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: