Background Cognitive Bias Modification (CBM) is a potentially effective intervention for social anxiety disorder (SAD). However, this has never been tested in a living systematic review and the relative efficacy of CBM subtypes remains uncertain. Methods We co-produced a living systematic review of controlled studies evaluating CBM in participants with SAD and in non-clinical participants undergoing a social stressor, seeking to triangulate these. Databases were searched until October 2025 and two independent reviewers screened, extracted and critically appraised studies. The primary outcome was reduction in SAD symptoms, but we collected data on other mental health outcomes. Random-effect network meta-analysis was conducted. Credibility was assessed using the Confidence In Network Meta-Analysis framework. Results CBM for attention (CBM-A) demonstrated the largest reduction in SAD symptoms relative to control CBM-A although this estimate was imprecise (Standardised Mean Difference (SMD) = -0.18, 95% CI: -0.41 to 0.05, 95% PI: -1.02 to 1.04). Opposite CBM-A, training attention towards negative stimuli, performed similarly (SMD -0.17, 95% CI: -0.65 to 0.31, 95% PI: -0.97 to 1.21). CBM for interpretation (CBM-I) reduced SAD symptoms (SMD = -0.47, 95% CI: -0.84 to -0.09, 95% PI: -0.53 to 1.46) and cognitive bias versus its structurally matched control. The SAD network showed high inconsistency and 95% of studies were at moderate or high risk of bias. Three comparisons involving CBM-A were rated as moderate confidence, all others were low or very low. Sparse data precluded NMA of outcomes in non-SAD participants. Conclusion Inconsistency and imprecision in the network preclude firm conclusions regarding CBM efficacy for SAD. CBM-A showed a small effect but its similarity to opposite CBM-A suggests benefits may not depend on training direction. Future studies should explore the mechanism of CBM and reporting on potential side-effects. We will update this review as part of the GALENOS project. Registration: PROSPERO-ID:CRD42024601380

Background Exercise for post-traumatic stress disorder (PTSD) is a potentially effective adjunct to psychotherapy. However, the biopsychosocial mechanisms of exercise are not well understood. This co-produced living systematic review synthesizes evidence from human and non-human studies. Methods We Included controlled human and non-human studies involving searches of multiple electronic databases (until 31.10.23). Records were screened, extracted, assessed for risk of bias, and reconciled by two independent reviewers. The primary outcome for human studies was PTSD symptom severity, while outcomes of interest for non-human studies included freezing behaviour, fear memory, fear generalization, startle response, and locomotion. Data were synthesised with random-effects meta-analysis. Results Eleven human studies met the eligibility criteria. Overall, exercise was not associated with symptom severity improvement compared to control (standardized mean difference [SMD] -0.08, 95% confidence interval [CI] -0.24 to 0.07; 8 studies, one at low risk of bias). High-intensity exercise reduced PTSD symptoms scores more than moderate-intensity exercise. There was insufficient data to examine the effects of exercise on functional impairment, PTSD symptom clusters, and PTSD remission. Only three studies, all at high risk of bias, examined mechanisms of exercise with inconclusive results. Exercise was associated with improvement in all behavioural outcomes, including locomotor activity (SMD 1.30, 95% CI 0.74 to 1.87, 14 studies), and changes in several neurobiological markers, including increase in brain-derived neurotrophic factor (SMD 1.79, 95% CI 0.56 to 3.01). Conclusions While non-human studies provide compelling evidence for the beneficial effects of exercise, human trials do not. Evidence from non-human studies suggest that exercise might increase the levels of brain-derived neurotrophic factor, enhance cognitive appraisal, and improve perceived exertion. Overall, the paucity of data on the effectiveness of exercise in PTSD and mechanisms of action underscore the need for rigorous trials. Registration The protocol was registered with PROSPERO (ID:453615; 22.08.2023).

