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Cognitive Therapy: Current Status and Future Directions

Aaron T. Beck1 and David J.A. Dozois2
1 Department of Psychiatry, University of Pennsylvania, Philadelphia, Pennsylvania; email: abeck@mail.med.upenn.edu 2 Department of Psychology, University of Western Ontario, London, Ontario, Canada; email: ddozois@uwo.ca

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Annu. Rev. Med. 2011. 62:397409 First published online as a Review in Advance on August 3, 2010 The Annual Review of Medicine is online at med.annualreviews.org This articles doi: 10.1146/annurev-med-052209-100032 Copyright c 2011 by Annual Reviews. All rights reserved 0066-4219/11/0218-0397$20.00

Keywords
cognitive vulnerability, psychotherapy, treatment outcome, cognitive behavior therapy

Abstract
Cognitive therapy is a system of psychotherapy with a powerful theoretical infrastructure, which has received extensive empirical support, and a large body of research attesting to its efcacy for a wide range of psychiatric and medical problems. This article provides a brief overview of the conceptual and practical components of cognitive therapy and highlights some of the empirical evidence regarding its efcacy. Cognitive therapy (often labeled generically as cognitive behavior therapy) is efcacious either alone or as an adjunct to medication and provides a prophylaxis against relapse and recurrence.

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OVERVIEW
Cognitive schema: a well-organized cognitive structure of stored information and memories that forms the basis of core beliefs about self and others

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From its inception more than 45 years ago (13), cognitive therapy has been theory driven. Specically, Becks objectives for deriving and evaluating this system of psychotherapy involved an overall plan to construct a comprehensive theory of psychopathology that maps clearly onto the treatment approach, to investigate scientic support for the theory, and to test the efcacy of therapeutic interventions (3, 4). Cognitive theory and therapy were rst developed for depression (1, 2) and later systematically applied to suicide prevention (5), anxiety disorders (6), personality disorders (7), substance abuse (8), and, most recently, schizophrenia (9, 10). Cognitive therapy (CT), often discussed under the generic label cognitive behavior therapy (CBT), is now widely represented in training programs in psychology, psychiatry, medicine, social work, nursing, and other allied health professions that value evidence-based practice (11). CT and CBT have been described as the fastest growing and most heavily researched systems of psychotherapy on the contemporary scene (12, p. 332). This article provides a brief overview of the conceptual, practical, and empirical aspects of CT. After highlighting some of its basic concepts and the research pertaining to Becks cognitive theory, we discuss the general approach to treatment and review the literature on its efcacy. We conclude by outlining some directions for future research.

COGNITIVE THEORY
Cognitive theory is based on the presumption that information processing is crucial for human adaptation and survival. Without the ability to process information from the environment, synthesize it, and formulate a plan for dealing with it, we would not survive. The cognitive (or information processing) system is intricately tied to other affective, motivational, and behavioral repertoires. Each of these repertoires, or systems, serves an individual function and also operates in synchrony toward
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coordinated, goal-oriented strategies (e.g., approaching pleasure, avoiding pain) (13, 14). The ght-ight response, for instance, arises from four systems (13): cognitive (perception of threat), affective (feelings of anxiety or anger), motivational (the impulse to confront or ee the threatening stimulus), and behavioral (the implementation of action). In this construct, onset of a particular condition (e.g., panic disorder) is believed to occur when these different systems shift from a fairly quiescent state to a highly activated state. In the example of panic disorder, this might occur when the ght-ight response is activated by false alarms (e.g., misperceiving bodily sensations as harmful to the organism). Cognitive theory suggests that psychopathology is characterized by the activation of a conglomerate of related or contiguous dysfunctional beliefs, meanings, and memories that operate in coordination with affect, motivation, behavior, and physiological responses. Different psychopathological conditions are associated with specic biases that inuence how an individual incorporates and responds to new information. According to Becks model (13, 6, 15, 16), the cognitive appraisal of internal or external stimuli inuences and is, in turn, impacted by these other systems. Thus, although cognition plays a key role in this model (i.e., the assignment of meaning is crucial to understanding maladaptive behavior), it is recognized that mental health problems involve a complex interplay among diverse and interrelated systems (17). Within the cognitive system are different levels of cognition, ranging from surface-level thoughts to deeper cognitive schemas (18, 19). Cognitive schemas are organized structures of stored information that contain individuals perceptions of self and others, goals, expectations, and memories. These elements are wellorganized within the cognitive structure (20) and inuence the screening, coding, categorization, and interpretation of incoming stimuli and the retrieval of stored information. Schemas are adaptive insofar as they afford efcient processing of information; however, when they

