Against the Biomedical Model of Mental Illness
“Nature does not appear to have provided us one critical level of explanation for psychiatric illness that stands out from the background. …For [cystic fibrosis], explanatory power is highly concentrated in the level of DNA base-pair variation. For psychiatric disorders, explanatory power is dispersed and diffuse …[M]ost probably, the nature of psychiatric disorders themselves … does not yield up unambiguous choices for the best level at which to define psychiatric illness etiologically. …[Science] will not yield a single clear level of explanation on which to ground our nosology.” — Kendler 2012: 16–17
Contemporary Psychiatric research is generally guided by two research paradigms: the biopsychosocial model of mental illness, and the biomedical model of mental disorders. The aim of this post is to cast doubt on the merits of the biomedical model as a research paradigm and to show why it cannot fully or sufficiently capture the reality, nature, and causes of mental illness in all their forms, and in the process attempting to highlight why the model’s underlying assumptions and methods ignore a wide variety of non-biological factors that are equally responsible in contributing to and/or causing mental illness. The biopsychosocial model remains the best approach to the understanding of mental illness, and reductive accounts of mental disorders should be replaced with a truly multi-disciplinary guideline to research.
To begin, we should lay out just what it is that the biomedical model consists of. The biomedical model is the view that:
“…what psychiatrists call ‘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. An example of the view is Nancy Andreasen’s argument that 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 the disorder have to completely destroy a brain system: it may be enough to put the system into a stable but chronically dysregulated state” (Murphy, 967).
I will begin my objection by noting the following: we know events like childhood trauma cause physiological changes in one’s body. These changes in turn correlate with behavioral changes that manifest themselves as symptoms, and what psychiatry and its DSM-5 do is assign labels to certain clusters and combinations of these symptomatic manifestations, with each label representing and naming an individual and distinct mental illness.
The problem with this psychiatric research paradigm (otherwise known as the biomedical model) is that it focuses on these physiological changes of the brain as the ultimate causes of these mental illnesses, while relegating trauma, abuse, poverty and environmental factors that contribute to these brain changes as irrelevant, secondary, or unaddressable in the study of the etiology of the disease. This worry has been expressed by the British Psychological Society in their 2011 Response to the American Psychiatric Association:
“The Society is concerned that clients and the general public are negatively affected by the continued and continuous medicalisation of their natural and normal responses to their experiences; responses which undoubtedly have distressing consequences which demand helping responses, but which do not reflect illnesses so much as normal individual variation. (p.1)”
“We believe that classifying these problems as ‘illnesses’ misses the relational context of problems and the undeniable social causation of many such problems. For psychologists, our well-being and mental health stem from our frameworks of understanding of the world, frameworks which are themselves the product of the experiences and learning through our lives. (p.4)”
This response is one that echoes critiques of psychiatric diagnosis and practice coming from within the field itself by some of its biggest names. My target in this piece is the continued overemphasis on locating biomarkers and neural correlates for mental illness to the exclusion or diminution of the social forces at play that are themselves equally important links in the causal chain that create the conditions for mental illness to manifest. The reasoning goes like this:
Environment → Brain changes → Behavioral changes.
The subtle move is to focus on those physiological changes as the sole relevant causes for the behavioral symptoms, and pharmacology then takes over to “fix” or counteract these changes in the brain. Note:
Leading the charge is the National Institute of Mental Health, whose Strategic Plan for Research states that “Fundamental to our mission is the proposition that mental illnesses are brain disorders expressed as complex cognitive, emotional,and social behavioral syndromes”. This statement goes well beyond the available scientific data (Satel & Lilienfeld, 2013). It assumes what remains to be proven. Yet this type of rhetoric is rampant in our field. Researchers refer to the “fundamental biological substrates of behavior” when they speak and write. Clinicians explain to patients how psychological disorders are caused by “underlying brain or neurotransmitter abnormalities.” Advertisements for psychotropic medications strongly reinforce this sentiment.
But by continuing to insist that brain changes are the ultimate causes of these symptoms, it gives us a reductionist account of mental illness that will lead to dead ends in research. Note for instance the effects that the childhood trauma of incest can have on our well-being:
After making sure that Marilyn was getting the proper medical care, I consulted with two of my colleagues at Massachusetts General, psychiatrist Scott Wilson and Richard Kradin, who ran the immunology laboratory there. I told them Marilyn’s story, showed them the picture she’d drawn, and asked them to collaborate on a study. They generously volunteered their time and the considerable expense of a full immunology workup. We recruited twelve women with incest histories who were not taking any medications, plus twelve women who had never been traumatized and who also did not take meds — a surprisingly difficult control group to find. (Marilyn was not in the study; we generally do not ask our clinical patients to be part of our research efforts.)