Background Exercise for post-traumatic stress disorder (PTSD) is a potentially effective adjunct to psychotherapy. However, the biopsychosocial mechanisms of exercise are not well understood. This co-produced living systematic review synthesizes evidence from human and non-human studies. Methods We Included controlled human and non-human studies involving searches of multiple electronic databases (until 31.10.23). Records were screened, extracted, assessed for risk of bias, and reconciled by two independent reviewers. The primary outcome for human studies was PTSD symptom severity, while outcomes of interest for non-human studies included freezing behaviour, fear memory, fear generalization, startle response, and locomotion. Data were synthesised with random-effects meta-analysis. Results Eleven human studies and 14 non-human studies met the eligibility criteria. Results of human studies showed that exercise was not associated with symptom severity improvement compared to control (standardized mean difference [SMD] -0.08, 95% confidence interval [CI] -0.24 to 0.07). High-intensity exercise reduced PTSD symptoms scores more than moderate-intensity exercise. There was insufficient data to examine the effects of exercise on functional impairment, PTSD symptom clusters, and PTSD remission. Only three studies, all at high risk of bias, examined mechanisms of exercise with inconclusive results. Results of non-human studies showed that exercise was associated with improvement in all behavioural outcomes, including locomotor activity (SMD 1.30, 95% CI 0.74 to 1.87, 14 studies), and changes in several neurobiological markers, including increase in brain-derived neurotrophic factor (SMD 1.79, 95% CI 0.56 to 3.01). Conclusions While non-human studies provide compelling evidence for the beneficial effects of exercise, human trials do not. Evidence from non-human studies suggest that exercise might increase the levels of brain-derived neurotrophic factor, enhance cognitive appraisal, and improve perceived exertion. Overall, the paucity of data on the effectiveness of exercise in PTSD and mechanisms of action underscore the need for rigorous trials. Registration The protocol was registered with PROSPERO (ID:453615; 22.08.2023).

Background Exercise for post-traumatic stress disorder (PTSD) is a potentially effective adjunct to psychotherapy. However, the biopsychosocial mechanisms of exercise are not well understood. This co-produced living systematic review synthesizes evidence from human and non-human studies. Methods We Included controlled human and non-human studies involving searches of multiple electronic databases (until 31.10.23). Records were screened, extracted, assessed for risk of bias, and reconciled by two independent reviewers. The primary outcome for human studies was PTSD symptom severity, while outcomes of interest for non-human studies included freezing behaviour, fear memory, fear generalization, startle response, and locomotion. Data were synthesised with random-effects meta-analysis. Results Eleven human studies met the eligibility criteria. Overall, exercise was not associated with symptom severity improvement compared to control (standardized mean difference [SMD] -0.08, 95% confidence interval [CI] -0.24 to 0.07; 8 studies, one at low risk of bias). High-intensity exercise reduced PTSD symptoms scores more than moderate-intensity exercise. There was insufficient data to examine the effects of exercise on functional impairment, PTSD symptom clusters, and PTSD remission. Only three studies, all at high risk of bias, examined mechanisms of exercise with inconclusive results. Exercise was associated with improvement in all behavioural outcomes, including locomotor activity (SMD 1.30, 95% CI 0.74 to 1.87, 14 studies), and changes in several neurobiological markers, including increase in brain-derived neurotrophic factor (SMD 1.79, 95% CI 0.56 to 3.01). Conclusions While non-human studies provide compelling evidence for the beneficial effects of exercise, human trials do not. Evidence from non-human studies suggest that exercise might increase the levels of brain-derived neurotrophic factor, enhance cognitive appraisal, and improve perceived exertion. Overall, the paucity of data on the effectiveness of exercise in PTSD and mechanisms of action underscore the need for rigorous trials. Registration The protocol was registered with PROSPERO (ID:453615; 22.08.2023).

