When a new client comes to me and reports feeling “depressed,” I always ask the same question: “how does that tend to look for you?” It’s always striking to me what a variety of answers I get to that question: depressed people might report low mood, lack of pleasure in doing things, difficulty sleeping, changes in appetite, suicidal thoughts or feelings, hopelessness, or sometimes all of the above. While none of those symptoms are surprising to hear, every client seems to experience a different combination of those symptoms. Some might have trouble sleeping, but a fine time eating. Some might have no appetite but never dream of hurting themselves.
Here’s the interesting thing about clinical depression: science doesn’t have a very clear picture of what it actually is. The DSM-5 defines Major Depressive Disorder as anybody experiencing “five (or more)…symptoms…during the same 2-week period” out of nine possible symptoms. If you do the math, that means there are hundreds of thousands of possible presentations of what we choose to call “depression.” But what exactly that looks like on a symptom level will vary from person to person. (Note that I’m using depression as an example here, but the same holds true for any mental health diagnosis.)
This reflects the DSM’s approach toward syndromal classification: the DSM and its proponents assume that biopsychosocial problems reflect identifiable latent diseases, or mental illness. This is what we call the “biomedical model,” and it aligns psychiatry within the broader medical field by assuming that there are potentially identifiable diseases underlying presentations that it would classify as “mental disorders.”
What we now call depression used to be called “melancholy,” and was thought to be caused by an excess of black bile in the system. (Harrington, 2019.) Spoiler: it wasn’t.
But notice what’s missing here: we don’t diagnose depression (or anything else in the DSM) based on biological criteria. We don’t measure someone’s serotonin or norepinephrine levels in order to ascertain the presence of depression. There are no blood tests, genetic tests, or brain scans that can be run. All we turn to from a diagnostic perspective is that checklist of nine symptoms. This approach isn’t wrong—but like most things, it’s helpful in some contexts and less helpful in others.
Indeed, criticisms of the biomedical model have been increasing in the past decade from many corners of the mental health world. DSM-IV task force chair Allen Frances (2014) has been working to disrupt the centrality of the DSM-5 and the validity of psychiatric diagnoses as a whole. NIMH director Thomas Insel (2013) has stated publicly that DSM diagnoses do not measure high in statistical validity, and a number of other books and articles have been written about the problems of the “chemical imbalance” theory of depression. (See, e.g., Angell, 2011; Kirsch, 2010; Whitaker, 2010; Spiegel, 2012). The problem, in short, is that no evidence of an imbalance has ever been found for any psychiatric disorder (Insel, 2015) and a growing contingent of respected doctors and psychiatrists are beginning to speak up about this “outmoded way of thinking” (Spiegel, 2012) that functions as an “urban legend” (Pies, 2011).
Indeed, Anne Harrington’s recent book Mind Fixers (2019) provides a thorough history of psychiatry’s attempts to promulgate a biomedical understanding of mental illness, which she argues at this point in time can only be understood as a complete failure. She makes a convincing argument that the widespread adoption of the biomedical model has been made possible in large part due to the influence of pharmaceutical companies—after all, if depression as framed as an imbalance, then medication can be sold to restore that balance.
What has the biomedical model meant for therapists? For those of us who practice evidence-based therapy, it’s resulted in a proliferation of individual protocols meant to be used with specific diagnoses. If we assume that General Anxiety is different from Social Anxiety which is different from OCD, etc., then it means we need to learn how to treat each diagnosis as if they are separate entities. The APA’s Society of Clinical Psychology lists scores of individual protocols that have been scientifically validated for use with various disorders (there are 13 listings for depression alone.) That leads to a lot of overlap and some confusion. Therapists can also begin thinking of a diagnosis as something a client “has” or “is”, rather than what a client is “experiencing.” This can lead to confusion if a therapist is preoccupied by questions of diagnosis in order to pick the right protocol, and it can lead the therapist to miss important data if they pigeonhole a client into a particular diagnosis.
What does it mean for clients? When a therapist rigidly sticks to a specific protocol, it can sometimes feel overbroad and/or underbroad. The protocol may target symptoms that are not present, and it may not target some symptoms that are present. Protocols lack specificity because they’re designed for a research lab, and study participants are usually excluded if they exhibit more than one diagnosis. As a result, protocols are not designed for the average individual in the room who may struggle with more than one thing. There’s even some evidence to suggest that treatment outcomes may be negatively impacted by fusing to a biomedical explanation for struggles. (Brett Deacon has done work here, e.g., Kemp, Lickel, & Deacon, 2014; Farrell, Lee, & Deacon, 2015; Deacon & Baird, 2009; Gershkovich, Deacon & Wheaton, 2018.) After all, if depression is something you “have” or you “are,” then you may have less hope that therapy will be effective. In other words, it can be useful to hold our diagnoses lightly.
