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DISCLAIMER: In an effort to expedite the publication of articles, AJHP is posting manuscripts online as soon as possible after acceptance. Accepted manuscripts have been peer-reviewed and copyedited, but are posted online before technical formatting and author proofing. These manuscripts are not the final version of record and will be replaced with the final article (formatted per AJHP style and proofed by the authors) at a later time. PURPOSE: Impella microaxial ventricular assist devices require a dextrose-based purge solution in combination with heparin or sodium bicarbonate to prevent device dysfunction and stoppage, but the dextrose in these solutions can interfere with positron emission tomography (PET) scans, necessitating an alternative approach. SUMMARY: We describe the short-term use in 2 cases of an alternative purge solution for patients with an Impella 5.5 ventricular assist device undergoing PET scans to rule out infection and malignancy. Sodium chloride solutions cannot be used with Impella ventricular assist devices even for short periods of time due to the potential for motor corrosion. We therefore selected a sterile water-based sodium bicarbonate purge solution, incorporating a short dextrose-free period before and during the PET scan. Imaging was successfully performed with this alternative solution, with monitoring of Impella performance levels and purge parameters throughout the procedure indicating no adverse effects on pump function. CONCLUSION: Our sterile water-based purge solution coupled with short-term restriction of dextrose is a practical option for PET imaging in patients with a Pella ventricular assist device.
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Women are at higher risk than men for developing posttraumatic stress disorder (PTSD), but underlying mechanisms are still unclear. Comprehensive knowledge about these mechanisms is necessary to develop tailored, sex- and gender-sensitive preventive interventions. This systematic review and meta-analysis examined sex-/gender-dependent risk factors, that is, risk factors with sex/gender differences in (a) vulnerability or (b) prevalence/severity, as well as sex-/gender-specific risk factors, that is, and (c) risk factors present in one sex/gender only. We searched PubMed, Web of Science, PsycINFO, PsycArticles, and PSYNDEX for articles published until October 16, 2022. We included prospective studies that assessed risk factors to predict subsequent PTSD symptom severity, as measured with the Clinician-Administered PTSD scale. The primary outcomes were sex/gender stratified pooled for sex-/gender-dependent vulnerability and sex-/gender-specific risk factors and pooled odds ratio (OR) or standardized mean difference (SMD) for sex-/gender-dependent risk factor prevalence/severity. We screened 17,270 records and included 117 reports from 45 studies (N = 13,752) in the systematic review. Seventeen studies (N = 4,257; 1,827 women, 2,430 men) were included in the meta-analysis. Regarding risk factor vulnerability, analyses revealed no significant sex/gender differences except for acute stress symptoms, with stronger associations for men (b = 0.11, SE = 0.06, p < .05). Regarding risk factor prevalence/severity, women reported more severe immediate psychological stress responses (range SMD = 0.23-0.56) and more commonly had a history of mental illness (OR = 1.81, 1.27-2.58). Men showed higher trauma load (SMD = -0.15, -0.29 to 0.01). Few women-specific and no men-specific factors were identified. Results suggest that women's heightened immediate psychological stress response drives sex/gender disparities in PTSD symptom severity. Preventive interventions should thus target women early after trauma. (PsycInfo Database Record (c) 2024 APA, all rights reserved).