Background Social anxiety is a heightened fear and discomfort in social situations. Cases of elevated distress and impaired functioning can lead to a clinical diagnosis of social anxiety disorder. Altering cognitive biases associated with social anxiety has been suggested as potentially beneficial; however, little is known about the comparative effectiveness of such interventions. The aim of this living systematic review is to examine the efficacy of cognitive bias modification for reducing social anxiety. Methods We will search multiple electronic databases for randomised controlled trials evaluating the efficacy of cognitive bias modification for people diagnosed with social anxiety and people exposed to a social stressor. The primary outcome will be change in social anxiety related symptoms; secondary outcomes will be changes in social functioning and quality of life and adverse events. Study selection, data extraction and risk of bias assessment will be done by at least two reviewers using pre-defined tools. We will synthesise data from people with social anxiety diagnosis and those subjected to a simulated social stressor separately using random effects meta-analyses. Heterogeneity will be evaluated by investigating characteristics of included studies and we will conduct a network meta-analysis in order to compare the efficacy of subtypes of cognitive bias modification for social anxiety disorder. We will appraise the strength of the evidence for each outcome by reviewing the overall association, internal and external validity, and reporting biases. Where data allows, we will triangulate the evidence from both sources with a multidisciplinary group of experts. We will also descriptively report factors reported to mediate cognitive bias modification, The review will begin in living mode and the database search will be rerun every three months to identify potential new evidence. We will co-produce this review with members of a global lived experience advisory board. This protocol was registered on 15.10.2024 (CRD42024601380)..

Background Exercise can play an important role in reducing symptom severity and improving functional impairment in patients with posttraumatic stress disorder (PTSD). However, the precise mechanisms underpinning the effect of exercise in PTSD management are not fully understood. This living systematic review aims to synthesize and triangulate the evidence from non-human and human studies to gain insight into the biopsychosocial mechanisms through which exercise reduces symptom severity and functional impairment. Methods Independent searches will be conducted in electronic databases to identify eligible studies. Two reviewers will independently conduct the study selection, data extraction, and risk of bias assessment. We will extract outcome data and variables that can act as effect modifiers or as mediators of the effect of exercise. For the non-human studies, outcome data will include the non-human equivalents of PTSD symptom clusters. For human studies, the primary outcome will be PTSD symptom severity. The secondary outcomes will be avoidance symptom severity, reexperiencing symptom severity, hyperarousal symptom severity, negative cognitions and mood severity, functional impairment, loss of PTSD diagnosis, and dropout rates. To explain the biopsychosocial mechanisms through which exercise affects the outcome of interest, we will extract effects that relate to the impact of exercise on potential mediating variables and the effect of the later outcomes. Comparison of within-study direct and indirect effects obtained from mediation analysis, when reported, will provide insight into the importance of the examined mediator. If appropriate, we will synthesize study results using meta-analyses. We will examine potential effect modifiers of the total exercise effect to understand better the impact of exercise on PTSD symptoms and function impairment (when possible). The evidence about the potential mediators of the association between exercise and PTSD-related outcomes will be considered in a consensus meeting when sufficient evidence is available. Protocol registration PROSPERO-ID: 453615

This document is a protocol for a living systematic review of the association between cardiovascular and metabolic factors and cognitive functioning in psychosis. This review is an output of the Global Alliance for Living Evidence on aNxiety, depressiOn, and pSychosis (GALENOS) project. The GALENOS project is a global, multidisciplinary consortium aimed at co-producing a continuously updated synthesis of the scientific literature on mental health. The consortium is focused on the underlying mechanisms of depression, anxiety, and psychosis, to inform their prevention and treatment. This protocol is registered on PROSPERO: CRD420251019425. The supplementary materials are on OSF (https://osf.io/b54a8/) and include the PRISMA-P checklist and example search strategies used.

