The interaction of sleep and hormones on emotion functioning

Insufficient sleep has been associated with deficits in emotion processing; sleepy individuals show increased emotional reactivity and decreased emotion regulation. Individual differences that predict performance after sleep loss has remained largely elusive. Concentrations of cortisol, progesterone, and testosterone are candidate predictors for variability in performance following sleep loss. These hormones are associated with emotion functioning under well-rested conditions and show interactions with sleep and circadian rhythms. The central aim of this dissertation was to investigate the interaction of natural sleep and hormones on measures of emotion functioning. Study 1 examined the role of cortisol in the relationship between sleep (across the first three years of university), and self reported emotion functioning in undergraduate students. Poor sleep was associated with worse emotion regulation and reactivity, and greater concentrations of cortisol and cortisol/DHEA-S. Consistently poor sleepers over three years, who had high cortisol, experienced the greatest difficulties with emotion regulation. Study 2 investigated the association between sleep satisfaction and objective measures of sleep on self-reported emotional functioning in a group of children and adolescents. Importantly, in girls who were dissatisfied sleepers, being further though puberty was associated with the greatest difficulties with emotion regulation. Study 3 examined natural sleep, hormones, and menstrual phase on processing emotional stimuli. Participants completed sleep diaries and wore actigraphy watches for 3-weeks and completed measures of emotion perception on two occasions in the laboratory, in different menstrual phases for women. The study supported dynamic relationships between hormone concentrations and various measures of sleep duration and quality on the processing of emotion stimuli. Many relationships emerged for threatening emotions, indicating that high concentrations of testosterone, progesterone or cortisol, combined with poor sleep resulted in increased sensitivity towards threat detection. Together these studies provide evidence that hormones are an important factor in understanding the link between poor sleep and emotion functioning. Hormone concentration plays a role in understanding individual differences in response to sleep loss and can compound with sleep loss to result in worse emotional outcomes. Consideration of hormonal factors may help identify certain at-risk populations for sleep related deficits or timing of interventions

Diurnal preference and depressive symptomatology: A meta-analysis

Copyright © 2021 The Author(s). Eveningness, a preference for later sleep and rise times, has been associated with a number of negative outcomes in terms of both physical and mental health. A large body of evidence links eveningness to Major Depressive Disorder (MDD). However, to date, evidence quantifying this association is limited. The current meta-analysis included 43 effect sizes from a total 27,996 participants. Using a random-effects model it was demonstrated that eveningness is associated with a small effect size (Fisher’s Z = − 2.4, 95% CI [− 0.27. − 0.21], p < 0.001). Substantial heterogeneity between studies was observed, with meta-regression analyses demonstrating a significant effect of mean age on the association between diurnal preference and depression. There was also evidence of potential publication bias as assessed by visual inspection of funnel plots and Egger’s test. The association between diurnal preference and depression is small in magnitude and heterogenous. A better understanding of the mechanistic underpinnings linking diurnal preference to depression and suitably powered prospective studies that allow causal inference are required

It is Time for Context - Determinants of the Negative Bias in Emotion Recognition in Borderline Personality Disorder

Patients with Borderline Personality Disorder (BPD) suffer from severe emotion dysregulation, instable relationships, and tend to perceive their interaction partners as hostile and rejecting. Causal to these negative perceptions of others might be deficits in social cognition, in particular a negative bias in emotion recognition (i.e. the attribution of negative emotions to neutral or ambiguous facial expressions). However, until now, findings regarding such a negative bias are heterogeneous, and influencing factors of its occurrence are neither well-described, nor systematically examined. The aim of this dissertation was to investigate internal and external determinants, as well as the specificity of the negative bias in BPD. A behavioral study combining affective priming, emotion recognition and a manipulation of the available processing time in one paradigm was conducted with BPD patients, a healthy and a clinical control group of schizophrenia patients. The results support the existence of a negative bias in patients with BPD, and suggest that preceding emotional information, as well as available processing time are relevant factors for the occurrence of the negative bias. In addition, an association between the negative bias and emotion dysregulation was revealed in BPD. While schizophrenia patients showed a similar error pattern, the extent of negatively biased responses was not associated with emotion dysregulation, pointing to distinct mechanisms underlying the disturbed processing of facial expressions. Further, an adapted task of affective priming combined with emotion recognition was applied to healthy participants in a functional magnetic resonance imaging study. Increased activation due to negative preceding information was revealed in brain regions such as the amygdala, the superior temporal sulcus, and the nucleus accumbens. These areas have been previously found to be disturbed in patients with BPD and also in patients with schizophrenia. The results of this study suggest that the brain’s response to facial expressions is sensitive to interfering negative emotional information, possibly reflecting a vulnerability factor for the emergence of the negative bias. The findings of this dissertation fit well into existing literature of a negative bias in BPD and provide new insights into the mechanisms of disturbed emotion recognition. It was shown that processing time as well as context information influence emotion recognition. Further, the results indicate a specific association between emotion dysregulation and the negative bias in BPD