Subject(s)
Stress Disorders, Post-Traumatic , Humans , Stress Disorders, Post-Traumatic/epidemiology , Stress Disorders, Post-Traumatic/psychology , Risk Factors , Female , Male , Sex Factors , Prospective Studies , PrevalenceABSTRACT
Women and men are at different risk for posttraumatic stress disorder (PTSD). It is unclear, however, how studies on PTSD risk factors integrate this knowledge into their research. Moreover, the temporal development of women's higher PTSD risk is unknown. In this systematic review and meta-analysis, we examine how prospective studies on PTSD development (k = 47) consider sex and gender across four domains (samples, terminology, analyses, and reporting). Further, we differentially analyze sex/gender differences within five time intervals from 1 month to 5 years posttrauma. PTSD prevalence (OR = 1.72 [1.27-2.34]) and severity (g = 0.31 [0.09, 0.53]) were increased for women relative to men at 1 month posttrauma already, that is, at the first timepoint of a possible PTSD diagnosis. PTSD severity was elevated for women compared to men across all time intervals, but evidence for increased PTSD prevalence for women relative to men was less stable with longer follow-ups. Despite women's higher PTSD burdens, they were clearly underrepresented in samples (68.3% male, 31.7% female participants). Only 5.0% of studies explained or described their understanding of sex and gender, and only 2.6% used sex as discovery variable, that is, investigating sex-dependent risk mechanisms. Sex and gender aspects in design, data, and discussion were considered by only one-third of studies each. Trauma research falls short of its potential to adequately consider sex and gender. Sex- and gender-sensitive practices can advance rigor, innovation, and equity in psychopathology research. (PsycInfo Database Record (c) 2024 APA, all rights reserved).
Subject(s)
Stress Disorders, Post-Traumatic , Humans , Stress Disorders, Post-Traumatic/epidemiology , Stress Disorders, Post-Traumatic/psychology , Male , Female , Sex Factors , Risk Factors , Prevalence , Psychological Trauma/epidemiology , Psychological Trauma/psychologyABSTRACT
BACKGROUND: Menstrual cycle regularity is an important marker of reproductive health and associated with physiological and psychological illnesses, as well as experiencing stress. We hypothesized that individuals with irregular menstrual cycles report higher depressive symptom severity, after controlling for stress occurrence. METHODS: The hypothesis was examined through two measurement approaches: a cross-sectional and a prospective, longitudinal study. In the cross-sectional study, participants (n = 394) reported depressive symptoms and their overall menstrual cycle regularity. In the longitudinal study, participants (n = 77) completed questionnaires on depressive symptoms and stress during the mid-follicular and periovulatory phase of one menstrual cycle. Depressive symptoms were compared between participants with regular and irregular cycles through a Welch t test and an ANCOVA. RESULTS: Participants with irregular menstrual cycles reported more depressive symptoms in the cross-sectional analysis. Similarly, in the longitudinal analysis, the group with a current irregular menstrual cycle reported more depressive symptoms after controlling for stress occurrence. When including only complete data sets without multiple imputation (n = 52), the direction of the effects remained but did not reach statistical significance. CONCLUSIONS: The results indicate an association between depressive symptoms and menstrual cycle irregularity. Limitations were that although we investigated the menstrual cycle prospectively, it would have been more precise to include two or more cycles and daily sex hormone measurements. Further limitations were the suboptimal statistical power and the data collection during the COVID pandemic. We give recommendations on how to incorporate the association of depressive symptoms and cycle irregularity in future study designs on women's mental health.
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Mitochondrial function plays an important role in the maintenance of male fertility. However, the mechanisms underlying mitochondrial defect-related infertility remain mostly unclear. Here we show that a deficiency of PARL (Parl-/-), a mitochondrial protease, causes complete arrest of spermatogenesis during meiosis I. PARL deficiency led to severe downregulation of proteins of respiratory chain complex IV in testes that did not occur in other tested organs, causing a deficit in complex IV activity and ATP production. Furthermore, Parl-/- testes showed an almost complete loss of HSD17B3, a protein of the sER responsible for the last step in testosterone synthesis. While testosterone production appeared to be restored by overexpression of HSD17B12, loss of the canonical testosterone synthesis led to an upregulation of luteinizing hormone (LH) and of LH-regulated responses. These results suggest an important impact of the downstream regulation of mitochondrial defects that manifest in a cell-type-specific manner and extend beyond mitochondria.
