Psychiatry’s Necessary Shadow
The Philosophy of Mental Illness
“The power to give names to our pain is a mighty thing and easy to abuse . . . Psychiatry’s appeal is not just about the possibility of cure, which is why the profession continues to flourish even when it cures nothing and relieves symptoms only haphazardly. It’s in the naming itself.”
–Gary Greenberg, The Book of Woe
“Physicians think they do a lot for a patient when they give his disease a name.”
— Immanuel Kant
On February 18th, 2015, former president of the American Psychiatric Association, Dr. Jeffrey Lieberman, penned a letter titled ‘What Does the New York Times Have Against Psychiatry?’ in which he bemoaned the fact that:
“Psychiatry has the dubious distinction of being the only medical specialty with an anti-movement. There is an anti-psychiatry movement. You have never heard of an anti-cardiology movement, an anti-dermatology movement, or an anti-orthopedics movement.”
He is right. Since the 1960’s, psychiatry has contended with a movement whose members have called into question the fundamental assumptions of the discipline. Whereas other medical professions face their own share of science denialism, no other field of medicine has had to grapple with decades-long criticism that its core concepts are fundamentally mistaken. What makes psychiatry special? How have closely related fields such as psychology and neurology avoided the same fate? Perhaps more importantly, are these criticisms worth taking seriously? Despite psychiatry being the only medical specialty with an anti-movement, various other non-medical scientific disciplines have faced similar opposition. Evolutionary biology and climatology are perhaps the best known examples of established science being routinely called into question by members outside of their respective fields.
As a lifelong skeptic, I want to make the case that the historical critiques of the biomedical approach to mental health ought to be taken seriously. The criticisms offered are dissimilar enough to evolution and climate change denialism that no facile comparison between the movements is justified. I want to explore how underlying philosophical assumptions about the nature and scope of explanation shape much of what on the surface seems like a scientific debate. My aim is to expose the weaknesses of the biomedical model of mental illness and thereby explain why psychiatry stands alone among medical disciplines in having its very own anti-movement.
The Biomedical Model And Its Critics
- Categories of mental illness, such as depression and schizophrenia, are not scientific. The process of compiling the Diagnostic and Statistical Manual of Mental Disorders is riddled with secrecy, dubious science, and arbitrariness.
- Pharmacological treatments for conditions like major depressive disorder do not work. Further, the emphasis on prescribing medicine over and above other forms of therapy is detrimental to the profession and treatment outcomes. These medications are potentially harmful to a vast number of people who take them.
- The mutually beneficial relationship between drug companies and the psychiatric profession is ethically repugnant and calls into question the reliability of the research done on these medications.
- Psychiatry and its biomedical model have slowly medicalized problems which are psychological and social in nature. Many common disorders are caused less by biology than cultural factors.
- The promises of the biomedical model in finding the biological roots of mental disorders have so far come up empty.
- Reductive analyses of the causes of mental illness leave out too many relevant variables external to the life of the individual and therefore fail to address much of what is at the root of their troubles.
Since this is a philosophical piece, my main interest lies in assessing those objections grounded on conceptual and philosophical grounds rather than empirical ones. Primarily, I am interested in the objection that a proper account of the causes of mental disorders should be a multi-level causal explanation. The insights from sociology, psychology, and biology must all be integrated into a holistic model that gives us a far richer and more accurate picture than any model which privileges one level of explanation over the others.
The psychiatric discipline is divided into two competing explanatory frameworks for the study of mental illness: the biopsychosocial and the biomedical models of mental illness. The distinction between the two isn’t always clear, nor do adherents of each view often recognize that the underlying root of their disagreement is not so often an empirical one but rather stems from hidden underlying philosophical assumptions about the nature of causation, the proper scope of scientific reduction, and what constitutes a comprehensive scientific explanation in the domain of medicine.
