An evolved module for fear elicitation and fear learning with 4 characteristics is proposed. (a) The fear module is preferentially activated in aversive contexts by stimuli that are fear relevant in an evolutionary perspective. (b) Its activation to such stimuli is automatic. (c) It is relatively impenetrable to cognitive control. (d) It originates in a dedicated neural circuitry, centered on the amygdala. Evidence supporting these propositions is reviewed from conditioning studies, both in humans and in monkeys; illusory correlation studies; studies using unreportable stimuli; and studies from animal neuroscience. The fear module is assumed to mediate an emotional level of fear learning that is relatively independent and dissociable from cognitive learning of stimulus relationships.

Research on relationships between anxiety and depression has proceeded at a rapid pace since the 1980s. The similarities and differences between these two conditions, as well as many of the important features of the comorbidity of these disorders, are well understood. The genotypic structure of anxiety and depression is also fairly well documented. Generalized anxiety and major depression share a common genetic diathesis, but the anxiety disorders themselves are genetically hetergeneous. Sophisticated phenotypic models have also emerged, with data converging on an integrative hierarchical model of mood and anxiety disorders in which each individual syndrome contains both a common and a unique component. Finally, considerable progress has been made in understanding cognitive aspects of these disorders. This work has focused on both the cognitive content of anxiety and depression and on the effects that anxiety and depression have on information processing for mood-congruent material.

Trait concepts are used extensively in psychopathology research, but much of this research has failed to consider recent advances in the dimensional structure of personality. Many investigators have discounted the importance of this structural research, arguing that (a) little progress has been made in this area, (b) structural models have little direct relevance for psychopathology research, and (c) the principal methodological tool of structural research--factor analysis--is too subjective to yield psychologically meaningful results. We dispute each of these objections. Specifically, we offer an integrative hierarchical model--composed of four higher order traits--that is congruent with each of the major structural subtraditions within personality. We also discuss the implications of this integrative scheme for basic trait research, for the conceptualization and assessment of psychopathology, and for the etiology of disorder.

Several theories of the development of panic disorder (PD) with or without agoraphobia have emerged in the last 2 decades. Early theories that proposed a role for classical conditioning were criticized on several grounds. However, each criticism can be met and rejected when one considers current perspectives on conditioning and associative learning. The authors propose that PD develops because exposure to panic attacks causes the conditioning of anxiety (and sometimes panic) to exteroceptive and interoceptive cues. This process is reflected in a variety of cognitive and behavioral phenomena but fundamentally involves emotional learning that is best accounted for by conditioning principles. Anxiety, an anticipatory emotional state that functions to prepare the individual for the next panic, is different from panic, an emotional state designed to deal with a traumatic event that is already in progress. However, the presence of conditioned anxiety potentiates the next panic, which begins the individual's spiral into PD. Several biological and psychological factors create vulnerabilities by influencing the individual's susceptibility to conditioning. The relationship between the present view and other views, particularly those that emphasize the role of catastrophic misinterpretation of somatic sensations, is discussed.

The authors describe how contemporary learning theory and research provide the basis for perspectives on the etiology and maintenance of anxiety disorders that capture the complexity associated with individual differences in the development and course of these disorders. These insights from modern research on learning overcome the shortcomings of earlier overly simplistic behavioral approaches, which sometimes have been justifiably criticized. The authors show how considerations of early learning histories and temperamental vulnerabilities affect the short- and long-term outcomes of experiences with stressful events. They also demonstrate how contextual variables during and following stressful learning events affect the course of anxiety disorder symptoms once they develop. This range of variables can lead to a rich and nuanced understanding of the etiology and course of anxiety disorders.