Subject(s)
Endopeptidases , Metalloproteases , Mitochondrial Proteins , Humans , Male , Mitochondria/genetics , Peptide Hydrolases , Spermatogenesis/genetics , Testosterone , Mitochondrial Proteins/genetics , Mitochondrial Proteins/metabolism , Metalloproteases/genetics , Metalloproteases/metabolismABSTRACT
A specific genetic variant associated with atrial fibrillation risk, rs17171731, was identified as a regulatory variant responsible for controlling FAM13B expression. The atrial fibrillation risk allele decreases FAM13B expression, whose knockdown alters the expression of many genes in stem cell-derived cardiomyocytes, including SCN2B, and led to pro-arrhythmogenic changes in the late sodium current and Ca2+ cycling. Fam13b knockout mice had increased P-wave and QT interval duration and were more susceptible to pacing-induced arrhythmias vs control mice. FAM13B expression, its regulation, and downstream effects are potential targets for investigation of patient-specific therapeutics.
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INTRODUCTION: Elevated levels of the hypothalamic-pituitary-adrenal axis hormone cortisol are a frequently replicated finding in major depressive disorder (MDD). However, the current state of research is inconclusive as to whether hypercortisolism represents a trait- or state-like biological signal of MDD. The aim of the present study was to investigate, for the first time, whether cortisol in fingernails, a highly accessible tissue, could distinguish currently remitted individuals with MDD from healthy controls. A further aim was to identify potential confounders of nail cortisol. METHODS: A total of N = 100 individuals from the general population were recruited. A structured clinical interview was administered, which resulted in two groups: n = 48 with lifetime MDD and n = 52 healthy controls. All participants answered questions on sociodemographic, lifestyle, and psychosocial characteristics. They also grew their nails for 14 days and cut them for the subsequent determination of cortisol. RESULTS: The groups differed in their nail cortisol concentrations, such that the individuals with lifetime MDD had significantly higher concentrations than the healthy controls (p = 0.041). Within the group of individuals with lifetime MDD, the number of experienced episodes was significantly correlated with cortisol (p = 0.011). Income emerged as the only significant confounder of cortisol (p = 0.008). CONCLUSION: Elevated fingernail cortisol appears to be a biological signal of MDD, even in the absence of a current major depressive episode. Its high accessibility and robustness render it a promising methodology for remote research as well as for the integration of biomarkers into clinical research and practice.
Subject(s)
Depressive Disorder, Major , Hydrocortisone , Humans , Depressive Disorder, Major/psychology , Nails , Hypothalamo-Hypophyseal System , Pituitary-Adrenal SystemABSTRACT
Obesity and metabolic disorders are increasing in epidemic proportions, leading to poor outcomes including heart failure. With a growing recognition of the effect of adipose tissue dysfunction on heart disease, it is less well understood how the heart can influence systemic metabolic homeostasis. Even less well understood is sex differences in cardiometabolic responses. Previously, our lab investigated the role of the amino-terminus of GRK2 in cardiometabolic remodeling using transgenic mice with cardiac restricted expression of a short peptide, ßARKnt. Male mice preserved insulin sensitivity, enhanced metabolic flexibility and adipose tissue health, elicited cardioprotection, and improved cardiac metabolic signaling. To examine the effect of cardiac ßARKnt expression on cardiac and metabolic function in females in response to diet-induced obesity, we subjected female mice to high fat diet (HFD) to trigger cardiac and metabolic adaptive changes. Despite equivalent weight gain, ßARKnt mice exhibited improved glucose tolerance and insulin sensitivity. However, ßARKnt mice displayed a progressive reduction in energy expenditure during cold challenge after acute and chronic HFD stress. They also demonstrated reduced cardiac function and increased markers of maladaptive remodeling and tissue injury, and decreased or aberrant metabolic signaling. ßARKnt mice exhibited reduced lipid deposition in the brown adipose tissue (BAT), but delayed or decreased markers of BAT activation and function suggested multiple mechanisms contributed to the decreased thermogenic capacity. These data suggest a non-canonical cardiac regulation of BAT lipolysis and function that highlights the need for studies elucidating the mechanisms of sex-specific responses to metabolic dysfunction.