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become negatively biased, maladaptive, rigid, and self-perpetuating, they can contribute to psychopathology. Maladaptive cognitive schemas are believed to develop during early periods of the life span and become increasingly consolidated and organized as new experiences are assimilated into the existing belief structure (3, 15). Poor early attachment experiences and other adverse events (e.g., childhood maltreatment), for example, may contribute to the development of a maladaptive belief system. Cognitive theory is essentially a diathesis-stress model. In other words, it is possible to have a maladaptive belief system and not exhibit symptoms so long as the cognitive schema (and related systems) is not activated. Once triggered by external events, drugs, or endocrine factors, however, the cognitive schema triggers a cascade of informationprocessing biases (1, 4, 15, 16, 18). These may be attention, memory, or interpretational biases. For instance, individuals with anxiety disorders perceive themselves as vulnerable and the world as dangerous. Such individuals attend selectively to threat-pertinent information at the expense of information that is inconsistent with threat or information that suggests one has sufcient resources for dealing with it. An individual who is vulnerable to depression, to consider another example, may have an underlying belief that he or she is unlovable. This belief may become especially salient when adverse circumstances activate an underlying negative schema. Such an individual may then attend selectively to and recall information that is consistent with this negative view of self (e.g., paying attention to cues that are suggestive of being unloved and minimizing information that is inconsistent with that belief). The activation of a maladaptive cognitive schema, along with the ensuing informationprocessing biases, is also apparent in more surface-level cognitions or what are referred to as automatic thoughts. This term refers to the stream of positive and negative thoughts that runs through an individuals mind unaccompanied by direct, conscious deliberation. Although such thoughts are more supercial and

proximal to a given situation than are other levels of cognition, they are functionally related to ones deeper beliefs and schemas and seem to arise associatively as different aspects of ones core belief system are activated. When negative cognitive schemas are activated, as in depression, they are not only identiable but can be shown to have an inuence on information processing, as manifested by cognitive biases, and have an impact on symptom development. When a depressive episode has remitted, the negative schemas are deactivated (or vice versa). Another aspect of Becks model is content specicity (16, 17). That is, different emotional experiences and forms of psychopathology are related to a unique cognitive prole or set of beliefs (see Table 1 for some examples of systematic biases associated with different disorders). To illustrate, depression is related to thoughts and beliefs concerning personal loss, deprivation, and failure (15). Persons with clinically signicant anxiety tend to overestimate the probability of risk while simultaneously underestimating their resources for coping with potential threats. Their thoughts focus on themes of the self as vulnerable, the world as dangerous, and the future as potentially catastrophic (6). A person with dependent personality disorder has a view of the self as weak, helpless, and incompetent (7). The empirical literature has provided considerable support for various aspects of Becks cognitive theory. Hundreds of studies have demonstrated that individuals lter information and respond to stimuli in a way that is consistent with their preexisting beliefs and assumptions. Some research has also demonstrated that negative cognitive biases precede the development of anxious (e.g., 21) and depressive (e.g., 22) symptoms. Supportive evidence has been obtained for the ideas that there are distinct levels of cognition that work in synchrony to impact emotional and behavioral responses and that an emotional experience or clinical disorder can be characterized by a unique set of beliefs and automatic thoughts (i.e., content specicity; see 16, 18). Schema
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Diathesis-stress model: a psychological theory that predicts that psychiatric disorders result from the interaction of a predisposition (e.g., genetic, cognitive diatheses) and negative life events. When an underlying vulnerability is strong, less stress is necessary to trigger the behavior or disorder; when the predisposition is weak, a greater amount of stress is typically needed before an individual develops the disorder Automatic thoughts: the ow of cognitions (considered the cognitive byproducts of activated schemas) that arise in our day-to-day lives and are not accompanied by direct deliberation or volition

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Table 1 Disorder

The cognitive prole of psychological disorders (14; reprinted with permission) Systematic bias in processing information Negative view of self, experience, and future Inated view of self and future Sense of physical or psychological danger Catastrophic interpretation of bodily/mental experiences Sense of danger in specic, avoidable situations Attribution of bias to others Concept of motor or sensory abnormality Repeated warning or doubts about safety Rituals to ward off perceived threat Hopelessness and deciencies in problem solving Fear of being fat Attribution of serious medical disorder

Depression Hypomania Anxiety disorder Panic disorder Phobia Paranoid state Hysteria Obsession Compulsion Suicidal behavior Anorexia nervosa

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Hypochondriasis

organization (see 18), activation (e.g., 23), and the contribution of cognitive vulnerability to the incidence of psychiatric disorders (e.g., 24) have also been supported by empirical research.

COGNITIVE THERAPY
CT rests on three main propositions (25, 26): The access hypothesis: With appropriate training, motivation, and attention, individuals can become aware of the content and process of their thinking. The mediation hypothesis: The manner in which individuals think about, interpret, and construe events inuences their emotional and behavioral responses. The change hypothesis: Individuals can become more functional and adaptive by intentionally modifying their cognitive and behavioral responses to the circumstances they face. Cognitive therapy is a structured, collaborative process that helps individuals to consider both the accuracy and usefulness of their thoughts through processes of exploration (determining ones idiosyncratic meaning system and maladaptive beliefs), examination (reviewing the evidence for and against a particular belief and considering alternative interpretations or explanations), and experimentation (testing
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the validity of ones belief system) (27). This general approach is used early in therapy to target more proximal and surface-level cognitions (e.g., automatic thoughts, dysfunctional attitudes) and in later sessions to modify deeper cognitive structures and core beliefs. CT is not the replacement of negative thoughts with positive ones; rather, it aims to help individuals shift their cognitive appraisals from ones that are unhealthy and maladaptive to ones that are evidence-based and adaptive. Essentially, patients learn how to become scientic investigators of their own thinkingto treat thoughts as hypotheses rather than as facts and to put these thoughts to the test. Framing a belief as a hypothesis provides an opportunity to test its validity, affords patients the ability to consider alternative explanations, and permits them to gain distance from a thought to allow more objective scrutiny (11). Patients learn to modify their thoughts so that they are congruent with existing evidence. When thoughts are aligned with evidence, and negative feelings exist, the cognitive therapist helps patients to deal with emotional sequelae by introducing coping strategies, fostering skill development and/or problem solving. Cognitive therapists help patients to move through the process of exploration, examination, and experimentation using collaborative empiricism, guided discovery, and Socratic