In addition, most psychiatric textbooks still formally accept the biopsychosocial model as the dominant research paradigm (though this is changing) yet in practice pursue a research agenda clearly directed by the assumptions and methodologies of the biomedical framework. Regardless of which label psychiatric texts embrace, most active research emphasizes molecular biology, genetics, biochemistry, neuroscience, and physiology as the target domains for understanding the nature and causes of mental illness while neglecting or minimizing the importance of life circumstances, social structures, impaired beliefs, and childhood adversities in their explanatory framework. In other words, psychiatry as a field formally embraces a research paradigm that in practice researchers abandon while emphasizing the ‘bio’ over and above the ‘psychosocial’.
In its simplest form, the biomedical model understands mental illnesses to be brain diseases, emphasizing pharmacological treatment to target presumed biological abnormalities (Deacon, 846).
Mental illness, on this view, is characterized as a type of disease, a disease every bit as real as diabetes, cancer, and pulmonary hypertension. The phrase “every bit as real as…” is taken to mean that a condition such as depression is a biological entity whose roots are to be found in brain processes, structures, and/or abnormalities. The causes are alleged to include neurotransmitter dysregulation, genetic anomalies, and defects in brain structure (Deacon, 847).
There are three core tenets (847)of the biomedical model:
- Mental disorders are caused by biological abnormalities principally located in the brain.
- There is no meaningful distinction between mental diseases and physical diseases.
- Pharmacological treatment is emphasized.
We should be extremely careful to note that when discussing these tenets, we should not understand them to be formally enshrined in psychiatry textbooks as the officially accepted views of mainstream psychiatry. As mentioned earlier, psychiatry still formally accepts the biopsychosocial model and is careful not to canonize the views above as part of official psychiatric doctrine. These tenets are instead understood to be guiding research principles that can be seen to be the operating underlying assumptions behind psychiatric research and clinical practice.
In other words, while psychiatrists may officially accept the biopsychosocial model of mental illness, their research and clinical practices are typically performed as if the biomedical model and its tenets are true. This is a sociological explanation of how psychiatric research is actually done and what kinds of underlying assumptions seem to be at play guiding research (Lilienfeld, 2007). Note the following statements from prominent sources:
It is clear that the current paradigm about the nature of mental illness is that of conceptualizing it in terms of a type of disease:
“What psychiatrists describe as ‘mental illnesses’ are diseases that are causally explained by their underlying pathophysiology. It is committed to specific causal hypotheses in terms of abnormalities in underlying neurobiological systems, which are responsible for the observed patterns of signs and symptoms.” (Murphy, 968)
“An explanation of mental illness will ultimately cite destructive processes in brain systems, just as bodily diseases are explained by such processes in other organs. The process can mediate the effects of cultural forces or other environmental risk factors. Nor does the cause of a disorder have to completely destroy a brain system: it may be enough to put the system into a stable but chronically dysregulated state…[there are], in psychiatry, phenomena that fit the conception of disease as a destructive process realized in bodily organs that predominates in biomedicine generally” (Murphy, 968).
In common english vernacular, the words “disorder”, “disease”, and “illness” are often used interchangeably. However, in the neurosciences and medicine more generally these words have different uses. A “disorder” refers to a malfunction of a biological process or organ when there is no known pathology. If the purpose of a kidney is to remove waste and extra fluid from our blood, then a kidney that is no longer able to remove waste or extra fluid is suffering from a malfunction and is therefore a type of disorder. Disorders can be caused by genetics, disease, or trauma. A disease or illness on the other hand refers to actually known pathophysiological processes. Hence the claim about the causes of disorders: there are many, with illnesses/diseases being just one type of cause.
Why this brief terminological digression? Because as we have seen above, the psychiatric profession continues to use the terms “mental illness” and “mental disorder” interchangeably, thereby obscuring the important distinction that unless the pathology of a mental condition is known, it cannot be called or said to be caused by an “illness”. But biomedical model proponents blur these distinctions, merely asserting that the 200+ disorders found in the DSM are rooted in biological illnesses without discovering the pathology of any of them to date.