Progress in relationship between chronotype and technology addiction and its mechanism

In the era of digitalization, the Internet has changed people's lifestyle and circadian rhythm, and has also brought the global problem of technology addiction. Many studies have shown that chronotype is significantly related to specific technology addiction (such as Internet, smartphones, video games and social media), which makes chronotype become a new perspective to explore the occurrence, development and maintenance of technology addiction. Individuals can be classified into three chronotypes: morning type (M-type), neither type (N-type) and evening type (E-type). Most studies showed that E-type was the risk factor in the onset and maintenance of problematic technology use. At present, most of the prior research focused on the relationship between chronotype and technology addiction, and there were few studies on the mechanism. Based on this situation, this paper discusses physiological factors (such as reward system), psychological factors (such as depression), individual factors (such as gender, age, personality traits and sleep patterns) and environmental factors (such as parental style), analyzes the relationship with Interaction of Person-Affect-Cognition-Execution (I-PACE) model and life history theory from the perspectives of etiology and evolution, and reviews the relationship between chronotype and technology addiction and its mechanism

Activation of the pro-resolving receptor Fpr2 attenuates inflammatory microglial activation

Poster number: P-T099 Theme: Neurodegenerative disorders & ageing Activation of the pro-resolving receptor Fpr2 reverses inflammatory microglial activation Authors: Edward S Wickstead - Life Science & Technology University of Westminster/Queen Mary University of London Inflammation is a major contributor to many neurodegenerative disease (Heneka et al. 2015). Microglia, as the resident immune cells of the brain and spinal cord, provide the first line of immunological defence, but can become deleterious when chronically activated, triggering extensive neuronal damage (Cunningham, 2013). Dampening or even reversing this activation may provide neuronal protection against chronic inflammatory damage. The aim of this study was to determine whether lipopolysaccharide (LPS)-induced inflammation could be abrogated through activation of the receptor Fpr2, known to play an important role in peripheral inflammatory resolution. Immortalised murine microglia (BV2 cell line) were stimulated with LPS (50ng/ml) for 1 hour prior to the treatment with one of two Fpr2 ligands, either Cpd43 or Quin-C1 (both 100nM), and production of nitric oxide (NO), tumour necrosis factor alpha (TNFα) and interleukin-10 (IL-10) were monitored after 24h and 48h. Treatment with either Fpr2 ligand significantly suppressed LPS-induced production of NO or TNFα after both 24h and 48h exposure, moreover Fpr2 ligand treatment significantly enhanced production of IL-10 48h post-LPS treatment. As we have previously shown Fpr2 to be coupled to a number of intracellular signaling pathways (Cooray et al. 2013), we investigated potential signaling responses. Western blot analysis revealed no activation of ERK1/2, but identified a rapid and potent activation of p38 MAP kinase in BV2 microglia following stimulation with Fpr2 ligands. Together, these data indicate the possibility of exploiting immunomodulatory strategies for the treatment of neurological diseases, and highlight in particular the important potential of resolution mechanisms as novel therapeutic targets in neuroinflammation. References Cooray SN et al. (2013). Proc Natl Acad Sci U S A 110: 18232-7. Cunningham C (2013). Glia 61: 71-90. Heneka MT et al. (2015). Lancet Neurol 14: 388-40