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Depression is one of the most poorly understood diseases due to its elusive pathogenesis. There is an urgency to identify molecular and biological mechanisms underlying depression and the gut microbiome is a novel area of interest. Here we investigate the relation of fecal microbiome diversity and composition with depressive symptoms in 1,054 participants from the Rotterdam Study cohort and validate these findings in the Amsterdam HELIUS cohort in 1,539 subjects. We identify association of thirteen microbial taxa, including genera Eggerthella, Subdoligranulum, Coprococcus, Sellimonas, Lachnoclostridium, Hungatella, Ruminococcaceae (UCG002, UCG003 and UCG005), LachnospiraceaeUCG001, Eubacterium ventriosum and Ruminococcusgauvreauiigroup , and family Ruminococcaceae with depressive symptoms. These bacteria are known to be involved in the synthesis of glutamate, butyrate, serotonin and gamma amino butyric acid (GABA), which are key neurotransmitters for depression. Our study suggests that the gut microbiome composition may play a key role in depression. Here, the authors analyze the relation of fecal microbiota diversity and composition with depressive symptoms in 1,054 participants from the Rotterdam Study cohort and in 1,539 subjects of the Amsterdam HELIUS cohort, finding associations with bacteria known to be involved in the synthesis of key neurotransmitters for depression.

Abstract The gut microbiome is thought to play a role in depressive disorders, which makes it an attractive target for interventions. Both the microbiome and depressive symptom levels vary substantially across ethnic groups. Thus, any intervention for depression targeting the microbiome requires understanding of microbiome-depression associations across ethnicities. Analysing data from the HELIUS cohort, we characterize the gut microbiota and its associations with depressive symptoms in 6 ethnic groups (Dutch, South-Asian Surinamese, African Surinamese, Ghanaian, Turkish, Moroccan; N = 3211), living in the same urban area. Diversity of the gut microbiota, both within (α-diversity) and between individuals (β-diversity), predicts depressive symptom levels, taking into account demographic, behavioural, and medical differences. These associations do not differ between ethnic groups. Further, β-diversity explains 29%–18% of the ethnic differences in depressive symptoms. Bacterial genera associated with depressive symptoms belong to mulitple families, prominently including the families Christensenellaceae, Lachnospiraceae , and Ruminococcaceae . In summary, the results show that the gut microbiota are linked to depressive symptom levels and that this association generalizes across ethnic groups. Moreover, the results suggest that ethnic differences in the gut microbiota may partly explain parallel disparities in depression.

To extrapolate the 'mood as information' theory to the unique and ecologically relevant setting of the COVID-19 pandemic; the specific aim was to inform health care providers of the impact of bringing the pandemic to salience during life satisfaction evaluations, assessing whether this 'prime' results in increased or decreased reports of satisfaction which are derived unconsciously. Prospective Randomised Interventional Study. Renal Transplant Department in a tertiary centre in the United Kingdom. 200 Renal transplant patients aged between 20 and 88 years. Telephone interviews were undertaken between 1st May, 2020 and 29th May, 2020, at the height of 'shielding' from COVID-19. Participants were randomised into 2 groups, with 1 group receiving a simple 'priming question' regarding the COVID pandemic and the other group having no prior contact. Individuals were then asked to rate their own overall lifetime happiness; desire to change; overall life satisfaction and momentary happiness on a scale of 1 to 10 for each measure. Independent sample t-tests were used to compare results between the two groups, with a type 1 error rate below 5% considered statistically significant. Participants' overall happiness with their life as a whole revealed that individuals who were primed with a question about COVID-19 reported increased overall happiness with their life compared to individuals who had not been primed (+0.88, 95% confidence interval 0.42 to 1.35, p = 0.0002). In addition, participants in the primed group reported less desire to change their life when compared to the non-primed group (-1.35, 95% confidence interval -2.06 to -0.65, p = 0.0002). Participants who were primed with the COVID-19 question also reported a higher overall satisfaction with their life than individuals who had not been primed (+1.01, 95% confidence interval 0.50 to 1.52, p = 0.0001). Finally, the participants who received the priming question demonstrated increased reported momentary happiness (+0.64, 95% confidence interval 0.03 to 1.24, p = 0.04). The results demonstrated that bringing salience to the COVID-19 pandemic with a simple question leads to positive changes in both momentary happiness and other components of global life satisfaction, thereby extrapolating evidence for the application of the mood-as-information theory to more extreme life circumstances. Given the importance of patient-reported evaluations, these findings have implications for how, when and where accurate and reproducible measurements of life satisfaction should be obtained.

