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Biomedical Model: Five Anecdotes

It is difficult to overstate the ubiquity and influence of the biomedical model that provides the foundation for psychiatric diagnosis and treatment in the United States. As a clinical psychologist who has spent the past 15 years working in medical centers, inpatient psychiatric hospitals, outpatient mental health clinics, a residential substance abuse treatment center, private practice, and academia, I have encountered the myriad effects of the biomedical model on a daily basis. Among these encounters, five are particularly memorable and help to illustrate the popularity and consequences of characterizing psychological problems in purely biomedical terms.

#1: “We act as if it were true.”

During my postdoctoral fellowship at the Mayo Clinic, I received an in-house employee health newsletter with a cover story on the recognition and treatment of depression. Major depressive disorder was described as a “medical disorder” that is “usually the result of a chemical imbalance.” I emailed the newsletter’s editor, expressing gratitude for highlighting an important topic but questioning the depiction of depression in a bioreductionistic manner. The editor politely acknowledged that the chemical imbalance explanation is an oversimplification of a complex phenomenon, but argued that it is nonetheless useful because it corrects the mistaken notion that depression is caused by laziness and/or character defects. He noted that, “While the chemical imbalance theory is speculative, we act as if it were true.” The editor was apparently unaware that biological explanations of depression do not reduce stigma (Schomerus et al., 2012) and may foster pessimism about recovery and bias individuals against psychosocial treatments (Deacon & Baird, 2009; Lebowitz, Ahn, & Nolen-Hoeksema, 2013).

#2: “Depression is a serious medical illness caused by [chemical] imbalances”

In 2008, I co-authored an article with psychologist Irving Kirsch and colleagues, published in PLoS Medicine, on the relationship between baseline depression severity and the therapeutic benefit of antidepressant medications. Using pharmaceutical industry data obtained from the United States Food and Drug Administration (FDA), we found that the advantage of antidepressants over placebo was small and clinically insignificant for all but the most severely depressed patients. Somewhat ironically, the editor’s summary of the article asserted that, “Depression is a serious medical illness caused by imbalances in the brain chemicals that regulate mood” (p. 0268). Three years prior, this same journal published an article by Jeffrey Lacasse and Jonathan Leo (2005) which underscored the disconnect between chemical imbalance claims in antidepressant consumer advertisements and the lack of scientific evidence in support of the chemical (serotonin) imbalance theory of depression. These authors noted, “The impact of the widespread promotion of the serotonin hypothesis should not be underestimated” (p. 1214). Indeed.

#3: “How many patients went off the medications due to that publication, without consulting their doctor?”

My co-authorship of the aforementioned article prompted an invitation to debate Hans-Jürgen Möller, the president of the European Psychiatric Association (EPA), on the efficacy of antidepressant medications at the 2008 European Congress of Psychiatry (Dr. Kirsch was unable to attend due to a scheduling conflict). The debate took place in front of a packed house of 300 psychiatrists, many of whom were concerned about the fallout from the substantial media attention our study had received in Europe. My opponent began his remarks by disclosing financial conflicts of interest with 14 pharmaceutical companies. The audience responded with apparent indifference, as though having dispensed with this formality an unbiased discussion of antidepressant efficacy could now begin.

In his opening statements, my opponent presented a slide in which digital smiley-faces were superimposed over the windows of his psychiatric hospital, with the title “Patients’ experience vs. meta-analytical evidence: My patients believe in the efficacy of antidepressants.” The next slide showed a picture of several dozen smiling staff members posing for a group portrait, apparently demonstrating that doctors also believe in the efficacy of antidepressants. The president of the EPA, a scientist who has co-authored more than 1,000 publications, was arguing that in the matter of antidepressant efficacy, clinical judgment trumps scientific evidence. After a debate largely focused on academic issues like publication bias and the integrity of the double blind in antidepressant trials, the audience was permitted to ask questions. A psychiatrist made a comment that, judging from the thunderous applause it received, captured the prevailing sentiment in the room. “I think you should consider your responsibility,” he stated. “How many patients went off the medications due to that publication, without consulting their doctor?” I validated this legitimate concern, but suggested that patients have a right to accurate information about the treatments they receive, and that deliberately withholding such information because it threatens the credibility of antidepressant treatment denies patients informed consent. One audience member politely clapped.

#4: “A study of the effect of an incorrect view, if not widely held, would not be important to do.”

In 2006, Grayson Baird and I submitted a study for publication to a clinical psychology journal on the effects of the chemical imbalance explanation of depression on perceptions of blame, prognosis, and treatment preferences. Eventually published in the Journal of Social and Clinical Psychology in 2009, this study was initially rejected from a different outlet. Both peer reviewers at this journal recommended rejection, and the editor concurred. The reviewers explicitly based their recommendation on the inappropriateness of our topic of study. One reviewer wrote, “The view that depression is caused only by biological factors is incorrect. A study of the effect of an incorrect view, if not widely held, would not be important to do.” The other reviewer stated, “The authors assert that a study of the degree to which mental health professionals endorse the biology-only causal model of depression is needed. I find this statement unconvincing, as this biology-only model is incorrect, and I don’t have any reason to expect that large numbers of mental health professionals hold an incorrect model of the causes of depression.” If only it were that simple. The needs of individuals with mental health problems are not served when pseudoscientific theories and practices are ignored by ivory tower academics with their heads in the sand.