Subject(s)
Cardiovascular Diseases , Insulin Resistance , Female , Male , Mice , Animals , Adipose Tissue, Brown/metabolism , Obesity/etiology , Obesity/metabolism , Diet, High-Fat/adverse effects , Mice, Transgenic , Cardiovascular Diseases/metabolism , Energy Metabolism , Thermogenesis , Mice, Inbred C57BLABSTRACT
The COVID-19 pandemic has been negatively associated with mental health. However, little is known about the temporal dynamics of mental health in the longer term of the pandemic. We aimed to investigate symptom levels and changes of depression, anxiety, posttraumatic stress, and loneliness spanning two years of the pandemic; and to examine associated risk factors. This five-wave, longitudinal online study from May 2020 to April 2022 included 636 adults (Mage = 39.5 years, SD = 16.11; 84.1% female) from the German general population who completed the international COVID-19 Mental Health Survey. Symptoms of anxiety (Generalized Anxiety Disorder-7; GAD-7), depression (Patient Health Questionnaire-9; PHQ-9), posttraumatic stress (PTSD Checklist for DSM-5; PCL-5), and loneliness ("Do you feel lonely?") were assessed using mixed-effects models. Associations with anxiety and depressive symptoms were examined with having children, student status, financial worries, contamination fear, and loneliness. PHQ-9, GAD-7, PCL-5, and loneliness scores overall decreased throughout the two-year period of the pandemic but exhibited an increase during two national lockdowns. Controlled for significant associations with female gender and younger age, increased PHQ-9 and GAD-7 scores were associated with contamination fear, financial worries, and loneliness. No associations were found with having children and student status. Symptoms of depression, anxiety, posttraumatic stress, and loneliness decreased over time but varied along with the dynamics of the pandemic. Longitudinal monitoring of mental health in vulnerable subgroups is required, especially those of younger age, females, and the financially insecure.
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Background: Pre-and post-traumatic hypothalamic-pituitary-adrenal (HPA) axis markers have been studied to predict posttraumatic stress disorder (PTSD) risk, but its acute reactivity cannot be measured in real-life settings. Experimental paradigms can depict the cortisol response to stimuli that simulate traumatic events.Objective: To review experimental studies on the cortisol response to traumatic stimuli and the correlation between cortisol and PTSD symptoms.Method: Experimental, (un-)published studies in German or English from any year were eligible if they confronted non-traumatized humans with traumatic stimuli, assessed cortisol before, during or after stimulus presentation and subsequent PTSD symptoms. The literature was searched via PubMed, PubPsych, PsychINFO, PsycArticle, Web of Science, EMBASE, ProQuest and ClinicalTrials.gov up to 16th February 2021. Risk of bias was assessed with the Cortisol Assessment List. Multilevel-meta-analyses were conducted under the random effects model. The standardized mean change (dSMC) indicated the cortisol response. Coefficient r indicated the correlations between cortisol and PTSD symptoms.Results: 14 studies, investigating 1004 individuals, were included. A cortisol response was successfully induced between 21 and 40â min post-presentation onset (kobservations = 25, dSMC = 0.15 [.03; .26]). Cortisol was not associated with overall or cluster-level PTSD symptoms. On a symptom-level, higher pre-presentation onset cortisol was correlated with lower state tension (k = 8, r = -.18 [-.35; -.01]), higher state happiness (k = 8, r = -.34 [-.59; -.03], variable inverted) and lower state anger (k = 9, r = -.14 [-.26; -.01]). Higher post-presentation onset cortisol was correlated with higher state happiness (k = 16, r = -.20 [-.33; -.06]) and lower state sadness (k = 17, r = -.16 [-.25; -.05]), whereas cortisol response was positively correlated with state anxiety (k = 9, r = .16 [0.04; 0.27]).Conclusions: Experimental paradigms effectively induce a cortisol response. Higher basal cortisol, higher cortisol, as measured after traumatic stimulus presentation, and a lower cortisol response were associated with more adaptive emotional reactions. These markers did not predict longer-term PTSD symptoms.
Experimental trauma paradigms successfully induced a cortisol response.Cortisol was predictive for single state, emotion-related symptoms, but not overall PTSD symptoms.Trauma paradigms shed light into the immediate post-trauma period that is hard to capture in real life, but the gap between experimental and naturalistic settings is difficult to overcome.