Depression is associated with metabolic alterations including lipid dysregulation, whereby associations may vary across individual symptoms. Evaluating these associations using a network perspective yields a more complete insight than single outcome-single predictor models. We used data from the Netherlands Study of Depression and Anxiety ( = 2498) and leveraged networks capturing associations between 30 depressive symptoms (Inventory of Depressive Symptomatology) and 46 metabolites. Analyses involved 4 steps: creating a network with Mixed Graphical Models; calculating centrality measures; bootstrapping for stability testing; validating central, stable associations by extra covariate-adjustment; and validation using another data wave collected 6 years later. The network yielded 28 symptom-metabolite associations. There were 15 highly-central variables (8 symptoms, 7 metabolites), and 3 stable links involving the symptoms Low energy (fatigue), and Hypersomnia. Specifically, fatigue showed consistent associations with higher mean diameter for VLDL particles and lower estimated degree of (fatty acid) unsaturation. These remained present after adjustment for lifestyle and health-related factors and using another data wave. The somatic symptoms Fatigue and Hypersomnia and cholesterol and fatty acid measures showed central, stable, and consistent relationships in our network. The present analyses showed how metabolic alterations are more consistently linked to specific symptom profiles.

CD34+ progenitor cells with angiogenic capabilities traffic into blood during exercise and extravasate afterwards but the magnitude of this response varies between people. We examined whether exercise‐induced progenitor cell trafficking is influenced by cardiorespiratory fitness (maximum oxygen uptake; V̇O2max ${{\\dot{V}}_{{{\\mathrm{O}}}_2}{\\mathrm{max}}}$ ). Ten males (age: 23 ± 3 years; V̇O2max ${{\\dot{V}}_{{{\\mathrm{O}}}_2}{\\mathrm{max}}}$ : 61.88 ± 4.68 mL kg min−1) undertook 1 h of treadmill running at 80% of V̇O2max ${{\\dot{V}}_{{{\\mathrm{O}}}_2}{\\mathrm{max}}}$ . Blood samples were collected before exercise (Pre), in the final minute of exercise (0 h) and afterwards at 0.25, 1 and 24 h. Pan‐progenitor cells (CD34+, CD34+CD45dim) and putative endothelial progenitor cells (CD34+CD133+, CD34+VEGFR2+, CD34+CD45dimVEGFR2+) were quantified using flow cytometry. Progenitor subpopulations (except for CD34+CD45dimVEGFR2+) increased at 0 h (P < 0.05) and returned to pre‐exercise levels by 1 h. V̇O2max ${{\\dot{V}}_{{{\\mathrm{O}}}_2}{\\mathrm{max}}}$was positively associated with the exercise‐induced progenitor cell response and there were statistically significant time × V̇O2max ${{\\dot{V}}_{{{\\mathrm{O}}}_2}{\\mathrm{max}}}$interactions for CD34+, CD34+CD45dim and CD34+CD133+ subpopulations but not VEGFR2‐expressing progenitor cells. There were statistically significant correlations between V̇O2max ${{\\dot{V}}_{{{\\mathrm{O}}}_2}{\\mathrm{max}}}$and ingress (r > 0.70, P < 0.025) and egress (r > −0.77, P < 0.009) of progenitor cell subsets (CD34+, CD34+CD45dim, CD34+CD133+), showing that cardiorespiratory fitness influences the magnitude of progenitor cell mobilisation into the blood and subsequent extravasation. These data may provide a link between high levels of cardiorespiratory fitness and vascular health. What is the central question of the study? Is the magnitude of progenitor cell trafficking into and out of the blood with a vigorous bout of exercise influenced by cardiorespiratory fitness? What is the main finding and its importance? Acute vigorous exercise bouts mobilise pan‐progenitor cells and their sub‐populations into blood, including endothelial progenitor cells, which subsequently extravasate to peripheral tissues post‐exercise. The magnitude of this response is strongly associated with cardiorespiratory fitness. Importantly, this finding identifies possible mechanisms underlying associations between an active lifestyle and endothelial health.

The determinants of telomere attrition, a potential marker of cellular aging, are not well understood. Persistent herpesvirus infections including cytomegalovirus (CMV) infection may be particularly important for telomere dynamics via mechanisms such as inflammation, oxidative stress, and their impact on peripheral blood lymphocyte composition. This study examined the association of 4 human herpesviruses (CMV, herpes simplex virus type 1, human herpesvirus type 6, and Epstein-Barr virus) with change in leukocyte telomere length (LTL) over 3 years in 400 healthy individuals (aged 53–76 years) from the Whitehall II cohort. CMV, herpes simplex virus type 1, and human herpesvirus 6 infection were independently associated with greater 3-year LTL attrition, with no association found for Epstein-Barr virus. The magnitudes of these associations were large, for example, the equivalent of almost 12 years of chronological age for those CMV seropositive. Seropositivity to more herpesviruses was additively associated with greater LTL attrition (3 herpesviruses vs none, β = −0.07 and P = .02; 4 infections vs none, β = −0.14 and P < .001). Higher immunoglobulin G antibody levels among those seropositive to CMV were also associated with shorter LTL at follow-up. These associations were robust to adjustment for age, sex, employment grade, body mass index, and smoking status. These results suggest that exposure to infectious agents should be an important consideration in future studies of telomere dynamics.