Background Exercise for post-traumatic stress disorder (PTSD) is a potentially effective adjunct to psychotherapy. However, the biopsychosocial mechanisms of exercise are not well understood. This co-produced living systematic review synthesizes evidence from human and non-human studies. Methods We Included controlled human and non-human studies involving searches of multiple electronic databases (until 31.10.23). Records were screened, extracted, assessed for risk of bias, and reconciled by two independent reviewers. The primary outcome for human studies was PTSD symptom severity, while outcomes of interest for non-human studies included freezing behaviour, fear memory, fear generalization, startle response, and locomotion. Data were synthesised with random-effects meta-analysis. Results Eleven human studies met the eligibility criteria. Overall, exercise was not associated with symptom severity improvement compared to control (standardized mean difference [SMD] -0.08, 95% confidence interval [CI] -0.24 to 0.07; 8 studies, one at low risk of bias). High-intensity exercise reduced PTSD symptoms scores more than moderate-intensity exercise. There was insufficient data to examine the effects of exercise on functional impairment, PTSD symptom clusters, and PTSD remission. Only three studies, all at high risk of bias, examined mechanisms of exercise with inconclusive results. Exercise was associated with improvement in all behavioural outcomes, including locomotor activity (SMD 1.30, 95% CI 0.74 to 1.87, 14 studies), and changes in several neurobiological markers, including increase in brain-derived neurotrophic factor (SMD 1.79, 95% CI 0.56 to 3.01). Conclusions While non-human studies provide compelling evidence for the beneficial effects of exercise, human trials do not. Evidence from non-human studies suggest that exercise might increase the levels of brain-derived neurotrophic factor, enhance cognitive appraisal, and improve perceived exertion. Overall, the paucity of data on the effectiveness of exercise in PTSD and mechanisms of action underscore the need for rigorous trials. Registration The protocol was registered with PROSPERO (ID:453615; 22.08.2023).

Background Social anxiety is a heightened fear and discomfort in social situations. Cases of elevated distress and impaired functioning can lead to a clinical diagnosis of social anxiety disorder. Altering cognitive biases associated with social anxiety has been suggested as potentially beneficial; however, little is known about the comparative effectiveness of such interventions. The aim of this living systematic review is to examine the efficacy of cognitive bias modification for reducing social anxiety. Methods We will search multiple electronic databases for randomised controlled trials evaluating the efficacy of cognitive bias modification for people diagnosed with social anxiety and people exposed to a social stressor. The primary outcome will be change in social anxiety related symptoms; secondary outcomes will be changes in social functioning and quality of life and adverse events. Study selection, data extraction and risk of bias assessment will be done by at least two reviewers using pre-defined tools. We will synthesise data from people with social anxiety diagnosis and those subjected to a simulated social stressor separately using random effects meta-analyses. Heterogeneity will be evaluated by investigating characteristics of included studies and we will conduct a network meta-analysis in order to compare the efficacy of subtypes of cognitive bias modification for social anxiety disorder. We will appraise the strength of the evidence for each outcome by reviewing the overall association, internal and external validity, and reporting biases. Where data allows, we will triangulate the evidence from both sources with a multidisciplinary group of experts. We will also descriptively report factors reported to mediate cognitive bias modification, The review will begin in living mode and the database search will be rerun every three months to identify potential new evidence. We will co-produce this review with members of a global lived experience advisory board. This protocol was registered on 15.10.2024 (CRD42024601380)..

Background Trace amine-associated receptor 1 (TAAR1) agonism shows promise for treating psychosis, prompting us to synthesise data from human and non-human studies. Methods We co-produced a living systematic review of controlled studies examining TAAR1 agonists in individuals (with or without psychosis/schizophrenia) and relevant animal models. Two independent reviewers identified studies in multiple electronic databases (until 17.11.2023), extracted data, and assessed risk of bias. Primary outcomes were standardised mean differences (SMD) for overall symptoms in human studies and hyperlocomotion in animal models. We also examined adverse events and neurotransmitter signalling. We synthesised data with random-effects meta-analyses. Results Nine randomised trials provided data for two TAAR1 agonists (ulotaront and ralmitaront), and 15 animal studies for 10 TAAR1 agonists. Ulotaront and ralmitaront demonstrated few differences compared to placebo in improving overall symptoms in adults with acute schizophrenia (N=4 studies, n=1291 participants; SMD=0.15, 95%CI: -0.05, 0.34), and ralmitaront was less efficacious than risperidone (N=1, n=156, SMD=-0.53, 95%CI: -0.86, -0.20). Large placebo response was observed in ulotaront phase-III trials. Limited evidence suggested a relatively benign side-effect profile for TAAR1 agonists, although nausea and sedation were common after a single dose of ulotaront. In animal studies, TAAR1 agonists improved hyperlocomotion compared to control (N=13 studies, k=41 experiments, SMD=1.01, 95%CI: 0.74, 1.27), but seemed less efficacious compared to dopamine D2 receptor antagonists (N=4, k=7, SMD=-0.62, 95%CI: -1.32, 0.08). Limited human and animal data indicated that TAAR1 agonists may regulate presynaptic dopaminergic signalling. Conclusions TAAR1 agonists may be less efficacious than dopamine D2 receptor antagonists already licensed for schizophrenia. The results are preliminary due to the limited number of drugs examined, lack of longer-term data, publication bias, and assay sensitivity concerns in trials associated with large placebo response. Considering their unique mechanism of action, relatively benign side-effect profile and ongoing drug development, further research is warranted. Registration PROSPERO-ID:CRD42023451628.

