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A significant body of research has investigated the effects of physical activity on sleep, yet this research has not been systematically aggregated in over a decade. As a result, the magnitude and moderators of these effects are unclear. This meta-analytical review examines the effects of acute and regular exercise on sleep, incorporating a range of outcome and moderator variables. PubMed and PsycINFO were used to identify 66 studies for inclusion in the analysis that were published through May 2013. Analyses reveal that acute exercise has small beneficial effects on total sleep time, sleep onset latency, sleep efficiency, stage 1 sleep, and slow wave sleep, a moderate beneficial effect on wake time after sleep onset, and a small effect on rapid eye movement sleep. Regular exercise has small beneficial effects on total sleep time and sleep efficiency, small-to-medium beneficial effects on sleep onset latency, and moderate beneficial effects on sleep quality. Effects were moderated by sex, age, baseline physical activity level of participants, as well as exercise type, time of day, duration, and adherence. Significant moderation was not found for exercise intensity, aerobic/anaerobic classification, or publication date. Results were discussed with regards to future avenues of research and clinical application to the treatment of insomnia.

Research over the past few decades has focused on the therapeutic effects of physical exercise among those affected by mood disorders. Only recently has attention turned to maladaptive and persistent expressions of anxiety, with a growing body of evidence indicating promise for exercise as an effective treatment for some of the anxiety disorders. The current review provides a comprehensive account of contemporary research examining the anxiolytic effects of exercise for anxiety disorders. We synthesize pertinent research regarding the effects of various types of exercise within the different anxiety disorders, consider impact of various types of exercise regimens on anxiety, and examine potential anxiolytic mechanisms responsible for positive mental health gains. We conclude with important considerations for implementing exercise as a treatment for clinically significant anxiety as well as future research directions.

Most adults and children in the United States fail to receive timely care for mental health symptoms, with even worse rates of care access for individuals who belong to racial and ethnic minority groups. Digital (ie, app-based) care has proven to be an efficacious and empirically supported treatment option with the potential to address low rates of care and reduce care disparities, yet little is known about the relative preference for such treatment. Furthermore, the rapid adoption of telehealth care during the COVID-19 pandemic may have shifted care preferences. This study aimed to examine relative treatment preferences for 4 different types of mental health care: in-person psychological care, telehealth psychological care, digital treatment, or pharmacologic care. Care preferences were also examined relative to potential predictors of care use (ie, gender, race, age, stigma, discrimination, and level of shame). In this cross-sectional online survey study of adults (N=237, mean age 35 years, range 19-68 years), we ranked 4 mental health care modalities based on care preference: (1) in-person care, (2) telehealth care, (3) digital care, and (4) pharmacologic care. Preference for treatment modality was assessed based on vignette presentation for generalized anxiety disorder and insomnia. In addition, participants completed self-report questionnaires for demographics, symptom severity, and psychological and stigma-related variables. We found no difference in overall preference for in-person versus both telehealth and digital care. For both generalized anxiety disorder and insomnia, participants preferred in-person care to telehealth care, although this finding was attenuated amongst older participants for insomnia treatment. Participants' depressed mood was associated with a greater relative preference for pharmacologic care. There was no evidence of differential preference for digital care according to demographics, symptom severity, or psychological and stigma-related variables. These results indicate that digital care now competes well in terms of treatment preference with in-person, telehealth, and pharmacologic treatment options.

The risks and benefits of standard antidepressants for patients with bipolar disorder are not well understood. In this randomized, placebo-controlled trial of patients with bipolar disorder, all of whom received a mood stabilizer, adjunctive treatment with an antidepressant did not reduce the symptoms of bipolar depression or increase the risk of mania. In patients with bipolar disorder, all of whom received a mood stabilizer, adjunctive treatment with an antidepressant did not reduce the symptoms of bipolar depression or increase the risk of mania. Bipolar disorder, the sixth-leading cause of disability worldwide, 1 is a chronic and recurrent psychiatric illness with a lifetime prevalence of just under 4% 2 and annual costs that exceed those of diabetes or recurrent (unipolar) major depressive disorder. 3 Although abnormal mood elevation is the cardinal diagnostic feature that distinguishes bipolar disorder from recurrent major depressive disorder, depression that alternates with manic episodes (bipolar depression) is the leading cause of impairment and death among patients with bipolar disorders. 4 – 6 Two main limitations related to standard antidepressant medications hamper their use in the treatment of bipolar depression. First, though these agents have proved . . .

Cues associated with alcohol consumption can trigger cravings, seeking behaviour and relapse after abstinence in individuals with alcohol use disorder (AUD). These conditioned responses can be attenuated through extinction learning, a core component of cue exposure therapy (CET). CET is effective in some individuals with AUD but not all, so it is necessary to develop strategies to identify and intervene with individuals unlikely to benefit from CET. Another method for attenuating conditioned responding is retrieval‐extinction, which renders the original associative memory labile via distinct neural mechanisms. We recently demonstrated that CO2 reactivity predicts extinction memory for both fear and food cues, and fear memory after retrieval‐extinction, and CO2‐induced orexin/c‐Fos colocalization predicts fear extinction memory. The purpose of the current study was to examine whether the predictive power of CO2 reactivity might extend to alcohol‐seeking behaviour after extinction or retrieval‐extinction in male and female rats. We also examined the relationship between CO2 reactivity, return of alcohol‐seeking behaviour and CO2‐induced orexin/c‐Fos colocalization. Male and female rats first underwent alcohol drinking induction in the homecage followed by dependence via exposure to chronic intermittent ethanol vapour or control air and homecage drinking. All rats then underwent Pavlovian alcohol conditioning followed by either standard extinction or retrieval‐extinction. They then received a long‐term memory (LTM) test and CO2 challenge followed by euthanasia for brain harvesting. CO2 reactivity differentially predicted LTM after extinction and retrieval‐extinction. There were no relationships between orexin/c‐Fos colocalization and CO2 reactivity or LTM. The predictive power of CO2 reactivity extends to alcohol‐seeking behaviour after extinction and retrieval‐extinction in alcohol dependent and nondependent male and female rats, while its relationship with orexin/c‐Fos colocalization does not. CO2 reactivity could be used as a screening tool to determine whether an individual may be a good candidate for CET or a retrieval‐extinction–based approach. CO2 reactivity differentially predicted alcohol‐seeking behaviour in alcohol dependent and non‐dependent male and female rats after extinction and retrieval‐extinction. However, there were no relationships between orexin/c‐Fos colocalization and CO2 reactivity or return of alcohol‐seeking behaviour. This supports the potential of CO2 reactivity to be used as a screening tool to determine whether an individual may be a good candidate for cue exposure therapy or a retrieval‐extinction‐based approach.