30 to 60% of the acute hospitalized older adults experience functional decline after hospitalization. The first signs of functional decline after discharge can often be observed in the inability to perform mobility tasks, such as raising from a chair or walking. Information how mobility develops over time is scarce. Insight in the course of mobility is needed to prevent and decrease mobility limitations. The objectives of this study were to determine (i) the course of mobility of acute hospitalized older adults and (ii) the association between muscle strength and the course of mobility over time controlled for influencing factors. In a multicenter, prospective, observational cohort study, measurements were taken at admission, discharge, one- and three months post-discharge. Mobility was assessed by the De Morton Mobility Index (DEMMI) and muscle strength by the JAMAR. The longitudinal association between muscle strength and mobility was analysed with a Linear Mixed Model and controlled for potential confounders. 391 older adults were included in the analytic sample with a mean (SD) age of 79.6 (6.7) years. Mobility improved significantly from admission up to three months post-discharge but did not reach normative levels. Muscle strength was associated with the course of mobility (beta = 0.64; p<0.01), even after controlling for factors as age, cognitive impairment, fear of falling and depressive symptoms (beta = 0.35; p<0.01). Muscle strength is longitudinally associated with mobility. Interventions to improve mobility including muscle strength are warranted, in acute hospitalized older adults.

Ambivalence in social interactions has been linked to health-related outcomes in private relationships and recent research has started to expand this evidence to ambivalent leadership at the workplace by showing that ambivalent supervisor-employee relationships are related to higher stress levels in employees. However, the mental health consequences of ambivalent leadership have not been examined yet. Using a multilevel approach, this study estimated associations of ambivalent leadership with mental health indicators (depression, anxiety, vital exhaustion, fatigue) in 993 employees from 27 work groups. A total effect of ambivalent leadership was found for all four mental health measures, as well as within-group and between-group effects. The consistent relationships of ambivalent leadership with higher symptoms of mental ill-health at the individual- (i.e., within-group) and the group-level (i.e., between-group) support the existence of an un-confounded association, as well as group effects of collective ambivalence.

Background: There is consistent evidence showing an interplay between psychological processes and immune function in health and disease processes. Objectives: The present systematic review and meta-analysis aims to provide a concise overview of the effectiveness of stress-reducing psychological interventions on the activation of immune responses in both healthy subjects and patients. Methods: Included are 3 types of challenges: in vivo, in vitro, and psychophysiological. Such challenges are designed to mimic naturally occurring immune-related threats. Results: A systematic literature search was conducted using PubMed, EMBASE, and PsychInfo, resulting in 75 eligible studies. The risk of bias was assessed with the Cochrane risk-of-bias tool. Across all studies, a small-to-medium effect size was found for the effects of psychological interventions on optimization of the immune function (g = 0.33; 95% CI 0.22–0.43). While the largest effects were found for in vivo immune-related challenges (g = 0.61; 95% CI 0.34–0.88; especially on studies that incorporated skin tests and wound healing), studies incorporating psychophysiological challenges and in vitro immune-related stimulations similarly suggest more optimal immune responses among those receiving stress-reducing interventions (g = 0.28; 95% CI 0.15–0.42). Conclusion: These findings showed substantial heterogeneity depending on the type of challenge, the study populations, and the intervention types. These data demonstrate support for the effectiveness of stress-reducing psychological interventions in improving immunity in studies that tested immune function by means of incorporating an in vivo,in vitro, or psychophysiological challenge. Future research should more consistently incorporate challenges into the study design to gather more insights in the mechanisms underlying the optimized immune function following a psychological intervention. This is also relevant for clinical practice, as psychological interventions can possibly supplement, or at least partially replace, current drug treatments in various somatic conditions to reduce side effects.

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a chronic disorder characterized by disabling fatigue. Several studies have sought to identify diagnostic biomarkers, with varying results. Here, we innovate this process by combining both mRNA expression and DNA methylation data. We performed recursive ensemble feature selection (REFS) on publicly available mRNA expression data in peripheral blood mononuclear cells (PBMCs) of 93 ME/CFS patients and 25 healthy controls, and found a signature of 23 genes capable of distinguishing cases and controls. REFS highly outperformed other methods, with an AUC of 0.92. We validated the results on a different platform (AUC of 0.95) and in DNA methylation data obtained from four public studies on ME/CFS (99 patients and 50 controls), identifying 48 gene-associated CpGs that predicted disease status as well (AUC of 0.97). Finally, ten of the 23 genes could be interpreted in the context of the derailed immune system of ME/CFS.