I grant that some disorders may, but it does not follow that all of them will. The declaration, before the biological pathologies are even established, that they either are illnesses or are caused by them is an ideological pronouncement, not an empirical finding. The biomedical model’s prediction of what we should expect to find about the causes of mental health conditions is instead asserted as what has already been established.
There are two key takeaways from this: the biomedical model is concerned with asking and providing answers to the following questions:
What is a mental disorder?
It’s a medical disease of the human brain.
What causes mental illness?
Destructive or dysregulating processes in brain systems.
Notice the confusion here. As seen above, disorders are typically understood to be caused by disease, but biomedical proponents fluctuate between claiming mental disorders are diseases and subtly talk about them being caused by illnesses instead. This terminological confusion is no doubt responsible for the intractability of the debate.
The biomedical model concerns itself with providing an explanation for both the nature and causes of mental illness. Just as cancer is understood to be a term for diseases in which abnormal cells divide without control and can invade nearby tissues, mental illness is a term for diseases in which certain dysfunctions of brain processes lead to the destruction or dysregulation of brain systems.
It is paramount to note that this is where the biomedical model diverges from the biopsychosocial: in giving us an account of the nature and causes of mental illness, the biomedical model will ultimately provide an explanation that is mechanistic. The ultimate aim is to show how the parts of a system (the brain) possess certain structures and activities which give rise to (cause or produce) the phenomena in question. It is a reductionist account that explains the nature of mental illness by appealing to underlying processes within that system itself.
By contrast, the biopsychosocial model eschews the reductionist approach by appealing to factors external to the brain that play an equally important role in the development of mental health disorders. External factors such as child abuse, the state of one’s marriage, history of substance abuse, as well as stressful environmental events like unemployment or bereavement (Murphy, 974). The objection is that by focusing our attention and research on causal factors within the brain, we are neglecting equally important links in the causal chain without which a complete explanation will be impossible.
Notice that whereas cancer is defined in terms of its causes, as in when the “body’s cells begin to divide without stopping and spread into surrounding tissues”, we do not yet know the specific causes for most of the mental illnesses found within the DSM. Therefore, “destruction or dysregulation of brain systems” is understood to be a placeholder causal definition of mental disorders until the specific underlying neurobiological mechanisms that give rise to these disorders are identified.
Until the underlying causal pathways for disorders such as schizophrenia are found, the biomedical model cannot define individual disorders by means of their actual known causes, as we do with cancer. This is so because psychiatry has yet to find any simple biological cause for any major mental disorder (Deacon, 856). As former head of the National Institute for Mental Health Thomas Insel writes regarding the DSM and psychiatry’s current nosology:
“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.
It became immediately clear that we cannot design a system based on biomarkers or cognitive performance because we lack the data. In this sense, RDoC is a framework for collecting the data needed for a new nosology. But it is critical to realize that we cannot succeed if we use DSM categories as the ‘gold standard.’ The diagnostic system has to be based on the emerging research data, not on the current symptom-based categories. Imagine deciding that EKGs were not useful because many patients with chest pain did not have EKG changes. That is what we have been doing for decades when we reject a biomarker because it does not detect a DSM category. We need to begin collecting the genetic, imaging, physiologic, and cognitive data to see how all the data — not just the symptoms — cluster and how these clusters relate to treatment response.” (Insel, 2013)
How The Debate Over Trump’s Diagnosis Refutes the Reductive Model
There’s a deeper problem here. During the recent public discussions surrounding Donald Trump’s mental health, Dr. Allen Frances objected to claims made by mental health professionals that the president suffers from Narcissistic Personality Disorder on the grounds that they:
“…ignore the further requirement that is crucial in defining all mental disorders — the behaviors also must cause clinically significant distress or impairment.
Trump is clearly a man singularly without distress and his behaviors consistently reap him fame, fortune, women, and now political power. He has been generously rewarded, not at all impaired by it.”
