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Depression: Causes and Treatment, by Aaron T. Beck M.D., Ph.D., Brad A. Alford
Download Ebook Depression: Causes and Treatment, by Aaron T. Beck M.D., Ph.D., Brad A. Alford
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More than forty years ago, Dr. Aaron T. Beck's pioneering Depression: Causes and Treatment presented the first comprehensive account of all aspects of depression and introduced cognitive therapy to health care providers and patients struggling with one of the most common and devastating diseases of the modern age. Since that classic text first appeared, the appreciation of the multifaceted nature of mood disorders has grown, and the phenomenological and biological aspects of psychology are increasingly seen as intertwined. Taking these developments into account, Beck and his colleague Brad A. Alford have written a second edition of Depression that will help patients and caregivers understand depression as a cognitive disorder.
The new edition of Depression builds on the original research and approach of the seminal first edition, including the tests of Freud's theory that led to a new system of psychological theory and therapy, one that addresses the negative schema and automatic thoughts that can trap people in painful emotional states. Beck and Alford examine selected scientific tests and randomized controlled trials that have enhanced the cognitive approach since the time it was first introduced.
Incorporating accepted changes in the definitions and categories of the various mood disorders into its discussion, Depression addresses the treatment role of revolutionary drugs, such as the selective serotonin reuptake inhibitors (SSRIs), electroconvulsive therapy (ECT), and transcranial magnetic stimulation (TMS) in relation to cognitive approaches. Beck and Alford explore research on neurotrophic and neurogenesis theories of depression. They also report on advances in psychosocial treatment of depression, including the value of cognitive therapy in the prevention of relapse.
- Sales Rank: #190264 in eBooks
- Published on: 2014-04-04
- Released on: 2014-04-04
- Format: Kindle eBook
Review
"The first edition of Beck's Depression: Causes and Treatments was published over 40 years ago with the goal of addressing firmly established aspects of the nature, causes, and treatment of depression. . . . The second edition has much the same goal as the first: it provides updates on previously reviewed topics; introduces aspects of the study of depression that have become relevant more recently; and provides an historical perspective on depression research. The book is well organized and well written, and manages to be both informative and satisfying for the reader."—Psychological Medicine
"The second edition of Depression: Causes and Treatment should appeal to clinicians interested in the symptom presentation of affective disorders, the cognitive model, and various treatment considerations as well as to researchers interested in the biological underpinnings of depression as well as research contributions and limitations. . . . The second edition will assume the position of the first edition as one of the most authoritative texts on the topic."—PsycCRITIQUES
About the Author
Winner of the Albert Lasker Award in Medical Science (known as "America's Nobel") and the Grawemeyer Award for Psychology, and recognized as the father of cognitive therapy, Aaron T. Beck, M.D., is University Professor Emeritus of Psychiatry at the University of Pennsylvania and President of the Beck Institute for Cognitive Therapy and Research. Brad A. Alford, Ph.D., is Professor of Psychology at the University of Scranton and coauthor with Aaron T. Beck of The Integrative Power of Cognitive Therapy and Scientific Foundations of Cognitive Theory and Therapy of Depression.
Excerpt. � Reprinted by permission. All rights reserved.
Preface to the Second Edition
The first edition of this book posed the question, "What has definitely been established regarding the nature, the causes, and the treatment of depression?" To answer it, Aaron Beck sifted through literally thousands of clinical and controlled studies and summarized representative research on the clinical, biological, psychological, and theoretical aspects of depression. Of greater significance, he described an original research program that, in retrospect, represented a breakthrough in understanding the cognitive components and treatment of depression.
Like the first edition, this one presents an update and overview of what is currently known about clinical depression, including developments that have taken place since the book was originally published 40 years ago and, also like that earlier volume, offers a historical perspective. Moreover, in Chapter 16 we review the randomized controlled trials that have built upon and elaborated cognitive theory and research.
What is new to the second edition? Definitions of the mood disorders have changed over the years, and new categories have been added. We now recognize major depression as the leading cause of disability worldwide, and it has received increased clinical and research attention. In the years since the book was first published additional types of bipolar disorder have been recognized, and research has been conducted on the relation between manic symptoms and life events. New drugs, such as the selective serotonin reuptake inhibitors, or SSRIs, have been developed. While comparable in efficacy (except in severe depression), they are chemically unrelated to tricyclic, heterocyclic, and other antidepressants discussed in the first edition, and they enjoy several advantages over those "first-generation" drugs. The newer medications can induce fewer adverse side-effects, provide greater safety in case of overdose, and promise improved tolerability and patient compliance. SSRIs may also be augmented with lithium, psychostimulants, and other agents.
There are even now many unresolved problems in pharmacotherapy. Drug treatment of depression - even using the newer SSRIs - still results in unwanted side effects, such as the sexual dysfunction that affects 60% of patients. There are potential lethal interactions between SSRI and MAOI drugs. Other unintended effects include gastrointestinal disturbance, nausea, and somnolence. Electroconvulsive therapy (ECT) causes side effects as well and alternatives are under review, including transcranial magnetic stimulation (TMS). We describe the results and conclusions of preliminary studies on this new treatment.
Since this book first appeared, we have made considerable progress in understanding the biological basis of depression. Steps have been taken in identifying the genetic basis of the mood disorders, including schizoaffective disorder. Research on changes in hippocampal neurons and amygdala enlargement appears promising. "Neurotrophic" (keeping cells alive) and "neurogenesis" (stimulating growth of new cells) theories abound and are being tested.
