by Michael D. Anestis, M.S.
Today marks the opening of a new school year at Florida State University. At 8am tomorrow morning, I will greet a classroom full of sleep deprived juniors and seniors and begin another semester of teaching Abnormal Psychology. I enjoy teaching this course immensely, although I am admittedly curious about the reception I will get now that I am teaching at an hour typically unseen by undergraduates rather than my standard late afternoon or early evening time slot. This could get ugly.
When I open the course, I generally spend a short time discussing the definition of mental illness and the basic requirements for a cluster of symptoms to be considered to meet criteria for a DSM-IV-TR diagnosis: deviation from the norm, distress, and/or impairment. The bulk of my opening lectures, however, are spent discussing the origins of mental illness. I often pose an open ended question to the class, asking them where they think mental illness comes from an I receive a thoughtful and diverse set of answers including genes, negative life events, early childhood experiences, and family environment. To this, I reply, that almost all of those answers could be considered correct depending upon the circumstance, but that current thinking involves an interaction of multiple factors rather than a single path to mental illness. Specifically, I say, clinicians and researchers often discuss the idea of a diathesis-stress model.
The word "diathesis" is often met with blank stares and, to be fair, I had never heard of it prior to arriving at graduate school, so I completely understand my students' initial confusion. Quite simply, the word means "vulnerability" and the diathesis-stress model of mental illness posits that symptoms of diagnoses such as depression and obsessive-compulsive disorder arise when individuals with a vulnerability (diathesis), typically a genetic predisposition, encounter negative life events (stress). So, while genes alone can be enough for some individuals, particularly for certain diagnoses (e.g., schizophrenia, bipolar disorder), and environmental stress can also be enough for some individuals, mental illness is most likely in individuals who have a genetic risk and who encounter sufficient life stress.
Aaron Beck, the creator of cognitive behavioral therapy (CBT) and one of the most influential researchers and clinicians in the history of the field, is a proponent of this model and uses it in his conceptualization of depression. In his view, dysfunctional attitudes serve as the diathesis and, when individuals with such attitudes encounter significant life stress, they are likely to develop depression. According to this model, the interaction of the diathesis and stress cause individuals to have depressive thoughts (e.g., "nothing in life works out for me"), which in turn lead to symptoms of depression. Beck, who is a medical doctor, is certainly not discounting the role of genetics by any means, but simply shining a light on another potential vulnerability based on cognitive style. After all, there is no rule that indicates that there must be one single vulnerability and genetic and cognitive risk factors are not mutually exclusive.
As we have said on PBB many times before, untested theories are a useful beginning, but not a good basis for strong conclusions. To be certain about the validity of a theory, we must empirically test it. Thus far, research on Beck's diathesis-stress model of depression has been fairly mixed, but some results are highly promising. Today, I would like to quickly describe one such study, published in Cognitive Therapy and Research by Joiner, Metalsky, Lew, and Klocek (1999). On a side note, we have discussed Joiner's interpersonal-psychological theory of suicidal behavior on PBB before and this model is another example of several risk factors interacting with one another to predict a particular outcome.
In this study, 119 undergraduates were given measures of their attitudes, depressive cognitions, anxious cognitions, and depression symptoms two weeks prior to and two days after receiving midterm grades in their abnormal psychology course. Joiner and colleagues (1999) anticipated that dysfunctional attitudes would predict increases in depression for individuals who received bad midterm grades, but not for individuals who received positive midterm outcomes. Additionally, they hypothesized that depressive cognitions, but not anxious cognitions, would explain the relationship between the interaction of dysfunctional attitudes and midterm outcomes and increases in depressive symptoms. In other words, they believed that depressive thoughts, but not anxious thoughts, would lead to increases in depression for individuals with dysfunctional attitudes who received poor midterm outcomes.
The results of this study confirmed the authors' hypotheses. Individuals with dysfunctional attitudes who received a poor midterm outcome experienced significant increases in depression symptoms whereas individuals without dysfunctional attitudes who received poor midterm outcomes did not. Additionally, individuals with dysfunctional attitudes who received positive midterm outcomes experienced a decrease in depression symptoms, a sign that objective evidence confirming high self-worth can help to combat depression. Also, when the authors examined their data, they found that depressive thoughts, but not anxious thoughts, mediated (explained) the link between increases in depressive symptoms and the interaction of dysfunctional attitudes and midterm outcomes. I realize that last sentence was a mouthful, but its meaning is actually not that complex. What Joiner and colleagues (1999) were saying was that a particular type of thought - depressive cognitions - is the source of the problem, not negative thoughts in general.
So what does all of this mean? First of all, this study provides some compelling evidence in support of the diathesis-stress model that I will be explaining to my students this week, at least with respect to depression. As always, a single study can neither confirm nor disconfirm a theory, but this evidence is promising. Additionally, this study demonstrated that depressive thoughts play a specific role in the onset of depression and that generally negative thoughts, including those related to anxiety, do not have the same effect. This is an important consideration in treatment, as therapists must be able to identify the types of thoughts that are most in need of remediation.
When we think about the origins of mental illness, many of us make the mistake of assuming that it is nature versus nurture rather than considering how those two might interact with one another. Even though the evidence is not universally supportive of this particular model, everything we know points towards a more dynamic, complicated situation than a simple nature versus nurture debate. So as you ponder the question of what causes mental illness, be careful to consider a variety of possibilities and remember, knowing the source is not the same as treating the condition.
If you would like to learn more about this type of model for mental illness, we recommend the following resources, all of which are available through out online store:
Cognitive Therapy of Depression
- by Aaron Beck, M.D.
Feeling Good: The New Mood Therapy Revised and Updated
- by David Burns, M.D.
Cognitive-Behavioral Treatment of Borderline Personality Disorder
- by Marsha Linehan, Ph.D.
Mike Anestis is a doctoral candidate in the clinical psychology department at Florida State University.