#5: “It’s true. But you shouldn’t say it.” 

My research lab initiated a study examining the effects of different types of causal information about obsessive-compulsive disorder (OCD) on perceived stigma, prognosis, and treatment expectancies. Participants belonging to OCD community support groups received information emphasizing either a biopsychosocial or biomedical causal explanation and subsequently completed a number of questionnaires. The biomedical explanation described OCD as a brain disease caused by abnormalities in genes, neurotransmitter levels, and the structure and function of different parts of the brain responsible for regulating emotions. The biopsychosocial explanation characterized OCD as the result of genetic, psychological, and environmental factors. In an ill-fated effort to distinguish the latter explanation from the former, we stated that the chemical imbalance causal explanation of OCD is not scientifically supported. We added that scientists do not have a valid test for measuring a chemical imbalance in the brain, and suggested that despite its popularity and use as an effective pharmaceutical marketing strategy, the chemical imbalance theory is not taken seriously by most scientists who study OCD.

Within 48 hours, the institutional review board at my university received a phone call from an angry psychiatrist who facilitated an OCD support group whose members had participated in the study. I subsequently spoke to the psychiatrist about his concerns. Apparently, our study had created a “firestorm” in the group, sparked by complaints from members who were upset about the causal information we provided. The participants were not troubled by the biomedical information despite what we regarded as its rather obvious omission of well-established psychosocial influences on OCD. Rather, support group members were “up in arms” about the portion of the biopsychosocial script disputing the chemical imbalance explanation. According to the facilitator, all group members believed, on the basis of what they had been told by treatment providers, that their OCD was the result of a chemical imbalance. Indeed, of the 13 patients who completed our survey before it was taken offline, nine (69.2%) reported being informed by their treatment provider that they needed to “take psychotropic medication to manage a chemical imbalance in the brain just as people with diabetes need to take insulin to manage their blood sugar.” Horrified at the prospect of interfering with participants’ treatment, we immediately terminated the study. Our naïve mistake was failing to appreciate the extent to which OCD patients in the community are socialized in the biomedical model of their disorder. The facilitating psychiatrist admitted during our conversation that the information we provided disputing the validity of the chemical imbalance explanation was accurate. “It’s true,” he noted. “But you shouldn’t say it.”

As these anecdotes illustrate, biomedical explanations of psychological experiences dominate our mental health system. Patients and the public are informed that depression, anxiety, and related problems are brain diseases caused by chemical imbalances. That such biomedical theories are neither scientifically credible nor useful in reducing stigma is apparently irrelevant to biomedical proponents seeking to bolster the credibility of psychiatric diagnosis and treatment, and to market and sell psychotropic drugs. The controversy surrounding DSM-5 has prompted a broader discussion about the biomedical model upon which the practice of contemporary American psychiatry, and its proprietary diagnostic system, are based. It is time for a broad, public, and critical discussion of the biomedical paradigm, and I’m pleased for this opportunity to contribute to it. For further critical analysis of the biomedical model, readers are referred to Deacon (2013). 

Like MIA bloggers Jonathan Leo and Jeffrey Lacasse (whose work I hold in high esteem), my vantage point is from within the mental health system as an academic whose work focuses on education and scientific research. I’m delighted to join the MIA community as a blogger and work together with individuals from diverse vantage points in an effort to improve the validity, utility, and credibility of our mental health system. I look forward to working with you!
References

Deacon, B. J. (2013). The biomedical model of mental disorder: A critical analysis of its assumptions, consequences, and effects on psychotherapy research. Clinical Psychology Review, 33, 846-861.

Deacon, B. J., & Baird, G. (2009). The chemical imbalance explanation of depression: Reducing blame at what cost? Journal of Clinical and Social Psychology, 28, 415–435.

Kirsch, I., Deacon, B. J., Huedo-Medina, T. B., Scoboria, A., Moore, T. J., & Johnson, B. T. (2008). Initial severity and antidepressant benefits: A meta-analysis of data submitted to the FDA. PLoS Medicine, 5, 0260-0268.

Lacasse, J., & Leo, J. (2005). Serotonin and depression: A disconnect between the advertisements and the scientific literature. PLoS Medicine, 2, 1211–1216.

Lebowitz, M. S., Ahn, W. K., & Nolen-Hoeksema, S. (2013). Fixable or fate? Perceptions of the biology of depression. Journal of Consulting and Clinical Psychology, 81, 518.

Schomerus, G., Schwahn, C., Holzinger, A., Corrigan, P. W., Grabe, H. J.,  Carta, M. G., et al. (2012). Evolution of public attitudes about mental illness: A systematic review and meta-analysis. Acta Psychiatrica Scandinavica, 125, 440-452.