Aaron Beck pioneered the way we view the nature of depression. He guided psychological theory from its overly Freudian emphasis to a simpler model capable of being scientifically evaluated. The field can now progress to integrate the major psychological elements. In proposing a new theory (Observer, Vol. 29, No. 4), Beck makes a major contribution to resolving the roles of the various elements of depression and demonstrates new pathways to treatment.
This article, however, only outlines the new proposal: A more detailed presentation of the supporting evidence is needed before we can judge the overall impact. For example, there are concerns about whether Beck has fully integrated what we have learned about the disorder since drug treatments were first introduced in the 1950s. The most impactful development then was the discovery that one-third of chronically depressed patients not only improved clinically but became symptom-free. That opened up new ways of thinking about the roots of the disorder (i.e., that the chemistry of the nervous system was substantially involved with creating and maintaining the illness). Many in the field conditioned to view depression as primarily psychological were reluctant to accept these new findings. However, decades of research on interactions between psychological and neurochemical factors have convinced most that a theory that does not find behavioral–biological interaction playing a major role in the disorder cannot be truly “integrative.” Beck’s theory downplays biological factors in depression, thus undermining his major thesis.
An analysis of the nature of the disorder must begin with an examination of why antidepressant drugs restored patients to their predepressed states. We accomplished that through empirical investigations of depression’s behavioral and neurochemical elements and how they interact. The theory recently presented (Katz, 2013) elaborates on the behavioral and cognitive elements, the components of the disorder based on phenomenological studies (Grinker et al., 1961; Katz, 2013; and Kendell, 1968), and their associations with the functioning of neurotransmitter systems shown to be directly acted on by antidepressant drugs (Morilak & Frazer, 2004). Those studies revealed specific associations, including those between the neurotransmitter serotonin and anxiety and anger as well as between norepinephrine and arousal. The findings point to a new view of depression as opposed emotional states — the “excited,” negatively aroused state of anxiety and feelings of anger, and the opposed “down” state of motor retardation and mood — as occurring concurrently and thereby creating a persisting state of turmoil and suffering for the afflicted patient.
This new theory of “opposed neurobehavioral states” does not speak to causes but only to the nature of the disorder; thus, it would not run counter to Beck’s theory about the psychological content that instigates the disorder. It would, however, alert investigators to the complicated interaction of behavioral and neurochemical factors that underlie the affliction. It reintroduces the major role that biology plays in this complex disorder and broadens the path to its understanding and the potential roles of the various treatments, cognitive–behavioral and neurochemical, in stemming and completely resolving it.
If Beck aims to create a truly integrative theory, he must find a place for these major developments in the neuropsychopharmacologic science alongside his pioneering contribution to the psychology of depression.
-Martin M. Katz
Grinker, R., Miller, J., Sabshin, M., Nunn R., & Nunnally, J. C. (1961). The phenomena of depressions. New York, NY: Hoeber.
Katz, M. M. (2013). Depression and drugs: The neurobehavioral structure of a psychological storm. New York, NY: Springer.
Kendell, R. E. (1968). The classification of depressive illnesses. London, United Kingdom: Oxford University Press.
Morilak, D. A., & Frazer, A. (2004). Antidepressants and brain monoaminergic systems: A dimensional approach to understanding their behavioral effects in depression and anxiety disorders. International Journal of Neuropsychopharmacology, 7, 193–218.