Several psychosocial treatments appear to be effective in treating posttraumatic stress disorder (PTSD). However, little is known about the predictors of treatment outcome. It is possible that some variables predict poor outcome for some treatments but not for other treatments. To investigate this issue, outcome predictors were investigated for three eight-session treatments: exposure therapy (entailing prolonged imaginal and in vivo exposure), relaxation training, and eye movement desensitization and reprocessing (EMDR). Sixty people with PTSD entered and 45 completed treatment. Treatments did not differ in attrition or perceived credibility. Exposure tended to be most effective, and EMDR and relaxation did not differ in efficacy. A number of clinical and cognitive variables were examined to identify predictors of treatment dropout as well as predictors of the likelihood that patients would be remitted from PTSD after treatment. These analyses were conducted by controlling for treatment condition. Low patient ratings of treatment credibility (assessed in session 2) predicted treatment dropout, regardless of treatment type. Severe reexperiencing symptoms (assessed prior to treatment) predicted poor outcome for relaxation training but not for the other therapies. These findings suggest that treatment outcome could be improved by improving treatment credibility. The findings also support the use of exposure therapy and, to a lesser extent, the use of EMDR in treating PTSD.

Empirically supported psychosocial treatments for posttraumatic stress disorder (PTSD) all entail some form of trauma-related exposure therapy. Although these treatments are often useful, none are effective for all patients. Even those who respond are often left with residual symptoms. A better understanding of the causes of PTSD may lead to more effective treatments. The present article reviews the nascent but steadily growing research on the role of anxiety sensitivity (fear of arousal-related sensations) in PTSD. Available research suggests that anxiety sensitivity may play an important role and that treatments that directly target anxiety sensitivity (such as interoceptive exposure) may improve outcome, particularly if these treatments are implemented before commencing trauma-related exposure therapy.

Hypochondriasis was once considered treatment resistant. Recent studies, however, suggest that several interventions can be effective. This article presents a narrative review of psychosocial and pharmacologic treatments for hypochondriasis, supplemented by a meta-analysis of treatments to identify the most promising interventions. Findings suggest that cognitive behavior therapy is the most effective treatment for hypochondriasis. Fluoxetine also is promising, although the long-term effects of this and other medications remain to be examined. Psychoeducation appears to be sufficient for mild hypochondriasis. Future research on the mechanisms of hypochondriasis may shed light on how we can improve treatments, particularly for severe cases, which are least likely to benefit from psychosocial and drug interventions.

Anxiety sensitivity is the fear of anxiety sensations based on beliefs that they have harmful physical, psychological, or social consequences. Anxiety sensitivity may represent a psychological vulnerability for panic attacks, but much of the research to date has been limited to selective college student or treatment-seeking samples. There is a paucity of research based on representative community-based samples. There is also a lack of longitudinal research in this regard. The current study addressed both of these issues by investigating the impact of anxiety sensitivity in a large community sample (N = 585) assessed longitudinally over a 1-year period. A hierarchical regression model was used to determine whether baseline scores on the Anxiety Sensitivity Index (ASI) could prospectively predict scores on the Beck Anxiety Inventory (BAI), a continuous scale that is largely a measure of panic-related symptomatology. Baseline BAI scores, neuroticism and stressful life events’ main effects, their interaction, and the ASI were all significant predictors of Time 2 BAI scores. The results thereby show that anxiety sensitivity predicts subsequent panic-related symptomatology even after adjusting for the effects of neuroticism, stressful life events, and their interaction.

The leading contemporary cognitive-behavioral model of excessive health anxiety (HA) emphasizes the importance of environmental factors, such as learning experiences. The model has little to say about the role of genetic factors and, by ignoring these factors, seems to imply that they are unimportant. In contrast, results from the University of British Columbia Twin Study, using a sample of 88 monozygotic and 65 dizygotic twin pairs, indicated that various facets of HA, such as excessive disease fear, unrealistic beliefs that one has a serious disease, and HA-related interference in functioning, are moderately heritable. The present study extended the analyses of this data set by investigating the extent to which the various facets of HA are due to genetic or environmental factors that are common to all facets versus specific to each facet. Results indicated that all facets of HA are influenced by a common set of genes—there was very little evidence of facet-specific genetic influences. There was considerably stronger evidence for facet-specific environmental influences, where each facet is strongly influenced by environmental experiences that are specific to that facet. However, there was also evidence that particular environmental influences—especially those that shape disease conviction—also influence some of the other HA facets (fear and interference). The importance of environmental factors is consistent with the cognitive-behavioral model of HA, although the model needs to be refined to account for the role of genetic factors. Possibilities for refining the model are discussed, along with promising research directions to better understand the role of genes and the environment in HA.

Health anxiety is an important but poorly assessed phenomenon. Manifesting along a continuum, health anxiety is the result of a catastrophic appraisal of somatic sensations and changes as indicative of disease. The Whiteley Index (WI) is one of the most widely used self-report measures for assessing health anxiety both for research and for clinical practice. It generally exhibits excellent and robust psychometric properties for internal consistency, test–retest reliability, convergent validity, and concurrent validity; however, both its item content and its factor structure are matters of debate. Moreover, the measure has rarely been assessed in nonclinical samples. For the present study, a sample of 300 participants from the University of Regina completed the WI. If the latent dimensions identified in factor analysis represent etiologic mechanisms, then the elucidation of the WI’s factor structure may enhance our understanding of health anxiety. Exploratory factor analysis was used to determine a robust and reliable item content and factor structure, resulting in a six-item two-factor structure that was invariant across gender. The two factors were denoted Somatic Symptoms/Bodily Preoccupation and Disease Worry/Phobia. Previous factor structure solutions were compared to the factor structure derived from this study by means of confirmatory factor analysis. The newly established item content and factor structure resulted in acceptable fit indices that were statistically superior to those found using the previous factor structure solutions. Implications and directions for assessment of health anxiety and future research are discussed.

Transdiagnostic cognitive-behavioral approaches attempt to develop broad theories of clinical conditions (e.g., general theories of mood and anxiety disorders) and corresponding treatment protocols that can be applied to a range of clinical conditions. These can be contrasted with diagnosis-specific theories and treatments, which focus on particular clinical conditions (e.g., theories of panic disorder and panic-specific treatments). In this introductory article we trace the history of transdiagnostic and diagnosis-specific cognitive-behavioral approaches. Both have their origins in the late 1950s and early 1960s. Over the subsequent decades there was waning interest in transdiagnostic approaches and a corresponding increase in interest in diagnosis-specific approaches to theory and treatment. Over the past several years, however, interest has been revived in transdiagnostic approaches. We summarize the reasons for this growing interest and provide an overview of the following articles in this special issue.

Transdiagnostic cognitive-behavioral therapy (CBT) for anxiety and depression has been of growing interest in psychotherapy research. In this article we discuss several fundamental issues raised by contributors to this special issue on transdiagnostic CBT for emotional disorders. Although researchers have tended to assume that interventions are transdiagnostic because they are labeled as such, the actual boundary between transdiagnostic and disorderspecific treatments may be far less clear than previously acknowledged. Nevertheless, there are many reasons to advocate for greater attention to a transdiagnostic perspective, not the least being the large shared variance in the emotional disorders, which is often overlooked in contemporary disorder-specific CBT protocols. Evidence of the efficacy of transdiagnostic CBT for anxiety and depression is limited, and issues facing comparative outcome and process studies are discussed. The article concludes by suggesting a programmatic framework for advancing a theory-driven, empirically based psychotherapy research agenda that could lead to the development of a truly integrated, transdiagnostic CBT for anxiety and depression.