Many of the biological aspects of depression still remain uncertain, though progress continues. One research area explores specific brain changes that correspond to the effective pharmacological and psychological treatments of depression. For example, studies have focused on differential effects in recovery for paroxetine (Paxil) therapy and cognitive therapy in modulating specific sites in limbic and cortical brain regions.
Researchers have continued to identify the pathophysiological aspects of major depressive disorder, including alterations in various monoamine brain systems. Neuropeptides such as corticotropin-releasing hormone are under investigation, as are hormonal variables such as glucocorticoid secretion. Dexamethasone nonsuppression of plasma cortisol has been suggested as a marker, although the same effects have been induced experimentally by sleep deprivation and dietary fasting.
Several studies have tested whether genetic markers can predict differential drug response, thus leading to the possibility of individualized pharmacologic treatment of depression. Response to paroxetine in relation to the serotonin transporter gene polymorphism (5-HTTLPR) have found reductions in depression ratings to be more rapid for certain genotypes than for others, despite equivalent paroxetine concentrations. Future studies in pharmacogenomics will continue to identify genetic markers in the hope of better predicting individual drug response, and the reasons for such response. The end result will be the possibility of individualized pharmacologic treatment of depression.
Clinical and psychosocial approaches to depression have made major strides. We now know a great deal more about cognitive vulnerability, the interaction of genetic predisposition with childhood and adult stress, and relapse than we did a generation ago. Most aspects of the cognitive theory of depression and suicide have been confirmed empirically, including negatively biased cognitions about the self, the importance of hopelessness as a predictor, content specificity of themes, and mood-congruent recall. Cognitive priming studies and studies utilizing longitudinal designs now support the theory of cognitive vulnerability in adults, and evidence is emerging for children as well.
Around the world, exciting research programs on clinical depression are underway. Cognitive therapies that target neurobiological mechanisms are being tested as adjuncts to conventional treatment. There is growing appreciation for the biopsychosocial nature of the mood disorders, and an increased sophistication concerning the action of psychological and somatic therapies across multiple dimensions. The dichotomy between the phenomenological and the "biological" are increasingly understood to be, in reality, two sides of the same coin. For example, we review one report that found changes in thyroid hormone levels in response to cognitive therapy of major depression, consistent with the effect on the thyroid axis found in various somatic antidepressant treatments. Future studies are needed to test the effects of the cognitive and the somatic therapies on neurogenesis, particularly in the granular cell level of the dentate gyrus (DG), the part of the hippocampus thought to be critical in laying down new cognitions.
As outlined above, depression research is vibrant and ever-changing. However, in addition to covering what is new, this Second Edition retains almost completely the original research and ideas of the First Edition (Beck, 1967). The basic theory of cognitive therapy was spelled out at that time. Part I CLINICAL ASPECTS OF DEPRESSION keeps the naturalistic research on the cognitive aspects of depression (Chapter 2: Symptomatology of Depression). This work led to the cognitive content formulation which links the cognitive system to the affective, motivational, and physical phenomena of depression (Chapter 12: Cognition and Psychopathology). Part II EXPERIMENTAL ASPECTS OF DEPRESSION includes the original tests of Freud's theory that led to an "anomalous finding" (Beck, 2006), one that eventually generated a new system of treatment, cognitive therapy. This research is preserved also, as part of Chapter 10, including the dream study and the "Masochism" Inventory (see Appendix A).
Part III THEORETCIAL ASPECTS OF DEPRESSION contains from the First Edition the original idea of the negative cognitive triad in depression, and the theory of mania and other disorders, including anxiety, phobia, somatization, paranoia, obsessive compulsive disorders, and psychosis. Likewise, Chapter 13, Development of Depression, articulates the various causes of depression, and has generated hundreds of studies. For these chapters, new sections add genetic findings, empirical support of the theory, and integrative theory that now underpins the general cognitive system of therapy. Thus, much of the first edition has been retained in the second, but the earlier work has been augmented and updated by the latest findings.
Part IV TREATMENT OF DEPRESSION summarizes advances in somaticpsychological therapies. We review findings of randomized controlled trials, with special focus on comparisons between psychotherapy and antidepressant medication are of special interest. Reviews of meta-analyses and conventional narrative reviews show certain psychological treatments and pharmacological therapy to be equally viable as clinical approaches to the mood disorders, with limited evidence suggesting the utilization of a combined approach. In addition, data now show the clear relapse prevention effect of cognitive therapy compared to medications. This includes group cognitive therapy for relapse of major depression, as well as for prevention of suicide reattempts in adults. Moreover, therapist experience with cognitive therapy is generally associated with better results.
Our comprehensive review of well-designed studies reveals that depressed patients treated with psychological interventions had a relapse rate of only 30%, compared to a relapse rate of 69% for those patients treated with pharmacotherapy alone. We review studies that now support the routine use of maintenance treatment for depression. One major study calculated that half of all depression during the five years following a major depressive episode can be averted by using maintenance treatment, either cognitive behavior therapy or antidepressants.
In summary, where significant advances have occurred, we have incorporated them in this revision of Aaron Beck's classic text. In cases where terminology is new, as in the case of the classification of disorders, current terms replace earlier ones or are included alongside them. In the new edition, thus, we attempt to preserve the timeless material of the first edition and to distill all the timely advances that have occurred since then.
Most helpful customer reviews
5 of 5 people found the following review helpful.
Great book
By Victor Slate
The book is very comprehensive. A lot of information packed into this book.
It isn't light reading, you have to understand medical jargon a little.
2 of 2 people found the following review helpful.
Four Stars
By Maira
Good review of the CBT approach for depression
0 of 0 people found the following review helpful.
Five Stars
By Paul Yeatts
Beck's description of his cognitive theory of depression is easy to digest.
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