the associated difficulties, to the reality of psychiatric illness.” (p 5)
Note the phrase “…we ought to… not lose sight of an underlying commitment, despite the associated difficulties, to the reality of psychiatric illness.” To which I can only ask: why not? The common and accepted meaning of the word “illness” is something going significantly awry with the structure or function of an organ. If what psychiatrists call major depression doesn’t actually conform to this description, why should psychiatry maintain an “underlying commitment to the reality of psychiatric illness?” Also, note the phrase “In our ongoing project to study and justify the nature of psychiatric disorders” [Emphasis added]. Isn’t this arguably the very opposite of valid science? Didn’t most of the great errors of science stem from efforts to justify the status quo often for the benefit of various powerful conflicting interests?
Despite Dr. Kendler’s writings on these matters, his polycausal model is not attracting a large following. Here are quotes from the websites of some psychiatric facilities:
Harvard Medical School: What causes depression?
“Certain areas of the brain help regulate mood. Researchers believe that — more important than levels of specific brain chemicals — nerve cell connections, nerve cell growth, and the functioning of nerve circuits have a major impact on depression. Still, their understanding of the neurological underpinnings of mood is incomplete.” [Note how the simplistic chemical imbalance theory is being nudged aside, and being replaced by the more generic notion of nerve “functioning”.]
This quote is followed by five pages of closely-written type under the following headings: (Brain) regions that affect mood; Areas of the brain affected by depression (with picture); Nerve cell communication; How the (neurological) system works; When the (neurological) system falters; Kinds of neurotransmitters; How neurons communicate (with picture); Genes’ effect on mood and depression; Temperament shapes behavior; Stressful life events; How stress affects the body; Early losses and trauma; Seasonal affective disorder; Medical problems; and Depression medications.
The material is heavily slanted towards a biological perspective. Even the headings that sound psychosocial are slanted. The section on stressful life events contains:
“Disturbances in hormonal systems, therefore, may well affect neurotransmitters, and vice versa.”
The section on early losses and trauma contains:
“Many researchers believe that early trauma causes subtle changes in brain function that account for symptoms of depression and anxiety. The key brain regions involved in the stress response may be altered at the chemical or cellular level.”
Mayo Clinic’s article Depression (major depressive disorder) under the section Causes:
“It’s not known exactly what causes depression. As with many mental disorders, a variety of factors may be involved, such as:
Biological differences. People with depression appear to have physical changes in their brains. The significance of these changes is still uncertain, but may eventually help pinpoint causes.
Brain chemistry. Neurotransmitters are naturally occurring brain chemicals that likely play a role in depression. Recent research indicates that changes in the function and effect of these neurotransmitters and how they interact with neurocircuits involved in maintaining mood stability may play a significant role in depression and its treatment.
Hormones. Changes in the body’s balance of hormones may be involved in causing or triggering depression. Hormone changes can result with pregnancy and during the weeks or months after delivery (postpartum) and from thyroid problems, menopause or a number of other conditions.
Inherited traits. Depression is more common in people whose blood relatives also have this condition. Researchers are trying to find genes that may be involved in causing depression.”
University of Rochester Medical Center, Major Depression, under the heading What causes depression?
“Researchers are studying the causes of depression. Several factors seem to play a role. It may be caused by chemical changes in the brain. It also tends to run in families. Depression can be triggered by life events or certain illnesses. It can also develop without a clear trigger.”
And so on. It’s clear that most pro-psychiatry writers have received the message to downplay the simplistic too-little-serotonin-in-the-brain theory. Many, however, are still relying on this notion but couching it in different terms or adding some token psychosocial material, usually referred to as “triggers.”
In psychiatry there is no actual illness behind the “symptoms.” “Major depressive disorder” and psychiatry’s other functional disorders are nothing more than loose collections of vaguely and arbitrarily defined thoughts, feelings, and behaviors. Psychiatry’s clear objective in the past fifty years has been to pathologize every significant difficulty of thinking, feeling, and/or behaving, and to sell these bogus illnesses to the general public, the media, insurance companies, and government officials. The only essential difference between psychiatrists and street-corner drug-pushers is that the latter don’t pretend that they are treating or curing illnesses.