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dialogue. Collaborative empiricism means that the patient and the therapist become coinvestigators both in ascertaining the goals for treatment and investigating the patients thoughts. Methods of guided discovery are used to help patients to test their own thinking through personal observations and experiments rather than via cajoling or persuasion. Through this process, patients are able to shift from a conviction mode to a questioning mode (28, p. 216). In addition, by collaboratively designing new experiences to try out (called behavioral experiments), patients are able to acquire a different perspective on themselves and their situations (14). Socratic dialogue is a method of guided discovery in which the therapist asks a series of carefully sequenced questions to help dene problems, assist in the identication of thoughts and beliefs, examine the meaning of events, or assess the ramications of particular thoughts or behaviors. CT is time limited. The average length of CT in outcome studies is between 12 and 24 weekly sessions, although there is more variability in clinical practice (25). The initial sessions are often focused on enhancing the therapeutic alliance, identifying the specic problem(s) that brought the patient into treatment, socializing the patient to the cognitive understanding of psychopathology, and symptom relief via behavioral strategies. At this time, the therapist plays a more active role than the patient. As therapy progresses, the emphasis shifts from symptom amelioration to the examination and modication of the patients patterns of thinking, and the patient assumes a more active role in identifying problems and solutions and developing homework assignments. Toward the end of therapy, sessions are usually spread apart so that the patient can consolidate gains and increase his or her condence in the application of newly learned skills. Booster sessions are frequently scheduled one or two months after the end of therapy. Homework assignments (also called action plans) are an important component of CT. Homework provides opportunities to enhance the mastery and generalization of skills learned

in the weekly therapy session by applying them in the real world, and improves treatment outcome (29). The specic techniques utilized in CT tend to vary depending on the disorder being treated and the case formulation. They typically include (a) establishing the therapy relationship, (b) behavioral change strategies, (c) cognitive restructuring strategies, (d ) modication of core beliefs and schemas, and (e) prevention of relapse/recurrence. Given that it is not possible to describe the science and art of CT in this brief article (interested readers are referred to more detailed discussions in 11, 14, 25, 30), we instead provide a capsule summary of these ve components. The therapeutic relationship is a key ingredient of all psychotherapies, including CT. There appears to be a bidirectional relationship between the patients perception of the therapeutic alliance and outcome: The connection between patient and therapist may facilitate change, and symptom change, in turn, enhances the bond between patient and therapist (11). Many of the basic interpersonal variables common to other psychotherapies (e.g., warmth, accurate empathy, unconditional positive regard) serve as an important foundation for cognitive and symptomatic change. As Beck et al. (15) noted, however, these characteristics in themselves are necessary but not sufcient to produce an optimum therapeutic effect (p. 45). Behavioral strategies are used to test and alter automatic thoughts and assumptions and to facilitate new learning. In a behavioral experiment, for instance, a patient may predict an outcome based on his or her automatic thoughts and beliefs, conduct an agreed-upon behavior, and evaluate the evidence in the context of the results of this new experiment. A related approach is hypothesis testing, which has both cognitive and behavioral components. A resident who insists, I am not a good doctor, for example, can be asked to generate a list of characteristics or criteria that would constitute being a good physician (e.g., ability to establish rapport; knowledge base; capacity for making
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decisions under pressure). The experiment would then involve collecting data by monitoring his or her behavior and seeking input from colleagues and supervisors which may help to modify this conviction (e.g., I am a good doctor for my level of experience and training) (14). Other behavioral techniques are used to alter the patients reinforcement schedule (thereby increasing pleasure or mastery), habituate to feared stimuli (exposure therapy), relax (progressive muscle relaxation), or prepare for upcoming situations (behavioral rehearsal). Given that these strategies are used to foster cognitive change, the therapist routinely assesses the patients perceptions, thoughts, and conclusions after each experiment (14). Cognitive restructuring strategies are also used to help patients identify and test the validity of their cognitions. One important technique for eliciting and evaluating negative automatic thoughts is the Daily Record of Thoughts (DRT). A DRT entry consists of three columns representing the situation encountered, the emotion or symptoms experienced, and associated thoughts. Once patients are reliably able to identify the automatic thoughts that carry the greatest emotional charge, the process of answering back to these thoughts (or putting them on trial) can begin. This process often involves writing down the evidence that pertains to a particular belief and developing an alternative thought that incorporates the facts that bear on the belief. By writing down an activating event, the mediating thoughts, and the ensuing emotional response, the patient maintaining a DRT achieves more objectivity about and distance from his or her thoughts. The evidence pertaining to a particular belief is then examined using guided discovery and collaborative empiricism. Specically, patients are asked a number of questions, including: What is the evidence for or against this belief? What are the alternative ways to think about this situation? If my best friend or loved one knew that I had this thought, what would he or she say to me? What would it mean about me even if this particular thought was true? (25, 3032). From
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this analysis of the evidence, patients are then taught to generate alternative thoughts that incorporate the evidence and lead to a shift in their emotional experience. If a given thought is inconsistent with the weight of factual evidence on the subject (e.g., I am unlovable), the therapist helps the patient to alter and realign the thought so that it is evidence-based and, consequently, more adaptive and helpful. Sometimes collecting more information or conducting a behavioral experiment is also used to test a certain belief. After a number of sessions using the DRT, the therapist and patient may notice a consistent pattern in the types of automatic thoughts that are elicited. This is because automatic thoughts and cognitive distortions (e.g., If I fail at X, then I am not worthwhile) are functionally related to deeper core beliefs and schemas. The modication of these core beliefs and schemas is believed to result in the most generalizable change and the greatest prevention of relapse (33, 34). These deeper beliefs are tested and recongured using Socratic dialogue and guided discovery, role plays, behavioral experiments, and other change strategies (11, 15, 25, 30). The nal sessions of treatment are focused on consolidating the skills learned and on the prevention of relapse/recurrence. This includes, among other things, a gradual titration of sessions and spreading apart of their timing, reviewing the treatment strategies that were utilized and were most helpful, creating a plan for the future, discussing feelings about the termination of therapy, preparing for setbacks, identifying possible triggers of relapse, and ensuring that the patient makes internal attributions for change.

