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BackgroundInternet-administered self-report measures of social anxiety, depressive symptoms, and sleep difficulties are widely used in clinical trials and in clinical routine care, but data loss is a common problem that could render skewed estimates of symptom levels and treatment effects. One way of reducing the negative impact of missing data could be to use telephone administration of self-report measures as a means to complete the data missing from the online data collection. ObjectiveThe aim of the study was to compare the convergence of telephone and Internet administration of self-report measures of social anxiety, depressive symptoms, and sleep difficulties. MethodsThe Liebowitz Social Anxiety Scale-Self-Report (LSAS-SR), Montgomery-Åsberg Depression Rating Scale-Self-Rated (MADRS-S), and the Insomnia Severity Index (ISI) were administered over the telephone and via the Internet to a clinical sample (N=82) of psychiatric patients at a clinic specializing in Internet-delivered treatment. Shortened versions of the LSAS-SR and the ISI were used when administered via telephone. ResultsAs predicted, the results showed that the estimates produced by the two administration formats were highly correlated (r=.82-.91; P

Telomere attrition is a hallmark of cellular aging and shorter telomeres have been reported in mood and anxiety disorders. Telomere shortening is counteracted by the enzyme telomerase and cellular protection is also provided by the antioxidant enzyme glutathione peroxidase (GPx). Here, telomerase, GPx, and telomeres were investigated in 46 social anxiety disorder (SAD) patients in a within-subject design with repeated measures before and after cognitive behavioral therapy. Treatment outcome was assessed by the Liebowitz Social Anxiety Scale (self-report), administered three times before treatment to control for time and regression artifacts, and posttreatment. Venipunctures were performed twice before treatment, separated by 9 weeks, and once posttreatment. Telomerase activity and telomere length were measured in peripheral blood mononuclear cells and GPx activity in plasma. All patients contributed with complete data. Results showed that social anxiety symptom severity was significantly reduced from pretreatment to posttreatment (Cohen's d = 1.46). There were no significant alterations in telomeres or cellular protection markers before treatment onset. Telomere length and telomerase activity did not change significantly after treatment, but an increase in telomerase over treatment was associated with reduced social anxiety. Also, lower pretreatment telomerase activity predicted subsequent symptom improvement. GPx activity increased significantly during treatment, and increases were significantly associated with symptom improvement. The relationships between symptom improvement and putative protective enzymes remained significant also after controlling for body mass index, sex, duration of SAD, smoking, concurrent psychotropic medication, and the proportion of lymphocytes to monocytes. Thus, indices of cellular protection may be involved in the therapeutic mechanisms of psychological treatment for anxiety.

Summary: Cognitive behavioural therapy for insomnia is efficacious and recommended for insomnia, but availability is scarce. Cognitive behavioural therapy for insomnia self‐help interventions could increase availability, especially if unguided. Optimizing cognitive behavioural therapy for insomnia methods and system user‐friendliness, we developed a short, digital, self‐help programme—FastAsleep—based on the behavioural components of sleep restriction and stimulus control. This study investigated its feasibility and preliminary effects. Thirty media‐recruited participants with moderate to severe insomnia were assessed via telephone before using FastAsleep for 4 weeks, and were interviewed afterwards. Self‐ratings with web questionnaires were conducted at screening, pre‐, mid‐ and post‐treatment, and at 3‐month follow‐up. Primary outcomes were feasibility (credibility, adherence, system user‐friendliness and adverse effects), and secondary outcomes were changes in symptom severity (insomnia, depression and anxiety). Adherence was generally high, participants' feasibility ratings were favourable, and adverse effects matched previously reported levels for cognitive behavioural therapy for insomnia. Symptoms of insomnia decreased after the treatment period (Hedge's g = 1.79, 95% confidence interval = 1.20–2.39), as did symptoms of depression and anxiety. FastAsleep can be considered feasible and promising for alleviating insomnia symptoms among patients fit for self‐care. Future controlled trials are needed to establish the efficacy of FastAsleep and its suitability in a stepped care model. [ABSTRACT FROM AUTHOR]

Introduction: Internet interventions for alcohol problems are effective, but not all participants are helped. Further, the importance of adherence has often been neglected in research on internet interventions for alcohol problems. Prediction analysis can help in prospectively assessing participants' probability of success, and ideally, this information could be used to tailor internet interventions to individual needs. Methods: Data were obtained from a randomized controlled trial on internet interventions for alcohol use disorders. Twenty-nine candidate predictors were run in univariate logistic regressions with two dichotomous dependent outcomes: adherence (defined as completing at least 60% of the treatment modules) and low-risk drinking (defined as drinking within national public health guidelines) at two time points – immediately post-treatment and at the 6-month follow-up. Significant predictors were entered hierarchically into domain-specific logistic regressions. In the final models, predictors still showing significant effects were run in multiple logistic regressions. Results: One predictor significantly predicted adherence: treatment credibility (as in how logical the treatment is and how successful one perceives the treatment to be) assessed during the third week of the intervention. Four predictors significantly predicted low-risk drinking at the post-treatment follow-up: pre-treatment abstinence (i.e., not drinking during the 7 days before treatment started), being of the male gender, and two personality factors – a low degree of antagonism and a high degree of alexithymia. At the 6-month follow-up, pre-treatment abstinence was the only significant predictor. Conclusion: Adherence was not predictive of low-risk drinking. Personality variables may have predictive value and should be studied further. Those who abstain from alcohol during the week before treatment starts have a higher likelihood of achieving low-risk drinking than people who initially continue drinking. [ABSTRACT FROM AUTHOR]

Treating comorbid insomnia is important for recovery from, and prevention of, depression. The objective of this study was to compare comorbidity and patient characteristics among patients having treatment for depression before and after implementation of cognitive behavioural therapy for insomnia (CBT‐I) in a routine care internet treatment clinic. We hypothesized that insomnia comorbidity would be lower among patients having treatment for depression after the treatment for insomnia became available, and that depression levels would be high among patients in the insomnia treatment group compared to previous studies of insomnia. Patients were assessed face‐to‐face by physicians and guided through internet‐delivered treatment by psychologists in a psychiatric setting. We retrieved patient data from 3 years before and 3 years after the CBT‐I implementation. Measures were the Montgomery‐Åsberg Depression Rating Scale‐Self rated (MADRS‐S) and Insomnia Severity Index (ISI). Pretreatment symptom levels were high in both the depression (MADRS‐S = 23, n = 1467) and insomnia treatment (ISI = 20, n = 552) groups, indicating a true psychiatric sample. Contrary to the hypothesis, there were no significant changes in the group having treatment for depression regarding insomnia severity or comorbid insomnia diagnosis (from 66% to 68%) after CBT‐I implementation. Also contrary to the hypothesis, comorbid depression levels among insomnia patients having CBT‐I were similar to or slightly higher than in previous studies. It is likely that more patients with this comorbidity, who currently receive treatment for depression, would benefit from CBT‐I. We suggest an emphasis on information on the benefits of CBT‐I among patients and clinical staff involved in the implementation of treatments for insomnia in psychiatry, and further research into possible differences between patients actively seeking treatment for insomnia or depression. [ABSTRACT FROM AUTHOR]