As the tide begins to turn against the biomedical model, we can look to advancements in evidence-based psychotherapy that seek to target core biopsychosocial processes in order to effect meaningful change in the lives of individuals. Adopting a process-based approach (Hayes et al., 2019) means shifting away from protocol-based treatment approaches (e.g., CBT for depression, CBT for anxiety, CBT for social anxiety, etc.) and toward “deploying effective treatment elements based on systems of therapeutic change processes as displayed by given people in given situations with given goals” (Hayes et al., 2019). In other words, clinicians must always return to the individual person and their goals for this moment rather than relying on a diagnosis to guide treatment. This approach gives us greater flexibility in targeting precisely what’s necessary for the person in the room.
References
Angell, M. (2011). The epidemic of mental illness: Why? The New York Times Review of Books. Retrieved May 23, 2019 from https://www.nybooks.com/articles/2011/06/23/epidemic-mental-illness-why/
Deacon, B.J., Baird, G.L. (2009). The chemical imbalance explanation of depression: Reducing blame at what cost? Journal of Social and Clinical Psychology, 28(4), 415-435. Retrieved May 23, 2019 from http://www.uw-anxietylab.com/uploads/7/6/0/4/7604142/chemical_imbalance_study.pdf
Deacon, B.J. (2013). The biomedical model of mental disorder: A critical analysis of its validity, utility, and effects on psychological therapy research. Clinical Psychology Review, 33(7), 846-861.
Farrell, N.R., Lee, A.A., Deacon, B.J. (2015). Biological or psychological? Effects of eating disorder psychoeducation on self-blame and recovery expectations among symptomatic individuals. Behaviour Research and Therapy, 74, 32-37. Retrieved May 23, 2019 from http://www.uw-anxietylab.com/uploads/7/6/0/4/7604142/ed_causal_explanations_brat.pdf
Frances, A. (2014). Saving Normal: An insider’s revolt against out-of-control psychiatric diagnosis, DSM-5, big pharma, and the medicalization of ordinary life. New York: William Morrow.
Gershkovich, M., Deacon, B.J., Wheaton, M.G. (2018). Biomedical causal attributions for obsessive-compulsive disorder: Associations with patient perceptions of prognosis and treatment expectancy. Journal of Obsessive-Compulsive and Related Disorders, 18, 81-85. Retrieved May 23, 2019 from http://www.illawarraanxietyclinic.com.au/uploads/7/6/0/4/7604142/biomedical_attributions_of_ocd.pdf
Harrington, A. (2019). Mind fixers: Psychiatry’s troubled search for the biology of mental illness. W.W. Norton: New York.
Hayes, S.C., Hofmann, S. G., Stanton, C. E., Carpenter, J. K., Sanford, B.T., Curtiss, J.E., et al. (2019). The role of the individual in the coming era of process-based therapy. Behavior Research and Therapy 117 (2019) 40-53. Retrieved May 23, 2019 from https://www.sciencedirect.com/science/article/pii/S000579671830158X?via%3Dihub
Insel, T.R. (2013). Director’s blog: Transforming diagnosis. Retrieved May 23, 2019, from http://www.nimh.nih.gov/about/director/2013/transforming-diagnosis.shtml.
Insel, T.R. (2015). Psychiatry is reinventing itself thanks to advances in biology. New Scientist. Retrieved May 23, 2019, from https://www.newscientist.com/article/mg22730353-000-psychiatry-is-reinventing-itself-thanks-to-a dvances-in-biology/
Kemp, J.J., Lickel, J.J., Deacon, B.J. (2014). Effects of a chemical imbalance causal explanation on individuals’ perceptions of their depressive symptoms. Behaviour Research and Therapy, 56, 47-52. Retrieved May 23, 2019, from http://www.uw-anxietylab.com/uploads/7/6/0/4/7604142/chemical_imbalance_brat.pdf
Kirsch, I. (2010). The emperor’s new drugs: Exploding the antidepressant myth. Basic Books: NY.
Pies, R. (2011). Psychiatry’s new brain-mind and the legend of the “chemical imbalance.” Psychiatric News. Retrieved May 23, 2019, from https://www.psychiatrictimes.com/articles/psychiatrys-new-brain-mind-and-legend-chemical-imbalance
Spiegel, A. (2012). When it comes to depression, serotonin isn’t the whole story. NPR Morning Edition. Retrieved May 23, 2019 from https://www.npr.org/sections/health-shots/2012/01/23/145525853/when-it-comes-to-depression-serotonin-isnt-the-whole-story
Whitaker, R. (2010). Anatomy of an epidemic: Magic bullets, psychiatric drugs, and the astonishing rise of mental illness in America. Random House: NY.