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EMPIRICAL EVIDENCE FOR COGNITIVE THERAPY

CT/CBT is one of the most actively researched psychotherapies (35) and has received consistent empirical support for a host of mental health problems and conditions (36, 37). We focus rst on the efcacy of CT for depression,

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as this has been most extensively studied, and also highlight ndings for other psychiatric disorders and medical illnesses.

CT for Unipolar Depression

More than 75 clinical trials and numerous metaanalyses have been published on CT for unipolar depression (35). For an acute episode of depression, the response achieved with CT is similar to that achieved with behavior therapy (38), other bona de psychological treatments (39), and antidepressant medication, and all of these produce results superior to placebo (see 27, 40). Early ndings (41) suggesting that CT was not effective for severe depression (42) have generated considerable controversy among researchers, and the perception that CT is not effective for severe depression has persisted despite compelling data to suggest otherwise (see 11 for review). DeRubeis et al. (43), for example, conducted a mega-analysis in which they pooled the data from four related trials and found that CT was as effective as antidepressants (imipramine and nortripyline) for the treatment of severely depressed individuals. More recent studies have also demonstrated that CT and pharmacotherapy (paroxetine) are equally effective for severe depression (44, 45). The weight of evidence suggests that CT/CBT is efcacious for depression, though it remains possible that the effect may be somewhat overestimated as a result of publication bias (e.g., the le-drawer effect; see 46). In addition to its efcacy for the acute phase of major depressive disorder, CT also carries an advantage, relative to antidepressant medication, for the prevention of relapse. Gloaguen et al. (47), for instance, reported that the average risk of relapse (based on follow-up periods of one to two years) was 25% following CT compared to 60% following antidepressant medication. Some studies also indicate that patients who receive CT alone are no more likely to relapse after treatment than are those who continue to receive medication (45, 48). Hollon et al. (45) found equal outcomes between medication and CT in the acute phase of

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treatment, but a lower relapse rate for CT compared to continuance medication. Consistent with these ndings are studies that have examined potential mechanisms for the prophylactic benets of CT. It appears that CT and antidepressant medication may both change certain aspects of negative thinking (such as information processing, automatic thoughts, and dysfunctional attitudes; e.g., 22, 33) but that CT may further modify some of the deeper cognitive structures (e.g., reduced activation of negative thinking following a negative mood manipulation1 in CT relative to pharmacotherapy) that give rise to relapse and recurrence (23, 33, 34, 49). Several studies have also assessed neuroimaging changes in cognitive therapy (50). Goldapple et al. (51), for example, examined neurobiological responses to CT (in unmedicated depressed outpatients) and compared these ndings to an independent sample of individuals treated with selective serotonin reuptake inhibitors (SSRIs). Differential pre- versus post-treatment changes in brain metabolic activity (measured by positron emission tomography) were obtained in individuals treated with CT compared to those treated with antidepressant medication. These researchers proposed that a top-down (cortical-limbic) therapeutic mechanism may have been active in CT, whereas a bottom-up (limbic-cortical) mechanism may have been active in antidepressant treatment.

CT for Other Psychiatric Disorders

Butler et al. (35) reviewed meta-analyses of treatment outcome for CT/CBT for a number of psychological disorders. A total of 16 methodologically rigorous meta-analyses were identied from 1967 to 2004, which incorporated 9,995 research participants in 332 studies. The review focused on effect sizes found by studies that compared outcomes of CT/CBT

1 A negative mood state is induced by prompting research participants to think of a sad time in their lives, by listening to sad music, etc.

