“What man sees depends both upon what he looks at and also upon what his previous visual-conception experience has taught him to see.”
― Thomas S. Kuhn, The Structure of Scientific Revolutions
Consider the following case vignette:
Ms. Jones is a 60-year old recently divorced accountant with a history of chronic, generalized anxiety. She has been increasingly depressed over the past four months and meets the full severity and duration criteria for DSM-5 Major Depressive Disorder.
Since her divorce six months ago, Ms. Jones describes herself as “lonely,” “isolated” and “totally without any connection” to others. Two months ago, her internist discovered that Ms. Jones has a mildly under-active thyroid (TSH 7.3, normal =0.45 and 4.12 mIU/L). Her psychotherapist of two years noted that Ms. Jones has a particular “cognitive style” that leads her to “catastrophize” relatively minor stressor, eg, she interpreted her boss’s bad mood one day as a reflection of his dislike for her, and concluded, “I’m about to get fired.”
If Ms. Jones were referred to you, how might you conceptualize her major depression? Would you be guided by the “biopsychosocial model” (BPSM), as formulated by Dr. George Engel? If so, how helpful would the BPSM be in guiding your treatment of Ms. Jones?
It turns out, the answers to these questions are by no means straightforward. Indeed, it is hard to think of another paradigm in the field of medicine that has had more influence—and inspired more debate—than the BPSM. (I will return to the term “paradigm” shortly, since it differs in important ways from the term “model”).
Most psychiatrists are generally familiar with some version of the BPSM, which was first introduced by Dr. George Engel in 1977.1,2 (Psychiatrists Dr. Roy Grinker and Dr. John Romano were also involved in the development of the BPSM).
Dr Engel himself provides us with the crux of his thesis:
“To provide a basis for understanding the determinants of disease and arriving at rational treatments and patterns of health care, a medical model must also take into account the patient, the social context in which he lives, and the complementary system devised by society to deal with the disruptive effects of illness, that is, the physician role and the health care system. This requires a biopsychosocial model.”1
A complete review of the nature, limitations, and applications of the BPSM is beyond the scope of this commentary, but at least two generalizations seem warranted:
(1) Within the realms of academic psychiatry and most residency training programs, the BPSM has been—at least nominally– the predominant guide to psychiatric diagnosis and treatment, over the past 30 or more years;3 and
(2) While many psychiatrists endorse and accept some version of the BPSM, the very concept has come under withering attack from within psychiatry itself.
How do we account for this seeming paradox? Are the criticisms leveled against the BPSM justified? If so, can the “model” be revised and salvaged, so that it serves as a useful conceptual and clinical tool in psychiatry? Is the term “model” really justified at all? These questions are the focus of the magisterial new book, “The Biopsychosocial Model of Health and Disease,” by philosopher Derek Bolton and ethicist Grant Gillett.4 And while the authors do not sound the death knell of the BPSM, their critique reveals deep and serious problems with it.
The Critics Have Their Say
Critiques of the BPSM are nothing new. My Tufts colleague, Dr. S. Nassir Ghaemi, launched a broadside against the BPSM in his 2010 book, “The Rise and Fall of the Biopsychosocial Model.”5 In essence, Dr. Ghaemi argued that,
“. . . the BPS [biopsychosocial] model has never been a scientific model or even a philosophically coherent model. It was a slogan whose ultimate basis was eclecticism.”5
Other psychiatrists, including Dr. Kenneth Kendler and the Australian psychiatrist, Dr. Niall McLaren, have also been critical of the BPSM.6,7
In large part, as Bolton and Gillett note, the critics have argued (to oversimplify greatly) that the BPSM lacks specific content; is too general and vague; lacks scientific validity as a “model”; and lacks philosophical coherence. These are serious charges, indeed. As Bolton and Gillett note:
“Given the popularity of the biopsychosocial model and its presumed status as overarching framework for medicine and healthcare, such radical criticisms signal significant underlying theory problems.”4(p6)
A complete discussion of these critiques would require a book in itself. My much more limited goal in this article is to suggest that at least part of the controversy stems from the unfortunate use of the term “model” in Engel’s original work, and the resultant conceptual and clinical burdens placed upon the BPSM.
When re-conceptualized as a paradigm rather than a scientific model, many of these burdens are lifted, and the biopsychosocial approach emerges as both conceptually coherent and clinically useful—within limits–as we’ll see when we return to our opening vignette.
What is a Scientific Model?
