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The recognition of noise exposure as a prominent environmental determinant of public health has grown substantially. While recent years have yielded a wealth of evidence linking environmental noise exposure primarily to cardiovascular ailments, our understanding of the detrimental effects of noise on the brain and mental health outcomes remains limited. Despite being a nascent research area, an increasing body of compelling research and conclusive findings confirms that exposure to noise, particularly from sources such as traffic, can potentially impact the central nervous system. These harms of noise increase the susceptibility to mental health conditions such as depression, anxiety, suicide, and behavioral problems in children and adolescents. From a mechanistic perspective, several investigations propose direct adverse phenotypic changes in brain tissue by noise (e.g. neuroinflammation, cerebral oxidative stress), in addition to feedback signaling by remote organ damage, dysregulated immune cells, and impaired circadian rhythms, which may collectively contribute to noise-dependent impairment of mental health. This concise review linking noise exposure to mental health outcomes seeks to fill research gaps by assessing current findings from studies involving both humans and animals.

Background The BSI-18 contains the three six-item scales somatization, depression, and anxiety as well as the Global Severity Index (GSI), including all 18 items. The BSI-18 is the latest and shortest of the multidimensional versions of the Symptom-Checklist 90-R, but its psychometric properties have not been sufficiently clarified yet. Methods Based on a representative sample of N  = 2516 participants (aged 14–94 years), detailed psychometric analyses were carried out. Results The internal consistency was good: Somatization α = .82, Depression α = .87, Anxiety α = .84 and GSI α = .93. Confirmatory factor analysis supported the three scales as second-order and GSI as first-order factors. The model fit based on RMSEA is good but that model fit based on CFI and TLI are too low. Conclusions Therefore, it is a very short, reliable instrument for the assessment of psychological distress. The BSI-18 can be used to reliably assess psychological distress in the general population. However, further studies need to evaluate the usefulness of standardization in clinical samples.

Alterations of the hypothalamus pituitary-axis on one hand and heightened rates of somatic diseases and mortality on the other hand are consistently found for PTSD and MDD patients. A possible link between these factors might be the immune system, in particular pro- and anti-inflammatory cytokines. A ‘low-grade inflammation’ in PTSD and MDD patients was found, whereas the influence of acute stress and the role of anti-inflammatory cytokines was rarely examined. In this study, 17 female PTSD patients participated in the Trier social stress test while serum cytokine levels (IL-6, IL-10) were assessed. Cytokine levels of PTSD patients were compared with levels of female depressive patients ( n  = 18) and female healthy controls ( n  = 18). Group differences were assessed using a 3 (group) x 8 (time: −15, −1, +1, +10, +20, +30, +45, +60 min) ANCOVA for repeated measures with baseline values as covariates. There was no group difference regarding IL-6 levels ( p  = 0.920) but PTSD patients showed significantly higher levels of IL-10 compared with depressive patients ( p  < 0.001, d  = 0.16) and healthy controls ( p  = 0.001, d  = 0.38). Under acute stress, PTSD patients did not show the widely found elevated IL-6 levels but showed an increase of anti-inflammatory IL-10. Therefore, acute stress seems to promote an imbalance of pro- and anti-inflammatory cytokine levels in PTSD and might indicate a hyperreactive immune response. This should be considered in future studies to further understand the role of the immune system as a link between stress response and somatic diseases.

There is a growing debate on the role of the physical environment and what constitute risk and protective factors for mental health. Various forms of air pollution have shown links to physical and mental health concerns and considering that Germany does not meet the WHO air quality standards—poor air quality affects a large proportion of Germans and is more important now than ever. This study investigates the physical environmental factor, air pollution, measured by particulate matter of particles with an aerodynamic diameter smaller than 10 µm (PM 10 ) and effects on determinants of mental health and well-being (life satisfaction, stress resilience, anxiety, depression, and self-esteem). A representative sample of N = 3020 German adults with 54% females (46% males) and an age range between 18 and 92 years (M = 49.04, S.D. ± 17.27) was used. Multivariate linear regression analyses show that higher life satisfaction, more self-esteem and higher stress resilience are predicted by less air pollution (PM 10 ). Individual income, age, and gender were taken into account for each regression model. Gender specific sub-analyses revealed similar predictions for PM 10 and stress resilience whereas PM 10 and self-esteem were only significantly associated for females. Associations between mental health or well-being determinants and air pollution (PM 10 ) are found in the representative German sample.