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with outcomes for control groups, providing an overview of the efcacy of CT/CBT. Large effect sizes were obtained for patients with unipolar depression, generalized anxiety disorder, panic disorder, social anxiety, and childhood internalizing problems (the latter included depressive, anxious, and somatic disorders). Moderate effect sizes were found for patients treated for couple distress, anger, childhood somatoform disorders, and chronic pain. Small effect sizes were obtained for recidivism in sexual offenders. CBT also showed promising results as an adjunct to medication for schizophrenia (10). Epp & Dobson (40) recently reviewed the treatment-outcome literature for CT/CBT and summarized the meta-analytic data according to absolute efcacy (the extent to which CBT demonstrates superior outcome to no treatment, waitlist controls, or treatment as usual), efcacy relative to pharmacotherapy, and efcacy compared to other forms of psychotherapy (see Table 2). Considerable empirical support has accumulated for the efcacy of CT/CBT. For some disorders (e.g., some anxiety disorders, bulimia nervosa), the evidence is compelling enough to suggest that CT/CBT should be considered the treatment of choice. The literature also suggests that CT/CBT is at least as effective as medication for a range of problems, although direct comparisons are not found for some disorders (e.g., bipolar disorder, psychosis) for which CT/CBT is used adjunctively (25). A recent meta-analysis of CT/CBT in the treatment of schizophrenia, severe depression, and bipolar disorder was less positive (52), suggesting that CT/CBT is no more effective than nonspecic interventions for the treatment of schizophrenia, although methodological aws in the meta-analysis tend to vitiate the ndings (53).

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physical illnesses including chronic pain, back pain, sleep disorders, fatigue and functional impairments related to cancer, health-related anxiety, rheumatoid arthritis, chronic fatigue syndrome, bromyalgia, irritable bowel syndrome, hypertension, tinnitus, headaches, sexual dysfunctions, and various neurological conditions (54, 55). CT/CBT has demonstrated efcacy for a number of psychological outcome variables (e.g., distress, attitudes, adherence to treatment regime, improved coping with pain) as well as physiological indices that are impacted by stress (e.g., lowered blood pressure, improved immune response; see Reference 54 for review). For some illnesses, there have been a sufcient number of studies to warrant systematic reviews and meta-analyses. This literature demonstrates various biopsychosocial benets of CT/CBT for back pain (56, 57), hypochrondriasis (58), irritable bowel syndrome (59), chronic fatigue (58, 60), bromyalgia (61), headache (62), insomnia (63, 64), adjustment to cancer (65, 66), and the management of diabetes (67).

SUMMARY AND FUTURE DIRECTIONS

Considerable empirical evidence has accumulated that supports the theory and practice of CT, and this model has been expanded over time to incorporate evidence from experimental cognitive science and the neurosciences (13, 16, 68). Moreover, several ofcial reports in the United Kingdom and the United States have recommended the use of CT/CBT for a number of common psychiatric conditions (4). Notwithstanding these treatment recommendations and the wealth of research underlying CT, it is not a panacea for all mental health problems (e.g., 69). For example, more purely behavioral interventions sometimes perform as well as CT/CBT for depression and anxiety in psychotherapy outcome trials. It is important to point out, however, that the use of behavioral interventions has always been part and parcel of CT proper (15). In addition, the theory states that whatever treatment is used so

CT for Medical Illnesses

CT/CBT is also effective for the treatment of anxiety and depression that are comorbid with medical problems (54). In addition, a number of randomized controlled trials have reported benets of CT/CBT for a wide range of
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Table 2

Summary of efcacy ndings by disorder or problem (40; reprinted with permission) Absolute Efcacy relative to medications + = + + Efcacy relative to other psychotherapies

Disorder Unipolar depression Bipolar disorder Specic phobia Social phobia Obsessive-compulsive disorder CBT CBT

Treatment

efcacy + + ++ ++ +

Exposure and cognitive restructuring Exposure and cognitive restructuring Exposure and response prevention and cognitive restructuring Exposure and cognitive restructuring Exposure and cognitive techniques CBT CBT CBT CBT CBT CBT CBT CBT CBT CBT CBT CBT CBT

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Panic disorder Chronic post-traumatic stress disorder Generalized anxiety disorder Bulimia nervosa Binge eating disorder Anorexia nervosa Schizophrenia Marital distress Anger & violent offending Sexual offending Chronic pain Borderline personality disorder Substance-use disorders Somatoform disorders Sleep difculties

++ + + + + + + + + + + + + + + + + + + +

+ = + + = = +

= + +

Symbols: A blank space indicates insufcient or no evidence; , negative evidence; +, positive evidence; = , approximate equivalence; ++, treatment of choice; equivocal evidence; CBT, efcacy of specic components unknown; , CBT is typically used as an adjunct to medication in these disorders; , efcacy relative to physical treatments (i.e., surgical castration and hormonal treatments).

that the patient improves (or if improvement occurs via spontaneous remission), the negative beliefs must also normalize. Indeed, Harmer et al. (22) recently found that the administration of antidepressant medication modulated emotional processing in depressed individuals prior to shifts in their mood state or symptoms. Such ndings support the primacy of cognition in therapeutic change and are consistent with the idea that there are myriad ways in which to modify cognition. In addition to altering information processing, however, we contend that