Background Trace amine-associated receptor 1 (TAAR1) agonism shows promise for treating psychosis, prompting us to synthesise data from human and non-human studies. Methods We co-produced a living systematic review of controlled studies examining TAAR1 agonists in individuals (with or without psychosis/schizophrenia) and relevant animal models. Two independent reviewers identified studies in multiple electronic databases (until 17.11.2023), extracted data, and assessed risk of bias. Primary outcomes were standardised mean differences (SMD) for overall symptoms in human studies and hyperlocomotion in animal models. We also examined adverse events and neurotransmitter signalling. We synthesised data with random-effects meta-analyses. Results Nine randomised trials provided data for two TAAR1 agonists (ulotaront and ralmitaront), and 15 animal studies for 10 TAAR1 agonists. Ulotaront and ralmitaront demonstrated few differences compared to placebo in improving overall symptoms in adults with acute schizophrenia (N=4 studies, n=1291 participants; SMD=0.15, 95%CI: -0.05, 0.34), and ralmitaront was less efficacious than risperidone (N=1, n=156, SMD=-0.53, 95%CI: -0.86, -0.20). Large placebo response was observed in ulotaront phase-III trials. Limited evidence suggested a relatively benign side-effect profile for TAAR1 agonists, although nausea and sedation were common after a single dose of ulotaront. In animal studies, TAAR1 agonists improved hyperlocomotion compared to control (N=13 studies, k=41 experiments, SMD=1.01, 95%CI: 0.74, 1.27), but seemed less efficacious compared to dopamine D2 receptor antagonists (N=4, k=7, SMD=-0.62, 95%CI: -1.32, 0.08). Limited human and animal data indicated that TAAR1 agonists may regulate presynaptic dopaminergic signalling. Conclusions TAAR1 agonists may be less efficacious than dopamine D2 receptor antagonists already licensed for schizophrenia. The results are preliminary due to the limited number of drugs examined, lack of longer-term data, publication bias, and assay sensitivity concerns in trials associated with large placebo response. Considering their unique mechanism of action, relatively benign side-effect profile and ongoing drug development, further research is warranted. Registration PROSPERO-ID:CRD42023451628.

Background Available empirical evidence on participant-level factors associated with dropout from psychotherapies for post-traumatic stress disorder (PTSD) is both limited and inconclusive. More comprehensive understanding of the various factors that contribute to study dropout from cognitive-behavioural therapy with a trauma focus (CBT-TF) is crucial for enhancing treatment outcomes.Objective Using an individual participant data meta-analysis (IPD-MA) design, we examined participant-level predictors of study dropout from CBT-TF interventions for PTSD.Methods A comprehensive systematic literature search was undertaken to identify randomised controlled trials comparing CBT-TF with waitlist control, treatment-as-usual or another therapy. Academic databases were screened from conception until 11 January 2021. Eligible interventions were required to be individual and in-person delivered. Participants were considered dropouts if they did not complete the post-treatment assessment.Findings The systematic literature search identified 81 eligible studies (n=3330). Data were pooled from 25 available CBT-TF studies comprising 823 participants. Overall, 221 (27%) of the 823 dropped out. Of 581 civilians, 133 (23%) dropped out, as did 75 (42%) of 178 military personnel/veterans. Bivariate and multivariate analyses indicated that military personnel/veterans (RR 2.37) had a significantly greater risk of dropout than civilians. Furthermore, the chance of dropping out significantly decreased with advancing age (continuous; RR 0.98).Conclusions These findings underscore the risk of premature termination from CBT-TF among younger adults and military veterans/personnel.Clinical implication Understanding predictors can inform the development of retention strategies tailored to at-risk subgroups, enhance engagement, improve adherence and yield better treatment outcomes.