Background Exposure-based therapy is an effective first-line treatment for anxiety-, obsessive–compulsive, and trauma- and stressor-related disorders; however, many patients do not improve, resulting in prolonged suffering and poorly used resources. Basic research on fear extinction may inform the development of a biomarker for the selection of exposure-based therapy. Growing evidence links orexin system activity to deficits in fear extinction and we have demonstrated that reactivity to an inhaled carbon dioxide (CO 2 ) challenge—a safe, affordable, and easy-to-implement procedure—can serve as a proxy for orexin system activity and predicts fear extinction deficits in rodents. Building upon this basic research, the goal for the proposed study is to validate CO 2 reactivity as a biomarker of exposure-based therapy non-response. Methods We will assess CO 2 reactivity in 600 adults meeting criteria for one or more fear- or anxiety-related disorders prior to providing open exposure-based therapy. By incorporating CO 2 reactivity into a multivariate model predicting treatment non-response that also includes reactivity to hyperventilation as well as a number of related predictor variables, we will establish the mechanistic specificity and the additive predictive utility of the potential CO 2 reactivity biomarker. By developing models independently within two study sites (University of Texas at Austin and Boston University) and predicting the other site’s data, we will validate that the results are likely to generalize to future clinical samples. Discussion Representing a necessary stage in translating basic research, this investigation addresses an important public health issue by testing an accessible clinical assessment strategy that may lead to a more effective treatment selection (personalized medicine) for patients with anxiety- and fear-related disorders, and enhanced understanding of the mechanisms governing exposure-based therapy. Trial registration ClinicalTrials.gov Identifier: NCT05467683 (20/07/2022).

Preclinical and clinical data have shown that D-cycloserine (DCS), a partial agonist at the N-methyl-d-aspartate receptor complex, augments the retention of fear extinction in animals and the therapeutic learning from exposure therapy in humans. However, studies with non-clinical human samples in de novo fear conditioning paradigms have demonstrated minimal to no benefit of DCS. The aim of this study was to evaluate the effects of DCS on the retention of extinction learning following de novo fear conditioning in a clinical sample. Eighty-one patients with social anxiety disorder were recruited and underwent a previously validated de novo fear conditioning and extinction paradigm over the course of three days. Of those, only 43 (53%) provided analyzable data. During conditioning on Day 1, participants viewed images of differently colored lamps, two of which were followed by with electric shock (CS+) and a third which was not (CS-). On Day 2, participants were randomly assigned to receive either 50 mg DCS or placebo, administered in a double-blind manner 1 hour prior to extinction training with a single CS+ in a distinct context. Day 3 consisted of tests of extinction recall and renewal. The primary outcome was skin conductance response to conditioned stimuli, and shock expectancy ratings were examined as a secondary outcome. Results showed greater skin conductance and expectancy ratings in response to the CS+ compared to CS- at the end of conditioning. As expected, this difference was no longer present at the end of extinction training, but returned at early recall and renewal phases on Day 3, showing evidence of return of fear. In contrast to hypotheses, DCS had no moderating influence on skin conductance response or expectancy of shock during recall or renewal phases. We did not find evidence of an effect of DCS on the retention of extinction learning in humans in this fear conditioning and extinction paradigm.

Cognitive control training (CCT) uses computer-based exercises to increase prefrontal cortex activation. Recent studies have found that depressed participants who received CCT significantly reduce their negative affect and rumination, and improve focus and concentration (Siegle et al. in Cogn Ther Res 31:235–262, 2007 ; Calkins et al. 2011 ). These promising findings raise questions about the degree to which this intervention may have use in other disorders; specifically, can CCT reduce the inflexible thinking characteristic of individuals with OCD? In the present study, we assessed the efficacy of three sessions of CCT, relative to a control intervention, on obsessive–compulsive (OC) symptoms in a community sample of individuals selected on the basis of elevated scores on the OCI-R. We hypothesized that those in the CCT condition would report a greater reduction in OC symptoms than those in the control condition. Additionally we assessed the ability to disengage from unattainable goals by using an unsolvable anagram task. To target the intervention to OC rather than mood symptoms, we excluded participants with elevated depression scores. Forty-eight participants (28 female, mean age 28.9 years) meeting eligibility criteria were randomized to receive three sessions of CCT or the control intervention (a computerized visual task) over a 2-week period. Following training, we did not find a significant difference between groups on OCI-R scores, indicating that this application of CCT was ineffective in meaningfully reducing OC symptoms (d = 0.27). Significant differences were found for affect ratings between groups, with participants in the CCT group showing larger decreases (d = 0.62) in negative affect scores across the three sessions of training. Hence, the CCT intervention may be more specific to mood than a direct modulator of cognitive inflexibility. Examination of the effects of additional sessions of CCT or CCT as an augmentation to exposure therapy remains to be investigated.