Current understanding of the bi-directional relationship of major depression with inflammation

Consistent evidence links major depression and its affective components to negative health outcomes. Although the pathways of these effects are likely complex and multifactorial, recent evidence suggests that innate inflammatory processes may play a role. An overview of current literature suggests that pathways between negative moods and inflammation are bi-directional. Indeed, negative moods activate peripheral physiologic mechanisms that result in an up regulation of systemic levels of inflammation. Conversely, peripheral inflammatory mediators signal the brain to affect behavioral, affective and cognitive changes that are consistent with symptoms of major depressive disorder. It is likely that these pathways are part of a complex feedback loop that involves the nervous, endocrine, and immune systems and plays a role in the modulation of peripheral inflammatory responses to central and peripheral stimuli, in central responses to peripheral immune activation and in the maintenance of homeostatic balance. Further research is warranted to fully understand the role of central processes in this feedback loop, which likely contributes to the pathophysiology of mental and physical health

Trait positive and negative emotionality differentially associate withdiurnal cortisol activity

Inter-individual variability in metrics of hypothalamic-pituitary-adrenocortical (HPA) activity, such asthe slope of the diurnal decline in cortisol, cortisol awakening response (CAR), and total cortisol out-put, have been found to associate inversely with trait ratings of extraversion and positive affect (E/PA)and positively with neuroticism and negative affect (N/NA) in some, but not all, investigations. Theseinconsistencies may partly reflect varied intensity of cortisol sampling among studies and reliance onself-rated traits, which are subject to reporting biases and limitations of introspection. Here, we furtherexamined dispositional correlates of HPA activity in 490 healthy, employed midlife volunteers (M age = 43years; 54% Female; 86% white). Trait ratings were requested from participants and 2 participant-electedinformants using the Positive and Negative Affect Schedule (PANAS) and Extraversion and Neuroticismdimensions of NEO personality inventories. CAR was assessed as percent increase in cortisol levels fromawakening to 30 min after awakening; and the diurnal slope and total output of cortisol [Area Underthe Curve (AUC)] were determined from cortisol measurements taken at awakening, +4 and +9 h later,and bedtime, across 3 workdays. Structural equation modeling was used to estimate multi-informantE/PA and N/NA factors. We used 3 days of measurement as indicators to model each of the three latentcortisol factors (slope, CAR, and AUC). With the two latent emotionality and three latent cortisol indicesincluded there was good fit to the data ( 2(200)= 278.38, p = 0.0002; RMSEA = 0.028, 90% CI = 0.02–0.04;CFI/TLI = 0.97/0.96; SRMR = 0.04). After controlling for covariates (age, sex, race), results showed higherlatent E/PA associated with a steeper diurnal slope (Standardized ˇ = −0.19, p = 0.02) and smaller CAR(Standardized ˇ = −0.26, p = 0.004), whereas N/NA did not associate with any cortisol metric (Standard-ized ˇ’s = −0.12 to 0.13, p’s = 0.10 to 0.53). These findings suggest that positive emotionality may be moreclosely associated with indices of diurnal cortisol release than negative emotionality

Trait positive and negative emotionality differentially associate withdiurnal cortisol activity

Inter-individual variability in metrics of hypothalamic-pituitary-adrenocortical (HPA) activity, such asthe slope of the diurnal decline in cortisol, cortisol awakening response (CAR), and total cortisol out-put, have been found to associate inversely with trait ratings of extraversion and positive affect (E/PA)and positively with neuroticism and negative affect (N/NA) in some, but not all, investigations. Theseinconsistencies may partly reflect varied intensity of cortisol sampling among studies and reliance onself-rated traits, which are subject to reporting biases and limitations of introspection. Here, we furtherexamined dispositional correlates of HPA activity in 490 healthy, employed midlife volunteers (M age = 43years; 54% Female; 86% white). Trait ratings were requested from participants and 2 participant-electedinformants using the Positive and Negative Affect Schedule (PANAS) and Extraversion and Neuroticismdimensions of NEO personality inventories. CAR was assessed as percent increase in cortisol levels fromawakening to 30 min after awakening; and the diurnal slope and total output of cortisol [Area Underthe Curve (AUC)] were determined from cortisol measurements taken at awakening, +4 and +9 h later,and bedtime, across 3 workdays. Structural equation modeling was used to estimate multi-informantE/PA and N/NA factors. We used 3 days of measurement as indicators to model each of the three latentcortisol factors (slope, CAR, and AUC). With the two latent emotionality and three latent cortisol indicesincluded there was good fit to the data ( 2(200)= 278.38, p = 0.0002; RMSEA = 0.028, 90% CI = 0.02–0.04;CFI/TLI = 0.97/0.96; SRMR = 0.04). After controlling for covariates (age, sex, race), results showed higherlatent E/PA associated with a steeper diurnal slope (Standardized ˇ = −0.19, p = 0.02) and smaller CAR(Standardized ˇ = −0.26, p = 0.004), whereas N/NA did not associate with any cortisol metric (Standard-ized ˇ’s = −0.12 to 0.13, p’s = 0.10 to 0.53). These findings suggest that positive emotionality may be moreclosely associated with indices of diurnal cortisol release than negative emotionality