CT also produces shifts in deeper levels of cognition (23, 33) and that targeting this depth of change may account for reduced relapse rates in CT relative to medication. There are a number of important future directions for the eld. During the past couple of decades, we have witnessed a tremendous increase in multiwave2 longitudinal studies that

2 Multiple points of assessment, not just pre- and postintervention.

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have supported the diathesis-stress model of cognitive vulnerability (18). Researchers are also better understanding gene-environment interactions in the context of psychopathology. For example, a replicable relationship has been found between negative cognitive processing and the short version of the serotonin transporter gene (68). Additional empirical work is necessary to further elucidate how genetic, neurophysiological, environmental, and cognitive factors contribute to psychopathology and to understand the intricate relationships among cognitive, affective, motivational, and behavioral systems. Future research will no doubt also

clarify the important mechanisms of change in CT. Some studies have, indeed, suggested that cognitive change is an important mediator of symptom change (11, 19, 33), but additional research is needed to ensure that these ndings are robust and, if they are, to determine which strategies (and psychotherapeutic doses) produce the most stable cognitive change. Enormous strides have been made in understanding, evaluating, and rening CT over the past four and a half decades. We believe that similar future progress will be made in improving our knowledge base of cognitive vulnerability and optimizing the delivery of CT.

SUMMARY POINTS 1. CT/CBT is the fastest growing and most researched contemporary system of psychotherapy. 2. The empirical literature has provided considerable support for Becks cognitive theory and therapy. 3. Three main propositions in CT are the access hypothesis (it is possible for individuals to become aware of the content and processing of their thinking), the mediation hypothesis (the way in which individuals think about themselves and their circumstances impacts subsequent emotional and behavioral responses), and the change hypothesis (by modifying cognitive and behavioral responses, an individual can become more functional and adaptive). 4. The main techniques used in CT focus on establishment of the therapeutic relationship, behavioral change strategies, cognitive restructuring, the modication of core beliefs and schemas, and the prevention of relapse and recurrence. 5. A key advantage of CT is that it effectively treats the acute episode of psychiatric disorders (with or without medication) and provides a prophylaxis against relapse.

DISCLOSURE STATEMENT
Aaron T. Beck is President Emeritus of the Beck Institute for Cognitive Therapy, a nonprot organization. He has no nancial interest in this organization.