Psychiatric diagnoses cannot be made unless there is clinically significant distress or impairment. The DSM does not define “clinically significant distress”, so that determination is usually made by the doctor tending to a patient on the basis of their professional judgment. Usually, a patient seeking help from a psychiatrist is good enough to establish the existence of clinically significant distress. The subjective judgment of the medical professional is not what I want to highlight. Instead, the criteria of clinically significant distress being a necessary condition for a diagnosis is the problem. If a condition like narcissistic personality disorder is a biological illness, then there should be no requirement that it causes distress to the patient.
According to Frances, Trump does not suffer from narcissistic personality disorder because he is rewarded for his behavior, not distressed by it. And since there is no distress, there can be no diagnosis. On the other hand, an individual with the exact same behavioral tendencies as Donald Trump who is shunned, criticized, and personally suffers because of their behavior would meet the criteria for NPD. Without a subjective personal assessment of how the condition affects your life, there can be no diagnosis.
Now, according to the biomedical model, all mental illnesses have an underlying pathology which, when discovered, will better help us identify their presence in patients by means of biomarkers. Suppose we discover a biomarker for NPD and find that both Trump and others sharing the same behavioral traits as he have this biomarker. Since Trump and those suffering from NPD share the same outward behavioral symptoms, and the presence of the biomarker in both is established, why would the lack of distress make a difference in the diagnosis? That society rewards Trump’s behavior while punishing others for it should have no bearing on the question of his mental health. By way of analogy, imagine not receiving a diagnosis of cancer on the basis that a patient reports not being personally distressed by their condition.
If societal expressions of praise or shunning as well as subjective assessments of distress play a role this crucial in the determination of the presence of a condition like NPD, then the reductive biological model is false.
The DSM-5 diagnostic criteria use what are known as practical kind definitions. Instead of defining an entity like depression on the basis of its underlying causal mechanisms, the DSM defines it instead pragmatically: for the sake of prediction, the discovery of risk factors, and direction of treatment (Murphy, 973). These are labels, not explanations. The DSM definition for major depressive disorder, for instance, recognizes depression as the presence of at least 5 of the following 9 symptoms during the same 2-week period:
- Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad, empty, hopeless) or observation made by others (e.g., appears tearful).
- Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account or observation).
- Significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body weight in a month), or decrease or increase in appetite nearly every day.
- Insomnia or hypersomnia nearly every day.
- Psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of restlessness or being slowed down).
- Fatigue or loss of energy nearly every day.
- Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick).
- Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others).
- Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide.
Notice what is absent from this criteria: there is no talk of causes nor is there any mention of contextual factors that ought to be taken into consideration when trying to determine if an individual suffers from major depressive disorder in contrast to normal sadness or grief.
Consider the following hypothetical case by Dr. Philip Hickey:
Consider the cases of two people, Peter and Paul, who come within the orbit of psychiatry. Both have had recent losses and both are living in difficult circumstances, and both are despondent. The examining psychiatrist, Dr. Checkem, runs them both through the APA’s facile and unvalidatable checklist for major depressive disorder. He finds that Peter meets the first five of the nine checklist items.
But Paul meets only four of the nine. Dr. Checkem works hard to “pin” a fifth item on Paul to clinch the “diagnosis”, but it just won’t fly, and he’s an honest doctor, so he notes “no diagnosis” in his assessment, and sends Paul home with advice to start a hobby, or have more sex, or take long walks, or whatever. But Peter gets a “diagnosis” of “major depressive disorder”, is enrolled as a “patient”, and given a prescription for a so-called antidepressant.
And incidentally, the only difference between the two men on the checklist items was that Peter reported a decrease in appetite and a 7% weight loss (from 150 to 140 pounds); but Paul reported no change in appetite and no loss of weight in the same time frame.
There is much to unpack here. One key insight is how this story highlights the seeming arbitrariness of the DSM’s cutoff criteria for who counts as depressed and who is merely suffering from “normal” sadness. Another insight is that cases like these bring into focus what I take to be the central issue of the psychiatric diagnosis debate: what counts as a cause for the conditions patients present to the clinic with?