Increased food intake, termed “comfort eating”, is a pathologic coping mechanism in chronic stress. Cortisol reactivity under stress is a potent predictor of stress-induced eating behavior affecting the body mass index (BMI). However, cortisol reactivity and food intake under stress in people with obesity has not been evaluated. The aim of this study was to investigate the effect of high/low cortisol reactivity on food intake in people with obesity and healthy weight test controls, following standardized stress induction and a resting condition. Thirty-six men and women with obesity (BMI: 33.00 ± 3.23 kg/m²), as well as 36 age- and gender-matched healthy weight controls (BMI: 21.98 ± 1.81 kg/m²) were categorized into high cortisol reactors (HCR) and low cortisol reactors (LCR) in the Trier Social Stress Test (TSST). Following the TSST and a resting condition, the food intake of all participants was recorded in a standardized laboratory meal. Obese HCR demonstrated a significantly higher food intake than LCR ( t (34) = −2.046, p  ≤ 0.05). However, there were no significant differences between HCR and LCR in the healthy weight controls ( p  = 0.26). In addition, HCR of the people with obesity showed lower values in the emotion coping strategy of cognitive reappraisal than obese LCR ( t (32) = 2.087, p  ≤ 0.05). In conclusion, the magnitude of the cortisol reactivity to stress predicts stress-induced food intake in people with obesity, but not in the healthy weight controls. Limited use of cognitive reappraisal in emotion regulation in the obese HCR may be a marker of vulnerability to stress-induced eating.

Panic attacks are characterized by intense feelings of uncontrollable threat and induce experiences of intense stress. As one of the major physiological stress systems of the body, the hypothalamic-pituitary-adrenocortical axis (HPA) may be a key to our understanding of a biological basis of this anxiety disorder. While recent studies have found evidence for short-term HPA changes in panic disorder with flattened cortisol responses to stimulation, no data have been available on tonic, i.e., long-term HPA activity in these patients. The current study therefore investigated the cumulative cortisol incorporation in hair over the period of three months in patients with panic disorder ( n  = 45) and healthy individuals ( n  = 45). Results showed higher hair cortisol concentration in patients with panic disorder compared to healthy controls. The duration and the severity of the disorder was unrelated to hair cortisol concentrations. In subsample analyses, patients with panic disorder and comorbid depression showed no significant differences in hair cortisol concentration compared to patients with pure panic disorder. The present findings do not support to the notion that a hypoactive HPA axis may be an important biological feature of patients suffering from panic disorder. Future studies will have to show in a large sample whether a changed HPA axis reactivity is present and causally related to the development and course of the disorder.

The SCL-K-9 is the latest short version of the multidimensional Symptom-Checklist 90-R. Up to now, its psychometric properties have not been clarified sufficiently as the nine items have not yet been presented exclusively in a representative sample. Therefore, psychometric properties, model fit values as well as norm-values were analyzed. For the sample, N = 2,507 participants aged 14 to 92, n = 1,379 women and n = 1,128 men, and a mean age of 48.79 (SD = 17.91), were selected from the general population by random-route sampling. Confirmatory factor analyses applying full information maximum likelihood (FIML) tested the model fit. The reliability estimations and effect sizes were reported. The items' discriminative power ranged between .49 to .65, and the Cronbach's Alpha was α = .87, which stands for a good reliability of the SCL-K-9. Norm values as well as gender and age specificities were presented in this section. The CFA with all nine items loading on one latent factor resulted in a good fit. There was evidence of invariance across age and gender groups. Based on these results, the short screening version SCL-K-9 of the Symptom-Checklist 90-R showed good reliability and good model fit; specific norm values could be determined. Further studies should evaluate the usefulness of the standardization in clinical samples.