LITERATURE CITED
1. Beck AT. 1963. Thinking and depression 0.1. Idiosyncratic content and cognitive distortions. Arch. Gen. Psychiatry 9:32433 2. Beck AT. 1964. Thinking and depression. 2. Theory and therapy. Arch. Gen. Psychiatry 10:56171 3. Beck AT. 1976. Cognitive Therapy and the Emotional Disorders. New York: Int. Univ. Press. 346 pp. 4. Beck AT. 2005. The current state of cognitive therapy: a 40-year retrospective. Arch. Gen. Psychiatry 62:95359
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5. Beck AT, Resnik HLP, Lettieri DJ, eds. 1974. The Prevention of Suicide. Bowie, MD: Charles Press 6. Beck AT, Emery G, Greenberg RL. 1985. Anxiety Disorders and Phobias: A Cognitive Perspective. New York: Basic Books 7. Beck AT, Freeman A, Davis D, et al. 1990. Cognitive Therapy of Personality Disorders. New York: Guilford 8. Beck AT, Wright FD, Newman CF, et al. 1993. Cognitive Therapy of Substance Abuse. New York: Guilford 9. Beck AT, Rector NA. 2005. Cognitive approaches to schizophrenia: theory and therapy. Annu. Rev. Clin. Psychol. 1:577606 10. Beck AT, Rector NA, Stolar N, et al. 2009. Schizophrenia: Cognitive Theory, Research, and Therapy. New York: Guilford 11. DeRubeis RJ, Webb CA, Tang TZ, et al. 2010. Cognitive therapy. In Handbook of Cognitive-Behavioral Therapies, ed. KS Dobson, pp. 277316. New York: Guilford 12. Prochaska JO, Norcross JC. 2010. Systems of Psychotherapy: A Transtheoretical Analysis. Belmont: Brooks/Cole 13. Beck AT. 1996. Beyond belief: a theory of modes, personality, and psychopathology. In Frontiers of Cognitive Therapy, ed. PM Salkovskis, pp. 125. New York: Guilford 14. Beck AT, Weishaar ME. 2011. Cognitive therapy. In Current Psychotherapies, ed. RJ Corsini, D Wedding, pp. 276309. Belmont: Brooks/Cole 15. Beck AT, Rush AJ, Shaw BF, et al. 1979. Cognitive Therapy of Depression. New York: Guilford 16. Clark DA, Beck AT, Alford BA. 1999. Scientic Foundations of Cognitive Theory and Therapy of Depression. New York: Wiley 17. Alford BA, Beck AT. 1997. The Integrative Power of Cognitive Therapy. New York: Guilford 18. Dozois DJA, Beck AT. 2008. Cognitive schemas, beliefs and assumptions. In Risk Factors in Depression, ed. KS Dobson, DJA Dozois, pp. 12143. Oxford, UK: Elsevier/Academic 19. Garratt G, Ingram RE, Rand KL, et al. 2007. Cognitive processes in cognitive therapy: evaluation of the mechanisms of change in the treatment of depression. Clin. Psychol. Sci. Pract. 14:22439 20. Dozois DJA, Dobson KS. 2001. Information processing and cognitive organization in unipolar depression: specicity and comorbidity issues. J. Abnorm. Psychol. 110:23646 21. Mathews A, MacLeod C. 2005. Cognitive vulnerability to emotional disorders. Annu. Rev. Clin. Psychol. 1:16795 22. Harmer CJ, OSullivan U, Massey-Chase R, et al. 2009. Effect of acute antidepressant administration on negative affective bias in depressed patients. Am. J. Psychiatry 116:117884 23. Segal ZV, Gemar M, Williams S. 1999. Differential cognitive response to a mood challenge following successful cognitive therapy or pharmacotherapy for unipolar depression. J. Abnorm. Psychol. 108:310 24. Alloy LB, Abramson LY, Whitehouse WG, et al. 2006. Prospective incidence of rst onsets and recurrences of depression in individuals at high and low cognitive risk for depression. J. Abnorm. Psychol. 115:14556 25. Dobson D, Dobson KS. 2009. Evidence-based Practice of Cognitive Behavioral Therapy. New York: Guilford 26. Dobson KS, Dozois DJA. 2010. Historical and philsophical bases of the cognitive-behavioral therapies. In Handbook of Cognitive-Behavioral Therapies, ed. KS Dobson, pp. 338. New York: Guilford 27. Hollon SD, Dimidjian S. 2009. Cognitive and behavioral treatment of depression. In Handbook of Depression, ed. IH Gotlib, CL Hammen, pp. 586603. New York: Guilford 28. Padesky CA, Beck AT. 2003. Science and philosophy: comparison of cognitive therapy and rational emotive behavior therapy. J. Cogn. Psychother. 17:21124 29. Kazantzis N, Whittington C, Dattilio F. 2010. Meta-analysis of homework effects in cognitive and behavioral therapy: a replication and extension. Clin. Psychol. Sci. Pract. 17:14456 30. Beck JS. 1995. Cognitive Therapy: Basics and Beyond. New York: Guilford 31. Dozois DJA, Bieling PJ. 2010. Cognitive behavioral treatment of depression. In Cognitive Behavioral Therapy, Acceptance, Mindfulness: Understanding and Applying the New Therapies, ed. JD Herbert, EM Forman. New York: Wiley. In press 32. Greenberger D, Padesky CA. 1995. Mind over Mood: Change How You Feel by Changing the Way You Think. New York: Guilford 33. Dozois DJA, Bieling PJ, Patelis-Siotis I, et al. 2009. Changes in self-schema structure in cognitive therapy for major depressive disorder: a randomized clinical trial. J. Consult. Clin. Psychol. 77:107888
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58. Looper KJ, Kirmayer LJ. 2002. Behavioral medicine approaches to somatoform disorders. J. Consult. Clin. Psychol. 70:81027 59. Blanchard EB, Scharff L. 2002. Psychosocial aspects of assessment and treatment of irritable bowel syndrome in adults and recurrent abdominal pain in children. J. Consult. Clin. Psychol. 70:72538 60. Malouff JA, Thorsteinsson EB, Rooke SE, et al. 2008. Efcacy of cognitive behavioral therapy for chronic fatigue syndrome: a meta-analysis. Clin. Psychol. Rev. 28:73645 61. H auser W, Thieme K, Turk DC. 2010. Guidelines on the management of bromyalgia syndromea systematic review. Eur. J. Pain 14:510 62. Holroyd KA. 2002. Assessment and psychological management of recurrent headache disorders. J. Consult. Clin. Psych. 70:65677 63. Wang MY, Wang SY, Tsai PS. 2005. Cognitive behavioural therapy for primary insomnia: a systematic review. J. Adv. Nurs. 50:55364 64. de Niet GJ, Tiemens BG, Kloos MW, et al. 2009. Review of systematic reviews about the efcacy of nonpharmacological interventions to improve sleep quality in insomnia. Int. J. Evidence-Based Health 7:23342 65. Osborn RL, Demoncada AC, Feuerstein M. 2006. Psychosocial interventions for depression, anxiety, and quality of life in cancer survivors: meta-analyses. Int. J. Psychiatry Med. 36:1334 66. Hersch J, Juraskova I, Price M, et al. 2009. Psychosocial interventions and quality of life in gynaecological cancer patients: a systematic review. Psychooncology 18:795810 67. Fisher EB, Thorpe CT, Devellis BM, et al. 2007. Healthy coping, negative emotions, and diabetes management: a systematic review and appraisal. Diabetes Educ. 33:1080103; discussion 1046 68. Beck AT. 2008. The evolution of the cognitive model of depression and its neurobiological correlates. Am. J. Psychiatry 165:96977 69. Longmore RJ, Worrell M. 2007. Do we need to challenge thoughts in cognitive behavior therapy? Clin. Psychol. Rev. 27:17387