The biomedical model emphasizes that people like Peter suffer from a mental illness, rooted in biology, whereas Paul is merely sad. The cause of Peter’s mental illness is allegedly some neurological abnormality in his brain. Paul doesn’t have a diagnosis of mental illness due to him only meeting 4 of the 9 diagnostic criteria for depression, whereas Peter meets the required minimum of 5.
In a case like this, what would we say caused major depressive disorder? Well, if we assume for the sake of argument that the chemical imbalance theory is true (though it isn’t), it would be true to say that Peter’s chemical imbalance is the cause of his depression. But it would also be true to say that the loss of his loved ones is the cause of his depression. Setting aside the question of whether grief at the loss of your loved ones should ever count as a mental illness in the first place, it seems plainly intuitive that a full explanation of the cause of Peter’s depression ought to incorporate multiple-levels of analysis that reveal the complexity of the causal web responsible for the manifestation of his condition.
The reductive biomedical model will merely emphasize what’s going on at the level of the brain but leaves out social and personal factors that play an equally important role in the development of his grief. Another example brings this into sharper focus.
Imagine that Peter works in law enforcement and picks up the habit of smoking cigarettes to deal with the stresses of the job. He smokes three packs a day for 5 years until, during a visit to his doctor, he is diagnosed with lung cancer, which ultimately leads to his death a year later.
What caused Peter’s death?
Well, it is uncontroversial that Peter’s lung cancer killed him. That’s true at one level of explanation. But isn’t it also true that Peter’s smoking habit caused his death? And wouldn’t it also be true that the stresses of his job should be included in the story we want to tell about the causal web of his death?
These are all true claims that allow us to paint a far richer and more colorful picture of the circumstances behind Peter’s death than any causal story we would tell that focused merely on one of the links in the chain.
Psychiatry’s biomedical model, in virtue of privileging the alleged biological underpinnings of mental disorders, gives us only a crude model of the vastly more complex web of the internal as well as external forces whose constant interactions create the inner mental life of the patient.
Currently, only 11% of psychiatrists offer talk therapy to their patients. That amounts to only 1 out of 10 psychiatrists offering psychotherapy as a form of treatment for mental illness. The preferred psychiatric form of treatment is psychopharmacology. Antidepressants are the third most commonly used class of prescription medication of any kind in the United states (Deacon, 850). As psychiatrist Daniel Carlatt writes about his profession:
Just as striking to me as the lack of typical doctorly activities in psychiatry is the dearth of psychotherapy. Most people are under the misconception that an appointment with a psychiatrist will involve counseling, probing questions, and digging into the psychological meanings of one’s distress. But the psychiatrist as psychotherapist is an endangered species. In fact, according to the latest data from a group of researchers at Columbia University, only one out of every ten psychiatrists offers therapy to all their patients.
Doing psychotherapy doesn’t pay well enough. I can see three or four patients per hour if I focus on medications (such psychiatrists are called “psychopharmacologists”), but only one patient in that time period if I do therapy. The income differential is a powerful incentive to drop therapy from our repertoire of skills, and psychiatrists have generally followed the money.
So, like most of my patients, Carol saw me for medications, and saw a social worker colleague for therapy. Her symptoms gradually improved, but whether this was due to the medications or the therapy, or simply the passage of time, I cannot say” (Carlat, 2010).
As we can see, psychiatry’s biomedical model and its emphasis on psychopharmacological treatment is largely the result of two factors:
- The identification of mental illness as strictly biological entities caused or facilitated by abnormal brain processes; and
- Financial incentives caused by insurance reimbursement rates. It simply makes more financial sense for the psychiatrist to focus on medication management and than to spend their clinical hours engaging in talk therapy.