Objective: Approximately 600 million adults worldwide suffer from obesity. In addition to individual’s eating behavior and lack of physical activity in the development of obesity and overweight, psychosocial stress as well as hormonal stress reactivity must also be considered as important contributing factors. In the current study we compared the cortisol stress response pathway in a psychosocial stress induction (Trier Social Stress Test; TSST) with obese individuals and normal-weight controls. Method: 32 obese individuals (17 females; mean age = 33.94 years, SD = 11.31 years) and 32 normal-weight controls (17 females; mean age = 29.09 years, SD = 10.46 years) underwent the TSST. The salivary cortisol responses and three appraisal questionnaires (Primary Appraisal Secondary Appraisal, Visual Analogue Scale, Trier Inventory for Chronic Stress) were measured. Results: After stress induction, there was a significant main group difference between the obese individuals and the normal-weight controls for cortisol, with lower baseline and post-stress cortisol levels in the obese individuals. Nevertheless, the obese individuals as well as the normal-weight controls showed no significant difference in the self-reported assessment of the stress condition but some significant differences in the cognitive appraisal of the TSST. Conclusion: In conclusion, the induction of psychosocial stress showed differences in the cortisol patterns between the obese individuals and the normal-weight controls. Furthermore, the present data suggest that obesity leads to lower cortisol activity, which may indicate alterations in the Hypothalamic-pituitary-adrencortical (HPA) axis.

The current study aimed to provide further evidence of the structural validity of the 16-item-short version of the Profile of Mood States (POMS), a widely-used tool for assessing an individual’s emotional state. This is significant for various research inquiries in clinical and social psychology. In order to cross-validate previous findings, an additional evaluation of the factorial structure and the psychometric properties is necessary in a newly collected dataset. A representative sample for age and gender of N  = 2503 with 1329 (53%) female, 1173 (47%) male, and 1 (< 1%) diverse, with a mean age of M  = 46 ( SD  = 18) was collected. The model fit for the four-factor model was acceptable, with good reliability for all factors. We found evidence for (partial) strict invariance between gender and age groups. There were small to moderate group differences for the Anger and Vigor subscales regarding age. We report normative percentile ranks. Our findings suggest that the POMS-16 is a dependable and structurally valid gauge of mood states. Especially in situations where a brief and cost-effective assessment is preferred, the POMS-16 should be a considered option.

PTSD patients show alterations of the immune system, mainly a ‘low-grade inflammation’. Psychotherapeutic treatments are meant to reduce symptom burden of PTSD patients but 30–50% of PTSD patients do not benefit from psychotherapy. Therefore, in this study, the predictive effect of cytokine levels on therapy outcome are investigated. Pro- (IL-6) and anti-inflammatory (IL-10) cytokines in female PTSD patients (N = 17) were assessed under acute stress during a Trier social stress test (TSST) before therapeutic treatment. The predictive effects of IL-6 and IL-10 on therapy outcome (SCL_GSI, BDI) after an inpatient psychotherapeutic treatment at the University Medical Center Carl Gustav Carus, Technische Universität Dresden was investigated. Areas under the curve with respect to ground (AUC G ) and increase (AUC I ) for IL-6 and IL-10 levels during the TSST were calculated and used as predictors in regression analyses with pre-treatment scores. Models including all three predictors show good model fits (R 2  = 0.255 to 0.744). Models including AUC G and AUC I scores show superior fits compared with models including pre-treatment scores alone (ΔR 2  = 0.196 to 0.444). IL-6 AUC G and AUC I scores are significant predictors for post-treatment SCL-GSI and BDI (β = −0.554 to 0.853), whereas IL-10 AUC G significantly predicts SCL-GSI and BDI (β = −0.449 to −0.509). Therefore, pro- and anti-inflammatory IL-6 and IL-10 levels under acute stress before therapy predict therapy outcome of female PTSD patients regarding general symptom burden and depressive symptoms. Future studies should further address the link between inflammation and therapy outcome, especially underlying mechanisms and influencing factors.