Background Trace amine-associated receptor 1 (TAAR1) agonism shows promise for treating psychosis, prompting us to synthesise data from human and non-human studies. Methods We co-produced a living systematic review of controlled studies examining TAAR1 agonists in individuals (with or without psychosis/schizophrenia) and relevant animal models. Two independent reviewers identified studies in multiple electronic databases (until 17.11.2023), extracted data, and assessed risk of bias. Primary outcomes were standardised mean differences (SMD) for overall symptoms in human studies and hyperlocomotion in animal models. We also examined adverse events and neurotransmitter signalling. We synthesised data with random-effects meta-analyses. Results Nine randomised trials provided data for two TAAR1 agonists (ulotaront and ralmitaront), and 15 animal studies for 10 TAAR1 agonists. Ulotaront and ralmitaront demonstrated few differences compared to placebo in improving overall symptoms in adults with acute schizophrenia (N=4 studies, n=1291 participants; SMD=0.15, 95%CI: -0.05, 0.34), and ralmitaront was less efficacious than risperidone (N=1, n=156, SMD=-0.53, 95%CI: -0.86, -0.20). Large placebo response was observed in ulotaront phase-III trials. Limited evidence suggested a relatively benign side-effect profile for TAAR1 agonists, although nausea and sedation were common after a single dose of ulotaront. In animal studies, TAAR1 agonists improved hyperlocomotion compared to control (N=13 studies, k=41 experiments, SMD=1.01, 95%CI: 0.74, 1.27), but seemed less efficacious compared to dopamine D2 receptor antagonists (N=4, k=7, SMD=-0.62, 95%CI: -1.32, 0.08). Limited human and animal data indicated that TAAR1 agonists may regulate presynaptic dopaminergic signalling. Conclusions TAAR1 agonists may be less efficacious than dopamine D2 receptor antagonists already licensed for schizophrenia. The results are preliminary due to the limited number of drugs examined, lack of longer-term data, publication bias, and assay sensitivity concerns in trials associated with large placebo response. Considering their unique mechanism of action, relatively benign side-effect profile and ongoing drug development, further research is warranted. Registration PROSPERO-ID:CRD42023451628.

In anxiety, depression and psychosis, there has been frustratingly slow progress in developing novel therapies that make a substantial difference in practice, as well as in predicting which treatments will work for whom and in what contexts. To intervene early in the process and deliver optimal care to patients, we need to understand the underlying mechanisms of mental health conditions, develop safe and effective interventions that target these mechanisms, and improve our capabilities in timely diagnosis and reliable prediction of symptom trajectories. Better synthesis of existing evidence is one way to reduce waste and improve efficiency in research towards these ends. Living systematic reviews produce rigorous, up-to-date and informative evidence summaries that are particularly important where research is emerging rapidly, current evidence is uncertain and new findings might change policy or practice. Global Alliance for Living Evidence on aNxiety, depressiOn and pSychosis (GALENOS) aims to tackle the challenges of mental health science research by cataloguing and evaluating the full spectrum of relevant scientific research including both human and preclinical studies. GALENOS will also allow the mental health community—including patients, carers, clinicians, researchers and funders—to better identify the research questions that most urgently need to be answered. By creating open-access datasets and outputs in a state-of-the-art online resource, GALENOS will help identify promising signals early in the research process. This will accelerate translation from discovery science into effective new interventions for anxiety, depression and psychosis, ready to be translated in clinical practice across the world.