Much has been written criticizing the perverse symbiotic relationship between pharmaceutical companies and the field of psychiatry. On Daniel Carlatt and psychiatric clinical practice in general, Doctor Marcia Angell writes:
His work consists of asking patients a series of questions about their symptoms to see whether they match up with any of the disorders in the DSM. This matching exercise, he writes, provides “the illusion that we understand our patients when all we are doing is assigning them labels.” Often patients meet criteria for more than one diagnosis, because there is overlap in symptoms. For example, difficulty concentrating is a criterion for more than one disorder.
One of Carlat’s patients ended up with seven separate diagnoses. “We target discrete symptoms with treatments, and other drugs are piled on top to treat side effects.” A typical patient, he says, might be taking Celexa for depression, Ativan for anxiety, Ambien for insomnia, Provigil for fatigue (a side effect of Celexa), and Viagra for impotence (another side effect of Celexa).
As for the medications themselves, Carlat writes that “there are only a handful of umbrella categories of psychotropic drugs,” within which the drugs are not very different from one another. He doesn’t believe there is much basis for choosing among them. “To a remarkable degree, our choice of medications is subjective, even random. Perhaps your psychiatrist is in a Lexapro mood this morning, because he was just visited by an attractive Lexapro drug rep.” And he sums up:
Such is modern psychopharmacology. Guided purely by symptoms, we try different drugs, with no real conception of what we are trying to fix, or of how the drugs are working. I am perpetually astonished that we are so effective for so many patients.
It is widely acknowledged within the profession that we are far from understanding the neurobiological underpinnings of mental disorders. Further, it is also acknowledged that we simply do not know how or why these drugs work.
What psychiatrists do claim is that these medications at least help alleviate and treat the symptoms of clients, even if we’re nowhere near discovering a cure for any of them. This is equally controversial and contested. On the alleged efficacy of antidepressant medication for the treatment of depression, Irving Kirsh writes:
Antidepressants are supposed to work by fixing a chemical imbalance, specifically, a lack of serotonin in the brain. Indeed, their supposed effectiveness is the primary evidence for the chemical imbalance theory. But analyses of the published data and the unpublished data that were hidden by drug companies reveals that most (if not all) of the benefits are due to the placebo effect. Some antidepressants increase serotonin levels, some decrease it, and some have no effect at all on serotonin. Nevertheless, they all show the same therapeutic benefit. Even the small statistical difference between antidepressants and placebos may be an enhanced placebo effect, due to the fact that most patients and doctors in clinical trials successfully break blind. The serotonin theory is as close as any theory in the history of science to having been proved wrong. Instead of curing depression, popular antidepressants may induce a biological vulnerability making people more likely to become depressed in the future.
Setting aside the empirical debate of whether psychopharmacology actually works, it is fairly clear and uncontested that it is the preferred modality of treatment offered by psychiatrists in the United States and a natural extension of the biomedical model’s implication for what kinds of solutions we should seek for our mental maladies. This emphasis on drug treatment is a pillar of the biomedical model that further distinguishes it from rival conceptions of mental illness and their suggested forms of treatment.
I have attempted to give a general overview of the biomedical model’s distinctive features and why adherence to this model has been one of the primary reasons why psychiatry stands apart from other mental health professions in having a history of sustained criticism. Why have psychology and neurology avoided this fate? One plausible reason is that psychology has historically opposed biomedical reductionism and continues to push back with each new edition of the DSM. On the other hand, neurology primarily focuses on conditions with known pathophysiologies, though the boundaries between the two are fuzzy, leading to many researchers calling for the two fields to merge.
The most likely answer is that the conditions neurology has medical domain over have identifiable biological markers and bases in human anatomy. Neurology is one field where the biomedical model has proven to widely successful, a claim that cannot be said for psychiatry. One way to interpret this is to hope some day psychiatry’s biomedical research program proves as successful as neurology’s. Another approach, the one I call for, is to abandon this reductionistic model and once again fully embrace the biopsychosocial research paradigm.
About the Author: Andrés Ruiz has an M.A. in Philosophy and is working on his MSW with the goal of becoming a licensed psychotherapist. He writes on Philosophy, Psychology, and Psychiatry.
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