Subject(s)
Stress Disorders, Post-Traumatic , Humans , Stress Disorders, Post-Traumatic/diagnosis , Stress Disorders, Post-Traumatic/psychology , Hydrocortisone/analysis , Pituitary-Adrenal System/chemistry , Anxiety Disorders , AnxietyABSTRACT
Sex disparities are evident in the biological response to acute stressors, with a suggested influence of ovarian hormones on hypothalamic-pituitary-adrenal (HPA) axis functioning. This systematic review and meta-analysis investigates differences in HPA axis reactivity to acute psychosocial or physiological stressors between menstrual cycle phases. A systematic literature search of six databases resulted in 12 longitudinal studies (n = 182) examining HPA axis reactivity in healthy, naturally-cycling, non-breastfeeding participants aged between 18 and 45 years in at least two cycle phases. The quality of cortisol and menstrual cycle assessment was rated and a descriptive synthesis and meta-analysis of HPA axis reactivity between two broader and five more precise cycle phases was conducted. Three studies provided sufficient data for the meta-analysis and showed a significant, small-sized effect, indicating higher cortisol reactivity in the luteal than in the follicular cycle phase. More primary studies with high-quality menstrual cycle and cortisol assessment are needed. The review did not receive funding and was pre-registered (PROSPERO; CRD42020181632).
Subject(s)
Hydrocortisone , Hypothalamo-Hypophyseal System , Female , Humans , Adolescent , Young Adult , Adult , Middle Aged , Hypothalamo-Hypophyseal System/physiology , Pituitary-Adrenal System/physiology , Stress, Psychological/psychology , Menstrual Cycle/physiologyABSTRACT
INTRODUCTION: Psychotherapeutic interventions for major depressive disorder (MDD) have been suggested to be associated with a normalization of biological stress system (i.e., the hypothalamic-pituitary-adrenal axis and the autonomic nervous system) dysregulation. Furthermore, pre-intervention cortisol parameters have been identified as prescriptive biological markers of treatment success. However, evidence of treatment effects on the biological stress systems is still sparse, and results are heterogeneous. The current study examined the effect of an internet-based intervention for MDD on salivary cortisol and alpha-amylase as well as hair cortisol concentrations. Moreover, the prescriptive capacity of pre-intervention cortisol and alpha-amylase concentrations on treatment response was explored. METHODS: Thirty-eight participants suffering from mild to moderate MDD collected saliva and hair samples throughout the intervention. Biological outcome parameters were salivary cortisol and alpha-amylase (awakening response, total diurnal output, diurnal slope) and hair cortisol concentrations. Treatment response was indicated by change in depression severity and perceived chronic stress. RESULTS: Treatment response on depression scores or chronic stress was not associated with changes in any of the cortisol or alpha-amylase parameters. Exploratory analysis indicated that non-responders showed a steeper alpha-amylase slope pre-intervention. DISCUSSION: The results indicate that changes in depressive symptoms did not correspond to changes of the biological stress systems, contradicting the suggested normalization of dysregulated hypothalamic-pituitary-adrenal axis or autonomic nervous system activity through a psychotherapeutic intervention. However, the results point to a potential role of pre-intervention alpha-amylase slope as a prescriptive marker of treatment response for depression.