Background: Anhedonia is a key symptom of depression, and it has been suggested as a potential target for future individualised treatments. However, much is unknown about how interventions enhancing dopaminergic pathways may affect anhedonia symptoms in the context of depression. Methods: We will perform independent searches in multiple electronic databases to identify clinical and animal experimental studies on pro-dopaminergic interventions in individuals with depression or animal models for depression. The primary outcomes will be overall anhedonia symptoms and their behavioural proxies in animals. Secondary outcomes will include side effects and neurobiological measures. At least two independent reviewers will conduct the study selection, data extraction, and risk of bias assessments using pre-defined tools according to each record’s study design. We will develop ontologies to facilitate study identification and data extraction. We will synthesise data from clinical and animal studies separately. If appropriate, we will use random-effects meta-analyses, or synthesis without meta-analyses. We will investigate study characteristics as potential sources of heterogeneity. We will evaluate the confidence in the evidence for each outcome and source of evidence, considering the summary of the association, potential concerns regarding internal and external validity, and reporting biases. When multiple sources of evidence are available for an outcome, we will draw an overall conclusion in a triangulation meeting involving a multidisciplinary team of experts. We plan updates of the review every 6 months, and any future modifications to the protocol will be documented. We will co-produce this review with multiple stakeholders. PROSPERO registration: CRD42023451821

Pets are an important part of many pet owners’ lives, yet very little is known about this complex relationship within a South African context. Most of the research on pet attachment and pet ownership stems from developed countries such as the USA. The present study used an online survey to investigate whether pet attachment was related to perceived stress and life satisfaction in a sample of South Africans. Group differences in perceived stress and life satisfaction between pet owners and non-pet owners, between male and female pet owners, between White and Black pet owners, and between dog and cat owners were also explored. The survey was distributed via Facebook and electronic mail. It comprised of a demographic and pet ownership questionnaire, the Comfort from Companion Animal Scale (CCAS), Perceived Stress Scale (PSS), and Satisfaction with Life Scale (SWLS). A total of 3,329 complete online responses were collected. The data were analyzed using Pearson’s correlations and independent t-tests. Results showed that pet attachment was not significantly related to pet owners’ perceived stress and life satisfaction. Female pet owners scored significantly higher on pet attachment than male pet owners, while White participants were significantly more attached to their pets than Black participants. Dog owners in this study were significantly more attached to their dogs, significantly more satisfied with their lives and had significantly less stress than cat owners. The results of the current study add to the body of knowledge on pet attachment, perceived stress, and life satisfaction in South Africa.

BACKGROUND:Posttraumatic stress disorder (PTSD) is a disorder that develops following exposure to severely stressful events. Altered cortisol secretion has been reported in PTSD; however, results have been inconsistent. Previous meta-analyses of cortisol levels in PTSD have combined results of studies that have used different tissue samples (blood, saliva, urine) for cortisol measurement and have not included newer methods of determining cortisol levels (e.g. hair samples). In this systematic review, we will synthesise evidence from studies evaluating basal cortisol levels in PTSD patients versus controls and stratify studies according to tissue type used for cortisol measurement. We will also determine whether results from different tissue types can be pooled and if any specific tissue samples have better utility in research studies on PTSD.METHODS:We will perform a systematic review of the scientific literature including all studies that have evaluated basal or baseline cortisol levels in adults with current PTSD versus controls, with and without trauma exposure. Independent reviewers will conduct searches in electronic databases (Medline, CINAHL, PTSDpubs, Web of Science, Scopus, ProQuest Dissertations & Theses A&I, ClinicalTrials.gov, and ICTRP), and additional studies will be obtained by searching the reference lists of articles. Two reviewers (LLvdH and SW) will independently conduct standardised screening, eligibility assessments, data extraction, and quality assessments before qualitative and, if appropriate, quantitative (meta-analysis and meta-regression) synthesis. Disagreements that arise at any stage will be resolved by a third reviewer (ShS).DISCUSSION:In line with previous reviews, we expect that cortisol levels will be lower in PTSD patients than in controls, but that patterns may vary somewhat according to the tissue sample in which cortisol is measured. This systematic review will assist in developing a better understanding of the acute and chronic patterns of basal cortisol secretion in PTSD and will inform future research.SYSTEMATIC REVIEW REGISTRATION:PROSPERO CRD42018091874.