The term “model” has been used in a multitude of ways, in both the scientific and philosophical contexts. In the broadest sense,
“…Models are vehicles for learning about the world. Significant parts of scientific investigation are carried out on models rather than on reality itself because by studying a model we can discover features of and ascertain facts about the system the model stands for…”8
Ideally, a scientific model has both specificity and predictive validity, and permits experimental verification (or refutation) of its various components. One example is the Bohr model of the atom:
“The Bohr model and all of its successors describe the properties of atomic electrons in terms of a set of allowed (possible) values. Atoms absorb or emit radiation only when the electrons abruptly jump between allowed, or stationary, states. Direct experimental evidence for the existence of such discrete states was obtained (1914) by the German-born physicists James Franck and Gustav Hertz.”9
Similarly, “. . . in biology, the meiotic model describes the process by which alleles segregate and independently assort during gamete formation. Given this model . . . it is possible to predict the possible allele combinations resulting from meiosis in a given sex cell or class of sex cells.”10
It is fair to say that nothing in Engel’s formulation of the BPSM remotely approaches this level of precision and predictive utility or validity—nor, to my knowledge, did Engel ever claim that his “model” possessed such ideal properties. At most, the BPSM is a scientific model only in the very general sense that it is a “vehicle for learning about the world.”
What is a Paradigm?
Indeed, I believe the biopsychosocial approach is better understood as a paradigm–the term made famous (and ubiquitous) by the historian and physicist Thomas Kuhn, in his classic work, The Structure of Scientific Revolutions.”11 To be sure: Kuhn used the term “paradigm” in a number of ways, and not always with great clarity. Kuhn himself understood “paradigms” as “…accepted examples of actual scientific practice–examples which include law, theory, application, and instrumentation together—[which] provide models from which spring particular coherent traditions of scientific research. These are the traditions which the historian describes under such rubrics as ‘Ptolemaic astronomy’ (or ‘Copernican’), ‘Aristotelian dynamics’ (or ‘Newtonian’), ‘corpuscular optics’ (or ‘wave optics’), and so on.”11(p10)
As I interpret Kuhn, a paradigm is essentially a world-view—a way of seeing things—that guides the practices within a given discipline. Paradigms often generate (“provide”) very specific models but are themselves both broader and more heterogeneous than models. Science writer John Horgan12 explains that “. . . Kuhn used the term [paradigm] to refer to a collection of procedures or ideas that instruct scientists, implicitly, what to believe and how to work.”
The Scope and Limits of the BPS Paradigm
Simply stated, the biopsychosocial (BPS) paradigm, as I conceive it, asserts that most (but not necessarily all) serious mental dis1orders are best understood as having a variety of causes and risk factors–including but not necessarily limited to biological, psychological and social components.
(Dr. Michael McGee13 has also emphasized the importance of the spiritual dimension in the origin and treatment of addictions and other psychiatric conditions, arguing for a “bio-psychosocialspiritual” approach).
As I conceive it, the BPS paradigm does not assert that all psychiatric disorders are, like ancient Gaul, divided into three parts: a biological, a psychological, and a social component. Nor does the paradigm assert “tripartite causation” for all or most diseases, though Engel’s 1977 paper briefly alludes to “the role of psychosocial variables in disease causation.”1(p132)
However, the BPS paradigm does encourage the clinician, heuristically, to investigate whether a particular disorder may arise from some combination of these factors; and, if so, whether the condition merits treatment in all three spheres—which will likely not be the case for all psychiatric illnesses.
The BPS paradigm imposes no need to solve the ancient “mind-body” conundrum that has bedeviled philosophy for millennia (eg, “What is the mind? Is it distinct from brain? How does mind interact with the brain?). Those issues, though philosophically important, are at a different epistemic level than that of the BPS paradigm.
To be sure, problems can arise if the BPS paradigm is untethered to the best available evidence. The actual treatment of the patient must always be evidence-based, and not promiscuously “eclectic.”5 It would indeed be a misuse of the paradigm to “throw a little of this, and a little of that” at the patient, hoping that some combination of biological, psychological, and social therapies will stick. That some practitioners may proceed in this helter-skelter fashion is regrettable but is not an indictment of the BPS paradigm itself, as I have delimited it.
Indeed, the BPS paradigm does have substantial limits. It does not readily lend itself to highly specific, quantitative predictions, along the lines of the Bohr model of the atom. But it does permit some broad, qualitative predictions, and can serve as a heuristic guide to diagnosis, treatment, and medical education. Let’s now return to our opening vignette and see how this might work.
Back to Ms. Jones
First, there is the issue of Ms Jones’ hypothyroidism—a well-known risk factor for depression that may require treatment. When the TSH level is above 10 mIU/L, there’s uniform agreement that treatment with levothyroxine is appropriate; however, for “borderline low” thyroid function (TSH 4-10), treatment with thyroid hormone may or may not be necessary, depending on a variety of factors.14
In any case, the BPS paradigm allows us to predict that, if Ms. Jones’s hypothyroidism is not corrected, she may have an inadequate response to an antidepressant; and that subsequent treatment of the thyroid problem may improve the antidepressant response. (This prediction may not be borne out, but the paradigm allows us to test the hypothesis).
