At a 2007 Mind and Life Conference at Emory University, I had the privilege of watching and listening as Charles Nemeroff, M.D., presented a professional paper to His Holiness the Dalai Lama. [As my older daughter would likely say, Dr. Nemeroff is a very fancy biological psychiatrist.] Nemeroff noted, with some authority, that we now know that one-third of all depressive disorders are genetically-based and two-thirds are environmentally-based. Following this statement, Nemeroff continued to discuss the trajectory of “depressive illness,” focusing, in particular, on findings linked to mice with early maternal deprivation and related findings regarding trauma and depression. His conclusion was that, for some individuals (and mice), the brain is changed by early childhood trauma, while for others, the brain seems unaffected. Interestingly, at that point in the conference the Dalai Lama interrupted and there were animated interactions between him and his interpreter. Finally, the interpreter directed a question to Nemeroff, stating something like, “His Holiness is wondering, if two-thirds of depression is caused by human experience and one-third is caused by genetics, but that humans who are genetically predisposed to depression have to have a trauma for the depression to be manifest, then wouldn’t it be true to say that all depression is caused by human experience?” After a brief silence, Nemeroff responded, “Yes. That would be true.”
Most of us have heard about the biopsychosocial model in contemporary medicine. Below I’ve included some information about its origin (this info is adapted from a 2009 Journal of Contemporary Psychotherapy Article; you can find the whole article here: http://www.coping.us/images/Sommers_Campbell_2009_EBP_for_Kids.pdf).
In his 1980 call to medicine, Engel (1980; 1997) encouraged adoption of a biopsychosocial model of health and illness. Despite this recommendation and the increased use of ‘biopsychosocial’ language among non-medical practitioners, medicine has demonstrated little movement toward embracing a biopsychosocial perspective (Alonso, 2004). To some extent, the Nemeroff-Dalai Lama interaction illustrates medical professionals’ tendencies to formulate mental health problems as disease states even when their own data are contradictory. At the Mind and Life Conference, Nemeroff continued to present his illness-based depression formulation even after conceding environmental causality of depression (Nemeroff, 2007).
Although we (Sommers-Flanagan & Campbell) generally advocate medicine’s biopsychosocial model, we see utility in a slightly more radical reconceptualization of depression–especially among youth. This belief rests upon knowledge about the etiology, course, and treatment of depression, equivocal data regarding antidepressant medication effectiveness, potential developmental and medical dangers associated with short- and long-term SSRI use, research on child development and trauma, and our own clinical experience (Sommers-Flanagan & Sommers-Flanagan, 1995a; Sommers-Flanagan & Sommers-Flanagan, 2007). In short, instead of a biopsychosocial model for understanding and treating youth depression, we believe a social-psychological-biological approach is more consistent with current scientific and clinical knowledge.
A Social-Psycho-Bio Model of Clinical Depression
All humans are born into pre-determined social and cultural settings, which directly influence emotional, psychological, social, and biological functioning and development (Christopher, 1996; Sue & Sue, 2013). Although space precludes complete articulation of the social-psycho-bio model, we describe the major components below.
Social-cultural components. Many cultural factors contribute to children’s emotional and psychological development. For example, in the United States, babies are often born to socially isolated mothers living in poverty. These mothers may also be depressed themselves and have little community and governmental support (Goosby, 2007; Knitzer, 2007). In contrast, more communal and supportive cultural settings place less of a parenting burden on individual mothers, thus possibly decreasing depression. It’s likely that different degrees of cultural support to families and children translate into different degrees of relative risk for depressive experiences in children.
Recent research affirms diverging cultural assumptions about depression etiology. Whereas South Asian immigrants viewed depressive symptoms as stemming from social and moral influences (Karasz, 2005), European Americans attributed depression to biological influences. These cultural formulations or expectations likely influence medication or psychotherapeutic efficacy. Although biomedical researchers emphasize genetic contributions to depression, an individual’s depressive predisposition may be strongly influenced by overarching cultural factors. Given Nemeroff’s admission that depression is rooted in human experience, it seems appropriate to us that depression formulations lead with social and cultural, rather than biological factors.
Early caretaker-child interactions. Early caretaker-baby interactions appear to stimulate depression development in very young children. The best example of this comes from studies of maternal depression, which demonstrate that mothers’ depressive behaviors influence their children’s own emotional suffering and other neurological changes (Ashman & Dawson, 2002). This evidence for a direct effect of caregiver behavior on children’s neural activity and possible brain development supports the social-psycho-bio model.