Dr. Kendler has written an interesting and thought-provoking essay, but, in my view, has missed the central point: that depression, regardless of severity, duration, or impact, is not an illness. In fact, the opposite is the case. Depression is an adaptive mechanism that encourages us to make changes in our lives, habits, or circumstances. Just as pain provides an incentive to remove our hand from a hot stove, so depression encourages us to leave home, change jobs, develop some assertion skills, find a partner, etc. It is a mechanism that we share with virtually all other animal species, though the precise nature, complexity, and impact of the depression varies enormously.
As a species we can experience a wide range of emotions. We have this ability because we have “machinery” in our brains, and other organs, that enables this to happen. It is widely believed in psychiatric circles that if neurobiologists could uncover the precise mechanisms involved in experiencing depression, this would prove that depression is an illness. But, in fact, uncovering such mechanisms would no more pathologize depression than the neurobiology of walking or seeing or writing poetry would pathologize these activities. All human activity has a neurobiological underpinning, without which the activity cannot occur. We cannot see without eyes and optic nerves, etc.; we cannot feel without feeling “machinery” though we don’t know exactly what this machinery is or how it works.
It certainly needs to be acknowledged that a person’s “feeling apparatus” can malfunction, but such malfunctions are almost certainly rare, and cannot be routinely inferred from the presence of depression, regardless of severity. I have personally worked with hundreds of depressed individuals in my career, but have never encountered anyone whose level of depression was incommensurate with his/her story. Psychiatrists have essentially numbed themselves to this reality, firstly because of their spurious atheoretical approach (if you’ve got the symptoms–regardless of why you’ve got them–then you have the illness); and secondly because their primary, or perhaps only, agenda is to clinch the diagnosis. It is particularly interesting in this regard that before the arrival of the pills, psychiatrists, most of whom practiced some kind of psychotherapy, had no difficulty recognizing the reality: that if people are given the opportunity to talk, they can tell you very clearly why they are depressed.
For several decades psychiatry has been lying to its customers that depression is a pathological state caused by a shortage of serotonin, and can, apparently miraculously, be diagnosed without ever examining the brain but simply by scoring yes on five of the nine items on the facile checklist. Some of the more prestigious facilities and colleges are stepping back from the serotonin hypothesis, largely as a result of being outed by the anti-psychiatry movement. But the “diagnostic” criteria are still the same, and the treatment hasn’t changed. It’s still “eat these pills every day and come back in three months.” And if that doesn’t work, we’ll try electric shocks.
Sometimes people feel trapped in their circumstances and are unable to muster the resources or skills to effect the necessary changes. An abused wife, for instance, might lack the economic or emotional means to leave her abusive husband. A man stuck in a job that he hates might not be able to see a way out. In cases like these, the depression can appear permanent and unrelenting. What people in these kinds of circumstances need is genuine help to identify the nature of the issues, generate positive targets, and begin the process of change. An abused wife needs a safe home for herself and her children, an effective safety network, and ongoing emotional and practical support. She does not need a “diagnosis” of major depressive disorder and a bottle of serotonin reuptake inhibitors.
Drugging a perfectly effective depression mechanism out of existence in order to reduce the immediate sense of discomfort and misery is a bit like sticking duct tape over the check engine light on one’s dashboard. It may reduce one’s negative feelings on the matter, but will produce no lasting benefits. Physicians who participate in these pharma-sponsored activities are not practicing medicine in any true sense of the term. Rather, they are drug pushers, pure and simple.
Dr. Kendler is proposing that psychiatry abandon the search for monocausal explanations of psychiatric “illness” and embrace the multicausal perspective. His reasoning is that this is a better perspective and is more in tune with present-day approaches to chronic non-communicable illnesses.
But he has perhaps revealed his true motivation in the 2016 paper:
“In our ongoing project to study and justify the nature of psychiatric disorders, we ought to be broadly pragmatic but not lose sight of an underlying commitment, despite the associated difficulties, to the reality of psychiatric illness.” (p 5)
In this very clear statement, Dr. Kendler is acknowledging an ongoing and underlying commitment to justify psychiatric disorders and to affirm their “reality.” But isn’t this the very antithesis of science? Isn’t it a fundamental requirement of science that we leave our beliefs–no matter how deeply cherished–at the door, and go where the science takes us? How much credence should we afford a scholar who acknowledges, apparently without compunction, that in his work and writings his agenda includes an underlying commitment to the reality of psychiatric illness?
“When scientifically investigating the natural world, the only thing worse than a blind believer is a seeing denier.” Neil deGrasse Tyson: Death by Black Hole, 2007, (p 292)