When the study was completed and the data analyzed, Rich reported that the group of incest survivors had abnormalities in their CD45 RA‑to‑RO ratio, compared with their nontraumatized peers. CD45 cells are the “memory cells” of the immune system. Some of them, called RA cells, have been activated by past exposure to toxins; they quickly respond to environmental threats they have encountered before. The RO cells, in contrast, are kept in reserve for new challenges; they are turned on to deal with threats the body has not met previously. The RA‑to‑RO ratio is the balance between cells that recognize known toxins and cells that wait for new information to activate. In patients with histories of incest, the proportion of RA cells that are ready to pounce is larger than normal. This makes the immune system oversensitive to threat, so that it is prone to mount a defense when none is needed, even when this means attacking the body’s own cells.
Our study showed that, on a deep level, the bodies of incest victims have trouble distinguishing between danger and safety. This means that the imprint of past trauma does not consist only of distorted perceptions of information coming from the outside; the organism itself also has a problem knowing how to feel safe. The past is impressed not only on their minds, and in misinterpretations of innocuous events (as when Marilyn attacked Michael because he accidentally touched her in her sleep), but also on the very core of their beings: in the safety of their bodies.
Research on childhood trauma provides a treasure trove of examples of the ways that social acts or events (war, incest, abuse) affect our biology, which in turn can lead to mental health illnesses such as borderline personality disorder, the etiology of which can be best described as both biological and environmental:
- One study found a link between the number and type of childhood traumas and the development of personality disorders. People with borderline personality disorder, for example, had especially high rates of childhood sexual trauma.
- Verbal abuse. Even verbal abuse can have an impact. In a study of 793 mothers and children, researchers asked mothers if they had screamed at their children, told them they didn’t love them or threatened to send them away. Children who had experienced such verbal abuse were three times as likely as other children to have borderline, narcissistic, obsessive-compulsive or paranoid personality disorders in adulthood.
Similarly, childhood trauma has been well documented to be linked to autoimmune diseases, the best evidence of which was provided by the famous ACE study:
We found a strong dose response relationship between the breadth of exposure to abuse or household dysfunction during childhood and multiple risk factors for several of the leading causes of death in adults. Disease conditions including ischemic heart disease, cancer, chronic lung disease, skeletal fractures, and liver disease, as well as poor self-rated health also showed a graded relationship to the breadth of childhood exposures. The findings suggest that the impact of these adverse childhood experiences on adult health status is strong and cumulative.
The literature abounds with examples in which social factors, such as food insufficiency are associated with DSM-IV disorders:
In South Africa the prevalence of household food insufficiency is very high compared with studies conducted in the developed world, and is independently associated with having a 12-month and lifetime DSM-IV diagnosis. The relationship between food insufficiency and mental health has implications for reducing the burden of common mental disorders in South Africa since, unlike a number of major risk factors for mental illness, food insufficiency may be relatively amenable to intervention.
In more philosophical terms: psychiatry continues to conflate proximate causes for ultimate causes, and gives us a false essentialist account of mental illness that will never truly capture the relevant causal web of each diagnosis, and by doing so it will continue to provide medical treatments for problems that are often sociologically grounded.
As this article from The Guardian correctly points out:
Psychological and social factors are at least as significant and, for many, the main cause of suffering. Poverty, relative inequality, being subject to racism, sexism, displacement and a competitive culture all increase the likelihood of mental suffering — as the survivor-led collective Recovery in the Bin brilliantly illuminates. Add into the mix individual experiences such as childhood sexual abuse, early separation, emotional neglect, chronic invalidation and bullying, and we get a clearer picture of why some people suffer more than others.
Crucially, all of these experiences affect our psychological and physiological makeup. For example, the Adverse Childhood Experiences studies show that childhood trauma, neglect and structural oppressions manifest later not just in mental distress but in chronically inflamed bodies stuck on hyper-alert (this we can pick up through blood tests).
Governments and pharmaceutical companies are not as interested in these results, throwing funding at studies looking at genetics and physical biomarkers as opposed to the environmental causes of distress. Sociologists argue that this is because citizens who consider themselves ill are easier to manage than people who consider themselves maddened by toxic families and injustice.
We should not wed ourselves to and ground our research agenda on the increasingly disputed and abandoned notion that all (or even most) mental health illnesses are “natural kinds”, or biologically grounded. Such a notion is philosophically problematic and scientifically dubious. Allen Frances, director of the DSM-IV, cites schizophrenia as one such disorder whose nature resists any facile reductionist attempts at explanation:
Take “schizophrenia” as an example. Our current construct is clearly a research nightmare: heterogeneous, overlapping with near neighbors, no uniform course or treatment response, and no clear pattern of gene or brain findings. Eventually this final common descriptive pathway — “schizophrenia” — will probably turn out to have hundreds of different causes and will require dozens of different treatments. But for now “schizophrenia” does very much inform clinical practice and RDoC has no replacement for it.