Child trauma. Garbarino’s (2001) statement, “Risk accumulates; opportunity ameliorates” (p. 362) suggests that repeated trauma in the absence of support or opportunity can deeply damage children. Trauma typically occurs within a social and cultural context, and without requisite support and opportunity, it can initiate cognitive, emotional, and social pathology. Sufficiently intense trauma may also produce lasting “psychic scars” (Terr, 1990). Additionally, early childhood trauma drains children and adults of meaningfulness (Garbarino, 2001). There is little doubt about the powerful contribution of trauma to the development of clinical depression and other mental disorders.
Psychological/cognitive development of depressive symptoms. Considerable evidence supports a cognitive model of depression in adults, and to some extent, in adolescents and children (Kazdin & Weisz, 2003). The pioneering work of Aaron Beck (1970) emphasizes that personal experiences lead individuals to acquire specific negative beliefs about themselves, the world, and the future (i.e., the cognitive triad). Although empirical support for the cognitive triad’s contributory and maintenance roles in depression is strong, these belief systems do not rise autonomously within the psyche. Instead, as Beck notes, these deeply ingrained beliefs are learned vis-à-vis interpersonal experiences.
The development of schemata or internal working models. Theorists spanning analytic, neoanalytic, cognitive, and attachment perspectives have proposed concepts that can be described as schemata or internal working models (Ainsworth, 1989; Glasser, 1998; Morehead, 2002; Young, Klosko, & Weishaar, 2003). Although each theoretical perspective articulates the concept somewhat differently, all involve development of a psychological pattern of repetitive automatic beliefs and expectations. These beliefs and expectations, which implicate the self, the world, and others (or objects), generate repetitive behaviors and affect. A cognitive schema or internal working model arises from early social interactions and may contribute to depression and other emotional and behavioral maladies. From a behavioral perspective, depressogenic working models involve early maladaptive reinforcement contingencies, which must be unlearned before one can acquire more adaptive behavior patterns.
Regardless of theoretical orientation, the internal working model concept forms the foundation of many psychological interventions. For example, it clearly underlies CBT and interpersonal therapy (IPT), two evidence-based practices for treating depression in youth (Kazdin & Weisz, 2003). Essentially, internal working models or schemata include internalized early experiences, and they constitute the “psycho” component of the social-psycho-bio model. When positive, adaptive, and healthy early experiences predominate, internalized working models buffer or immunize the individual against stress and trauma. When critical, negative, and maladaptive experiences predominate, schemata can predispose an individual to acute, chronic, or recurrent depressive episodes.
Neurological (brain-based) manifestations of depression. In addition to social, cognitive, emotional, and motivational experiences, current and recent research has identified cortical functioning correlates of depression. These correlates include neurochemical changes and neural activity, which can be observed via Positron Emission Tomography or functional Magnetic Resonance Imaging. Typically, brain imaging studies in animals, youth, and adults are presented as evidence of biomedical or biogenetic causal factors of depression. In the social-psycho-bio model described here, we suggest that neural changes are natural and inevitable correlates of internalized depressive life experiences. Because we are all biological organisms, observable neural changes associated with clinical depression should come as no surprise. It is important to note, however, that brain changes represent a physical phenomenon correlated with depression; these changes may or may not be causative.
Individuals with more extreme, recurrent, or chronic depressive experiences are perhaps more likely to evidence neurochemical states that add to or maintain depression. Again, we view this as a natural biological process. In some circumstances, this state might require a biological agent (or medication) to be used in combination with psychotherapy to facilitate depression recovery.
Our social-psycho-bio model advocacy does not exclude biomedical contributors to depression. Instead, it identifies biological manifestations as correlates of social and psychological dimensions of depression. This argument has been articulated before, but without much success. We attribute the failure of this view to the din of medication marketing and a cultural orientation toward quick fixes. In fact, we are all biological creatures with intricately interconnected brains characterized by dazzlingly complex electrochemical communication. The search for fMRI and PET scan differences between depressed and non-depressed individuals represents a logical and natural development in our understanding of depression as it exists within the whole person. Although neurochemical changes might maintain depression, it is not necessarily the case that neurochemical factors (or the vernacular ‘chemical imbalances’) initiate depressive processes. Indeed, these neurochemical changes are just as likely to be consequences of depressive conditions. Based on this depression re-formulation, we believe that it would be appropriate to initiate antidepressant medication treatment as an adjunctive approach if previously attempted experiential interventions, including exercise, dietary adjustments, and psychotherapy failed to achieve desired effectiveness. Further, conceptualizing neurochemical changes as depressive correlates rather than causes, lead us to agree with others who maintain that medication treatment should be considered a palliative and not curative treatment (Overholser, 2006).
[Again, please note that much of the preceding is adapted from a previously published article in the Journal of Contemporary Psychotherapy. The article was titled, “Psychotherapy and (or) Medications for Depression in Youth? An Evidence-Based Review with Recommendations for Treatment.” Citations are available in the original article.]