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Contents
Role of Postmarketing Surveillance in Contemporary Medicine Janet Woodcock, Rachel E. Behrman, and Gerald J. Dal Pan p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 1 Genome-Wide Association Studies: Results from the First Few Years and Potential Implications for Clinical Medicine Joel N. Hirschhorn and Zoa K.Z. Gajdos p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 11 Imaging of Atherosclerosis D.R.J. Owen, A.C. Lindsay, R.P. Choudhury, and Z.A. Fayad p p p p p p p p p p p p p p p p p p p p p p p p p p p 25 Novel Oral Factor Xa and Thrombin Inhibitors in the Management of Thromboembolism Bengt I. Eriksson, Daniel J. Quinlan, and John W. Eikelboom p p p p p p p p p p p p p p p p p p p p p p p p p p p 41 The Fabry Cardiomyopathy: Models for the Cardiologist Frank Weidemann, Markus Niemann, David G. Warnock, Georg Ertl, and Christoph Wanner p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 59 Kawasaki Disease: Novel Insights into Etiology and Genetic Susceptibility Anne H. Rowley p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 69 State of the Art in Therapeutic Hypothermia Joshua W. Lampe and Lance B. Becker p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 79 Therapeutic Potential of Lung Epithelial Progenitor Cells Derived from Embryonic and Induced Pluripotent Stem Cells Rick A. Wetsel, Dachun Wang, and Daniel G. Calame p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 95 Therapeutics Development for Cystic Fibrosis: A Successful Model for a Multisystem Genetic Disease Melissa A. Ashlock and Eric R. Olson p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 107 Early Events in Sexual Transmission of HIV and SIV and Opportunities for Interventions Ashley T. Haase p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 127 HIV Infection, Inammation, Immunosenescence, and Aging Steven G. Deeks p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 141

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The Increasing Burden of HIV-Associated Malignancies in Resource-Limited Regions Corey Casper p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 157 Biliary Atresia: Will Blocking Inammation Tame the Disease? Kazuhiko Bessho and Jorge A. Bezerra p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 171 Advances in Palliative Medicine and End-of-Life Care Janet L. Abrahm p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 187 Clostridium difcile and Methicillin-Resistant Staphylococcus aureus: Emerging Concepts in Vaccine Development David C. Kaslow and John W. Shiver p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 201
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Antiestrogens and Their Therapeutic Applications in Breast Cancer and Other Diseases Simak Ali, Laki Buluwela, and R. Charles Coombes p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 217 Mechanisms of Endocrine Resistance in Breast Cancer C. Kent Osborne and Rachel Schiff p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 233 Multiple Myeloma Jacob Laubach, Paul Richardson, and Kenneth Anderson p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 249 Muscle Wasting in Cancer Cachexia: Clinical Implications, Diagnosis, and Emerging Treatment Strategies Shontelle Dodson, Vickie E. Baracos, Aminah Jatoi, William J. Evans, David Cella, James T. Dalton, and Mitchell S. Steiner p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 265 Pharmacogenetics of Endocrine Therapy for Breast Cancer Michaela J. Higgins and Vered Stearns p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 281 Therapeutic Approaches for Women Predisposed to Breast Cancer Katherine L. Nathanson and Susan M. Domchek p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 295 New Approaches to the Treatment of Osteoporosis Barbara C. Silva and John P. Bilezikian p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 307 Regulation of Bone Mass by Serotonin: Molecular Biology and Therapeutic Implications Gerard Karsenty and Vijay K. Yadav p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 323 Alpha-1-Antitrypsin Deciency: Importance of Proteasomal and Autophagic Degradative Pathways in Disposal of Liver DiseaseAssociated Protein Aggregates David H. Perlmutter p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 333 Hepcidin and Disorders of Iron Metabolism Tomas Ganz and Elizabeta Nemeth p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 347

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Interactions Between Gut Microbiota and Host Metabolism Predisposing to Obesity and Diabetes Giovanni Musso, Roberto Gambino, and Maurizio Cassader p p p p p p p p p p p p p p p p p p p p p p p p p p p p 361 The Brain-Gut Axis in Abdominal Pain Syndromes Emeran A. Mayer and Kirsten Tillisch p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 381 Cognitive Therapy: Current Status and Future Directions Aaron T. Beck and David J.A. Dozois p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 397 Toward Fullling the Promise of Molecular Medicine in Fragile X Syndrome Dilja D. Krueger and Mark F. Bear p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 411
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Stress- and Allostasis-Induced Brain Plasticity Bruce S. McEwen and Peter J. Gianaros p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 431 Update on Sleep and Its Disorders Allan I. Pack and Grace W. Pien p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 447 A Brain-Based Endophenotype for Major Depressive Disorder Bradley S. Peterson and Myrna M. Weissman p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 461 Indexes Cumulative Index of Contributing Authors, Volumes 5862 p p p p p p p p p p p p p p p p p p p p p p p p p p p 475 Cumulative Index of Chapter Titles, Volumes 5862 p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 479 Errata An online log of corrections to Annual Review of Medicine articles may be found at http://med.annualreviews.org/errata.shtml

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