Changes in stress pathways as a possible mechanism of aerobic exercise training on brain health: a scoping review of existing studies

Physical activity (PA) in the form of aerobic exercise (AE) preserves and improves neurocognitive function across the lifespan. However, a mechanistic understanding of the pathways by which aerobic exercise impacts brain health is still lacking, particularly with respect to stress-related pathways. One mechanistic hypothesis is that AE improves neurocognitive health in part by modifying circulating levels of stress-related hormones and signaling factors associated with the hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system (ANS), as commonly measured by the biomarkers cortisol (CORT) and salivary α-amylase (sAA). Thus, this hypothesis predicts that changes in stress biomarkers, such as CORT and sAA, are possible explanatory pathways mediating the positive effects of AE on neurocognitive health. In the present review article, we provide a summary of available studies examining the possibility that exercise-induced changes to stress biomarkers could partly account for exercise-related improvements in neurocognitive health. Our review indicates that despite the intuitive appeal of this hypothesis, there is insufficient evidence available to conclude that chronic and habitual AE affects neurocognitive health by altering stress biomarker pathways. The cross-sectional nature of the majority of reviewed studies highlights the need for well-controlled studies to adequately test this hypothesis

Psychology Meets Biology in COVID-19: What We Know and Why It Matters for Public Health

Psychosocial factors are related to immune, viral, and vaccination outcomes. Yet, this knowledge has been poorly represented in public health initiatives during the COVID-19 pandemic. This review provides an overview of biopsychosocial links relevant to COVID-19 outcomes by describing seminal evidence about these associations known prepandemic as well as contemporary research conducted during the pandemic. This focuses on the negative impact of the pandemic on psychosocial health and how this in turn has likely consequences for critically relevant viral and vaccination outcomes. We end by looking forward, highlighting the potential of psychosocial interventions that could be leveraged to support all people in navigating a postpandemic world and how a biopsychosocial approach to health could be incorporated into public health responses to future pandemics

Brain iron accumulation in unexplained fetal and infant death victims with smoker mothers-The possible involvement of maternal methemoglobinemia

<p>Abstract</p> <p>Background</p> <p>Iron is involved in important vital functions as an essential component of the oxygen-transporting heme mechanism. In this study we aimed to evaluate whether oxidative metabolites from maternal cigarette smoke could affect iron homeostasis in the brain of victims of sudden unexplained fetal and infant death, maybe through the induction of maternal hemoglobin damage, such as in case of methemoglobinemia.</p> <p>Methods</p> <p>Histochemical investigations by Prussian blue reaction were made on brain nonheme ferric iron deposits, gaining detailed data on their localization in the brainstem and cerebellum of victims of sudden death and controls. The Gless and Marsland's modification of Bielschowsky's was used to identify neuronal cell bodies and neurofilaments.</p> <p>Results</p> <p>Our approach highlighted accumulations of blue granulations, indicative of iron positive reactions, in the brainstem and cerebellum of 33% of victims of sudden death and in none of the control group. The modified Bielschowsky's method confirmed that the cells with iron accumulations were neuronal cells.</p> <p>Conclusions</p> <p>We propose that the free iron deposition in the brain of sudden fetal and infant death victims could be a catabolic product of maternal methemoglobinemia, a biomarker of oxidative stress likely due to nicotine absorption.</p

North Atlantic simulations in Coordinated Ocean-ice Reference Experiments phase II (CORE-II). Part I: Mean states

Simulation characteristics from eighteen global ocean–sea-ice coupled models are presented with a focus on the mean Atlantic meridional overturning circulation (AMOC) and other related fields in the North Atlantic. These experiments use inter-annually varying atmospheric forcing data sets for the 60-year period from 1948 to 2007 and are performed as contributions to the second phase of the Coordinated Ocean-ice Reference Experiments (CORE-II). The protocol for conducting such CORE-II experiments is summarized. Despite using the same atmospheric forcing, the solutions show significant differences. As most models also differ from available observations, biases in the Labrador Sea region in upper-ocean potential temperature and salinity distributions, mixed layer depths, and sea-ice cover are identified as contributors to differences in AMOC. These differences in the solutions do not suggest an obvious grouping of the models based on their ocean model lineage, their vertical coordinate representations, or surface salinity restoring strengths. Thus, the solution differences among the models are attributed primarily to use of different subgrid scale parameterizations and parameter choices as well as to differences in vertical and horizontal grid resolutions in the ocean models. Use of a wide variety of sea-ice models with diverse snow and sea-ice albedo treatments also contributes to these differences. Based on the diagnostics considered, the majority of the models appear suitable for use in studies involving the North Atlantic, but some models require dedicated development effort

Impact of childhood cancer on emerging adult survivors\u27 romantic relationships: a qualitative account

ix, 69 hlm. : 23,5 c