Reviews and Overviews The Evolution of the Cognitive Model of Depression and Its Neurobiological Correlates Aaron T. Beck, M.D. Although the cognitive model of depres- now possible to sketch out possible ge- sion has evolved appreciably since its first netic and neurochemical pathways that formulation over 40 years ago, the poten- interact with or are parallel to cognitive tial interaction of genetic, neurochemical, variables. A hypersensitive amygdala is and cognitive factors has only recently associated with both a genetic polymor- been demonstrated. Combining findings phism and a pattern of negative cognitive from behavioral genetics and cognitive biases and dysfunctional beliefs, all of neuroscience with the accumulated re- which constitute risk factors for depres- search on the cognitive model opens new sion. Further, the combination of a hyper- opportunities for integrated research. active amygdala and hypoactive prefron- Drawing on advances in cognitive, per- tal regions is associated with diminished sonality, and social psychology as well as cognitive appraisal and the occurrence of clinical observations, expansions of the depression. Genetic polymorphisms also original cognitive model have incorpo- rated in successive stages automatic are involved in the overreaction to the thoughts, cognitive distortions, dysfunc- stress and the hypercortisolemia in the tional beliefs, and information-processing development of depression—probably biases. The developmental model identi- mediated by cognitive distortions. I sug- fied early traumatic experiences and the gest that comprehensive study of the psy- formation of dysfunctional beliefs as pre- chological as well as biological correlates disposing events and congruent stressors of depression can provide a new under- in later life as precipitating factors. It is standing of this debilitating disorder. (Am J Psychiatry 2008; 165:969–977) I was privileged to start my research on depression at a clinical research in depression because the field was wide time when the modern era of systematic clinical and bio- open—and besides, I had a testable hypothesis. logical research was just getting underway. Consequently, the field for new investigations was wide open. The cli- Cross-Sectional Model of Depression mate at the time was friendly for such research. The Na- I decided at first to make a foray into the “deepest” level: tional Institute of Mental Health had only recently been the dreams of depressed patients. I expected to find signs funding research and providing salary support for full- of more hostility in the dream content of depressed pa- time clinical investigators. The Group for Advancement of tients than nondepressed patients, but they actually Psychiatry, under the leadership of pioneers like David showed less hostility. I did observe, however, that the Hamburg, was providing guidelines as well as the impetus dreams of depressed patients contained the themes of for clinical research. loss, defeat, rejection, and abandonment, and the Caught up with the contagion of the times, I was dreamer was represented as defective or diseased. At first I prompted to start something on my own. I was particularly assumed the idea that the negative themes in the dream intrigued by the paradox of depression. This disorder ap- content expressed the need to punish one’s self (or “mas- peared to violate the time-honored canons of human na- ochism”), but I was soon disabused of this notion. When ture: the self-preservation instinct, the maternal instinct, encouraged to express hostility, my patients became the sexual instinct, and the pleasure principle. All of these more, not less, depressed. Further, in experiments, they normal human yearnings were dulled or reversed. Even vi- reacted positively to success experiences and positive re- tal biological functions like eating or sleeping were attenu- inforcement when the “masochism” hypothesis predicted ated. The leading causal theory of depression at the time the opposite (summarized in Beck [1]). was the notion of inverted hostility. This seemed a reason- Some revealing observations helped to provide the basis able, logical explanation if translated into a need to suffer. for the subsequent cognitive model of depression. I noted The need to punish one’s self could account for the loss of that the dream content contained the same themes as the pleasure, loss of libido, self-criticism, and suicidal wishes patients’ conscious cognitions—their negative self-evalu- and would be triggered by guilt. I was drawn to conducting ations, expectancies, and memories—but in an exagger- Am J Psychiatry 165:8, August 2008 ajp.psychiatryonline.org 969 EVOLUTION OF THE COGNITIVE MODEL OF DEPRESSION ated, more dramatic form. The depressive cognitions con- activity. These symptoms are also subjected to negative tained errors or distortions in the interpretations (or evaluation (“My poor functioning is a burden on my fam- misinterpretations) of experience. What finally clinched ily” and “My loss of motivation shows how lazy I am”). the new model (for me) was our research finding that Thus, the depressive constellation consists of a continu- when the patients reappraised and corrected their misin- ous feedback loop with negative interpretations and at- terpretations, their depression started to lift and—in 10 or tentional biases with the subjective and behavioral symp- 12 sessions—would remit (2). toms reinforcing each other. Thus, I undertook the challenge of attempting to inte- grate the different psychological pieces of the puzzle of de- Developmental Model of Depression pression. The end product was a comprehensive cognitive model of depression. At the surface, readily accessible Cognitive Vulnerability level was the negativity in the patients’ self-reports, in- What developmental event or events might lead to the cluding their dreams and their negative interpretations of formation of dysfunctional attitudes and how these events their experiences. These variables seemed to account for might relate to later stressful events leading to the precip- the manifestations of depression, such as hopelessness, itation of depression was another piece of the puzzle. In loss of motivation, self-criticism, and suicidal wishes. The our earlier studies, we found that severely depressed pa- next level appeared to be a systematic cognitive bias in in- tients were more likely than moderately or mildly de- formation processing leading to selective attention to neg- pressed patients to have experienced parental loss in ative aspects of experiences, negative interpretations, and childhood (6). We speculated that such a loss would sensi- blocking of positive events and memories. These findings tize an individual to a significant loss at a later time in ad- raised the question: “What is producing the negative olescence or adulthood, thus precipitating depression. bias?” On the basis of clinical observations supported by Brij Sethi, a member of our group, showed that the combi- research, I concluded that when depressed, patients had nation of a loss in childhood with an analogous loss in highly charged dysfunctional attitudes or beliefs about adulthood led to depression in a significant number of de- themselves that hijacked the information processing and pressed patients (7). The meaning of the early events (such produced the negative cognitive bias, which led to the as “If I lose an important person, I am helpless”) is trans- symptoms of depression (1, 3, 4). formed into a durable attitude, which may be activated by A large number of studies have demonstrated that de- a similar experience at a later time. A recent prospective pressed patients have dysfunctional attitudes, show a sys- study observed that early life stress sensitizes individuals tematic negative attentional and recall bias in laboratory to later negative events through impact on cognitive vul- experiments, and report cognitive distortions (selective nerability leading to depression (8). abstraction, overgeneralizing, personalization, and inter- The accumulated research findings have supported the pretational biases [4]). Dysfunctional attitudes, measured original cognitive vulnerability model derived from clini- by the Dysfunctional Attitudes Scale (5), are represented cal observations (4). As shown in Figure 1, early adverse by beliefs such as “If I fail at something, it means I’m a total events foster negative attitudes and biases about the self, failure.” During a full-blown episode of depression, the hy- which are integrated into the cognitive organization in the persalient dysfunctional attitudes lead into absolute nega- form of schemas; the schemas become activated by later tive beliefs about the self, their personal world, and the fu- adverse events impinging on the specific cognitive vulner- ture (“I am a failure”). I suggested that these dysfunctional ability and lead to the systematic negative bias at the core attitudes are embedded within cognitive structures, or of depression (1, 9). schemas, in the meaning assignment system and thus Much of the early research by others on the cognitive have structural qualities, such as stability and density as model overlooked the role of stress in activating previ- well as thresholds and levels of activation. The degree of ously latent dysfunctional schemas. Scher and colleagues salience (or “energy”) of the schemas depends on the in- (10) provided a comprehensive review of the diathesis- tensity of a negative experience and the threshold for acti- stress formulation