For years theorists have hypothesized on the basis of meagre evidence that observational conditioning is involved in the origins of many human and nonhuman primates* fears and phobias The present experiments provide strong support for this hypothesis by demonstrating observational conditioning of snake fear in rhesus monkeys Experiment l demonstrated the usefulness of a new index of snake fear in rhesus monkeys and, using this new measure, also demonstrated that young monkeys raised by parents who have a fear of snakes do not acquire this fear in the absence of any specific experience with snakes In Experiment 2, however, five out of six adolescent/young-adult rhesus monkeys did acquire an intense and persistent fear of snakes as a result of observing their wild-reared parents behave fearfully in the presence of real, toy, and model snakes for a short period of time. The fear was not context specific and showed no significant signs of diminution at 3-month follow-up Implications of the present results for current theories of the origins of human fears and phobias are discussed.

Overgeneral autobiographical memory (OGM) is a robust phenomenon in depression, but the extent to which OGM predicts the course of depression is not well-established. This meta-analysis synthesized data from 15 studies to examine the degree to which OGM 1) correlates with depressive symptoms at follow-up, and 2) predicts depressive symptoms at follow-up over and above initial depressive symptoms. Although the effects are small, specific and categoric/overgeneral memories generated during the Autobiographical Memory Test significantly predicted the course of depression. Fewer specific memories and more categoric/overgeneral memories were associated with higher follow-up depressive symptoms, and predicted higher follow-up symptoms over and above initial symptoms. Potential moderators were also examined. The age and clinical depression status of participants, as well as the length of follow-up between the two depressive symptom assessments, significantly moderated the predictive relationship between OGM and the course of depression. The predictive relationship between specific memories and follow-up depressive symptoms became greater with increasing age and a shorter length of follow-up, and the predictive relationship was stronger for participants with clinical depression diagnoses than for nonclinical participants. These findings highlight OGM as a predictor of the course of depression, and future studies should investigate the mechanisms underlying this relationship. KeywordsAutobiographical memory specificity; Overgeneral autobiographical memory; Course of depression; Meta-analysis Overgeneral Autobiographical Memory as a Predictor of the Course of Depression: A Meta-AnalysisOver the past 20 years, a large body of research has accumulated on the overgeneral autobiographical memory (OGM) phenomenon in depression. First described by Williams and Broadbent (1986) in their study of suicidal patients, OGM refers to the finding that, when asked to come up with a specific memory in response to a cue word, some individuals are less specific Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptBehav Res Ther. Author manuscript; available in PMC 2011 July 1. Published in final edited form as:Behav Res Ther. 2010 July ; 48(7): 614-625. doi:10.1016/j.brat.2010.03.013. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscriptand/or more overgeneral in their memory retrieval than others. In particular, much research has shown that individuals with depression are characterized by higher levels of OGM than nondepressed controls . Mor...

Levels of the stress-sensitive hormone cortisol increase dramatically in the first 30-40 minutes after waking, an effect known as the cortisol awakening response (CAR). There is considerable crosssectional evidence that psychosocial stress is associated with an increased CAR, and the CAR has been found to be altered in the presence of stress-related diseases, including Major Depressive Disorder (MDD). To date, no prospective longitudinal studies have examined whether individual differences in the CAR serve as a premorbid risk factor for MDD. In a sample of 230 late adolescents, clinical diagnoses of MDD were predicted from the CAR as well as other indicators of basal cortisol functioning gathered one year earlier, including: waking cortisol levels, bedtime cortisol levels, the size of the CAR, average cortisol, and the slope of the diurnal cortisol rhythm across the waking day. Age and gender, health and health behaviors, baseline neuroticism, exposure to stressful life events and past episodes of mood and anxiety disorders were included as covariates, to help ensure effects are attributable to the CAR rather than related variables. A higher baseline CAR was associated with a significantly increased risk of developing MDD by follow-up, even when excluding individuals with baseline MDD. No other baseline cortisol measures were significant prospective predictors of MDD. In summary, the CAR is a significant prospective risk factor for the development of MDD in young adults, providing some support for the possibility that a heightened CAR may play a role in the etiology of Major Depressive Disorder.