Moreover, it is a dangerous myth to assume that patients who meet criteria for “schizophrenia” suffer only from a brain disease. Contextual forces play a large role in the onset of schizophrenia and very often are the most crucial elements in its successful management. A supportive environment, a decent place to live, and therapeutically encouraged engagement with school, work, and social activities are now, and always will be, absolute essentials.
If Not Biological, Then What?
It started by my recalling something Paula J. Caplan had mentioned to me days earlier. “Mental disorders,” she had said, “are nothing more than constellations.” At the time I’d not given the comment much thought, but now, after having spoken to Spitzer, her analogy seemed perfect. Just think about it. As far back as historical records go, we have tried to order this chaos of sparkling orbs into meaningful patterns or configurations, drawing lines between individual stars to create the constellations we know from our schoolbooks: Orion, Leo, Apus, and Aquarius. Most other cultures have also engaged in this astrological map making; Hindu, Chinese, Inca, and Australian Aboriginal have all forged their unique celestial maps. This is why when someone from Bangalore or Sichuan looks up at the very same night sky as you, she identifies different constellations. Her culture has taught her to read the sky differently. She sees her own, not your, astral designs.
And that’s why Caplan’s analogy now made so much sense to me: mental disorders are also man-made maps. Maps linking up our separate feelings and behaviors like astrologers do the galactic stars. One star characterizes sleeplessness, another a visual hallucination, another a constant tick, a violent outburst, or sexual lethargy. And when these separate items are joined with lines, a new pattern — a new disorder — is forged.
Viewed from this standpoint, the DSM committee did not actually discover mental disorders, at least not in any traditional scientific sense. Rather, they literally contrived them, by drawing lines between painful, emotional experiences. One disorder linked up fear, panic, and uncontrolled bouts of anxiety (this would be called Specific Phobia); another disorder linked up low self-esteem, lethargy, and a low capacity for pleasure (and this would be called Dysthymia). And so it went until hundreds of separate patterns had all been given individual names: major depressive disorder, self-defeating personality disorder, oppositional defiant disorder, somatization disorder, and so on.
Looked at in this way…mental disorders aren’t therefore waiting to be discovered, like molecules or bacteria. They are much like man-made constellations which are imposed upon the night sky. Sometimes these map-makers draw patterns that make sense, but sometimes they do not, and sometimes they make mistakes so dramatic that it’s hard to put things right again.
Of course the stars that make up a constellation are physically real and exist in the actual, real world. Similarly, of course behavioral symptoms often and in fact do have underlying neural correlates (even if we haven't found them for many, if not most, of the DSM's disorders). But the actual categories that we create out of these cluster symptoms are constantly shifting, morphing, and at the mercy of scientific and social fads and trends. Some, like homosexuality, were removed from the DSM not because of some new scientific breakthrough, but as a result of a popular vote taken by the APA’s voting members. The decision to remove homosexuality as a mental illness from the DSM was upheld by a 58% majority of 10,000 voting members. Of course, it never should have been in the DSM in the first place, but that reinforces the influence that societal norms have had on our categorization of mental illness throughout history. The categories are social constructs, even if the underlying material out of which we construct them are very much real. It needs to be noted, however, that this notion of social construction by no way means “imaginary” or “not real". Social constructs still need raw materials out of which to do the constructing. The edifice is a complex relationship between the raw materials provided by the objectively existing natural world “out there” and our own mental ordering of those raw materials into new categories by which we organize the material universe. A recent paper by Eiko Fried lists a number of frameworks for understanding mental illness that integrate the biopsychosocial advances in our understanding, one of which (and my own current view) is that of psychological constructs as “complex kinds”:
Conceptualizing psychological concepts through a “complex” approach involves understanding natural processes that co-occur, forming a cluster connected by an underlying causal force. This relationship is probabilistic, not deterministic, and the features of these properties aggregate in imperfect, inconsistent ways. For example, if depression is viewed as a “complex kind,” it would be consistent with the notion that some features of depression are caused by other features, and that different patients may present with various clusters of symptoms. Unlike “natural kinds,” “complex kinds” do not have defined necessary and sufficient features, yet their existence is not purported to be symbolic in the case of “practical” and “social” kinds.
I here conclude with a relevant excerpt from the Oxford Handbook of Philosophy of Psychiatry:
Reference:
- Fulford, Kwm, Martin Davies, Richard Gipps, George Graham, John Sadler, Giovanni Stanghellini, and Tim Thornton. 2013. The Oxford Handbook of Philosophy and Psychiatry. OUP Oxford.
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