Secondly, we know that Ms. Jones’s divorce has left her feeling lonely and isolated. The BPS paradigm allows us to predict that, unless this “social” component is adequately addressed, the patient may not reach full remission of her depression. (Perhaps Ms. Jones also needs to grieve for the loss of her marriage).
Thirdly, we know that Ms. Jones’s habitual cognitive style involves “catastrophizing” minor stressors, and perhaps misinterpreting certain social cues as reflecting badly on her. Though it is unclear what role, if any, these chronic cognitive distortions played in the current bout of major depression, the BPS paradigm may steer us in the direction of recommending cognitive-behavioral therapy for the patient.
Commenting on the pointed critiques of Engel’s original biopsychosocial model, Bolton and Gillette observe that “What [the critiques] signal is not the end of the model—witness the fact that it persists, for good reasons already indicated—but the need to rethink and reinvigorate it. The answer to the content problem, we suggest, is that the content lies in scientific and clinical specifics, not generalities.”4(p8)
I have argued here that the original BPSM is often held to a standard more befitting a true “scientific model”—like the Bohr atom—when, in reality, what George Engel described is better characterized as a paradigm: a world-view with clear implications for practice. That said, the BPS paradigm needs to be sharpened and “particularized” to specific psychiatric disorders. We need to understand the “scientific and clinical specifics” for all the major psychiatric disorders.
For example, when considering schizophrenia, what relative contribution does “biology” make to the etiology of this disease, as distinct from psychological and social risk factors or causes? (My guess: biology is by far the overwhelming factor). What about obsessive-compulsive disorder or PTSD? To what degree does the controlled evidence support biological vs. psychosocial treatments for these and other psychiatric conditions? And what role does combination treatment play?
In the meantime, I wouldn’t start hanging crepe for Engel’s biopsychosocial “model”—or for the BPS paradigm. It is clear that many psychiatrists still find the basic paradigm useful, for all its flaws. For example, a recent talk by Dr. Anita Clayton nicely illustrates the utility of a BPS approach to sexual dysfunction.15
Until psychiatrists devise a better framework for understanding the diseases we treat, some form of the BPS paradigm will almost certainly survive. Patients like Ms. Jones will see to that.
Note: I wish to thank Dr. Nassir Ghaemi and Dr Awais Aftab for their thoughtful commentaries on this piece, which are posted on the Psychiatric Times website.
1.Engel GL. The need for a new medical model: a challenge for biomedicine. Science. 1977; 196:129–136.
2. Engel GL. The clinical application of the biopsychosocial model. Am J Psychiatry. 1980;137:535–544.
3. Pies RW. Comments on “cyclical swings” by Professor Hannah Decker: The underappreciated “solid center” of psychiatry. Hist Psychol. 2016;19:60–65. https://doi.org/10.1037/hop0000019
4. Bolton D, Gillett G. The Biopsychosocial Model of Health and Disease . Palgrave Pivot, 2019 5. Ghaemi SN: The Rise and Fall of the Biopsychosocial Model Johns Hopkins University Press; 2010
6. Kendler K. The rise and fall of the biopsychosocial model: reconciling art and science in psychiatry. Am J Psychiatry. 2010;167:999–1000.
7. McLaren NA. Critical review of the biopsychosocial model. Aust N Z J Psychiatry. 1998;32:86–92.
8. Models in Science: Section 2.4 Descriptions. Stanford Encyclopedia of Philosophy. February 27, 2006. https://plato.stanford.edu/entries/models-science/#Des. Accessed January 19, 2020.
9. Bohr Model. Encyclopedia Britannica. https://www.britannica.com/science/Bohr-model. Accessed January 19, 2020.
10. Carter J, Rudolph J, Stewart J. The Nature and Structure of Scientific Models. The National Center for Improving Student Learning and Achievement in Mathematics and Science. January 2001. http://courses.umass.edu/educ512f/512readingmaterials/nature%20of%20sci%20models.pdf. Accessed January 19, 2020.
11. Kuhn T. The Structure of Scientific Revolutions. Chicago, IL: University of Chicago Press; 1970.
13. McGee MD. Awakening and Recovery. Alcohol Treat Q. 2019. DOI: 10.1080/07347324.2019.1632766.
14. Godman H. For borderline underactive thyroid, drug therapy isn’t always necessary. Harvard Health Publishing. October 9, 2013. https://www.health.harvard.edu/blog/for-borderline-underactive-thyroid-drug-therapy-isnt-always-necessary-201310096740. Accessed January 19, 2020.
15. Clayton AH. The Biopsychosocial Model of Sexual Response. Consultant 360. https://www.consultant360.com/video/consultant360/biopsychosocial-model-sexual-response. Accessed January 19, 2020.