Subject(s)
Depressive Disorder, Major , Internet-Based Intervention , Humans , Hydrocortisone , alpha-Amylases/metabolism , Depressive Disorder, Major/therapy , Hypothalamo-Hypophyseal System/metabolism , Depression/therapy , Pituitary-Adrenal System/metabolism , Saliva/metabolism , Stress, Psychological/therapyABSTRACT
PURPOSE: ß-Adrenergic receptors (ßAR) are essential targets for the treatment of heart failure (HF); however, chronic use of ßAR agonists as positive inotropes to increase contractility in a Gs protein-dependent manner is associated with increased mortality. Alternatively, we previously reported that allosteric modulation of ß2AR with the pepducin intracellular loop (ICL)1-9 increased cardiomyocyte contractility in a ß-arrestin (ßarr)-dependent manner, and subsequently showed that ICL1-9 activates the Ras homolog family member A (RhoA). Here, we aimed to elucidate both the proximal and downstream signaling mediators involved in the promotion of cardiomyocyte contractility in response to ICL1-9. METHODS: We measured adult mouse cardiomyocyte contractility in response to ICL1-9 or isoproterenol (ISO, as a positive control) alone or in the presence of inhibitors of various potential components of ßarr- or RhoA-dependent signaling. We also assessed the contractile effects of ICL1-9 on cardiomyocytes lacking G protein-coupled receptor (GPCR) kinase 2 (GRK2) or 5 (GRK5). RESULTS: Consistent with RhoA activation by ICL1-9, both Rho-associated protein kinase (ROCK) and protein kinase D (PKD) inhibition were able to attenuate ICL1-9-mediated contractility, as was inhibition of myosin light chain kinase (MLCK). While neither GRK2 nor GRK5 deletion impacted ICL1-9-mediated contractility, pertussis toxin attenuated the response, suggesting that ICL1-9 promotes downstream RhoA-dependent signaling in a Gi protein-dependent manner. CONCLUSION: Altogether, our study highlights a novel signaling modality that may offer a new approach to the promotion, or preservation, of cardiac contractility during HF via the allosteric regulation of ß2AR to promote Gi protein/ßarr-dependent activation of RhoA/ROCK/PKD signaling.
Subject(s)
Heart Failure , Myocytes, Cardiac , Mice , Animals , Signal Transduction , Protein Kinase C/metabolism , Protein Kinase C/pharmacology , Heart Failure/metabolism , Myocardial ContractionABSTRACT
Biological markers, particularly endocrine measurements, are increasingly being integrated into clinical psychological research. We introduce a systematic framework that classifies different functions of such biomarkers. The framework distinguishes between diagnostic biomarkers which add a biological perspective to conventional clinical assessments, prognostic biomarkers that inform about an individual's risk to develop or maintain a mental health disorder, and intervention-related biomarkers. Regarding interventions, including prevention and treatment, it further distinguishes between prescriptive biomarkers which predict an individual's response to an intervention, outcome biomarkers which evaluate intervention-related changes on a biological level and indicators of change mechanisms. We demonstrate how to apply the framework by exemplarily classifying and describing previously published systematic reviews and primary empirical studies on endogenous, peripheral cortisol concentrations as a biomarker for posttraumatic stress disorder (PTSD). The evidence on cortisol's diagnostic and prognostic value is heterogeneous and still sparse regarding parameters based on multiple cortisol measurements, such as the cortisol awakening response. With regard to interventions, most research focused on trauma-focused psychotherapy and cortisol reactivity to trauma reminders. This field of research appears to be growing and very promising due to its potential to optimize PTSD-related interventions. The proposed framework can help in gaining a systematic overview of existing research. It can assist in structuring, comparing, summarizing and evaluating empirical studies, and in identifying research gaps.
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Heart disease remains the leading cause of death, and mortality rates positively correlate with the presence of obesity and diabetes. Despite the correlation between cardiac and metabolic dysregulation, the mechanistic pathway(s) of interorgan crosstalk still remain undefined. This study reveals that cardiac-restricted expression of an amino-terminal peptide of GRK2 (ßARKnt) preserves systemic and cardiac insulin responsiveness, and protects against adipocyte maladaptive hypertrophy in a diet-induced obesity model. These data suggest a cardiac-driven mechanism to ameliorate maladaptive cardiac remodeling and improve systemic metabolic homeostasis that may lead to new treatment modalities for cardioprotection in obesity and obesity-related metabolic syndromes.
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Background: The reliable assessment of cortisol is a necessary requirement to produce replicable research. Several recommendations to increase cortisol assessment reliability exist. However, cortisol assessment methodology is still rather heterogeneous. For this reason, the Cortisol Assessment List (CoAL) was created.The CoAL can be used to guide researchers during the planning phase and document which measures were taken to increase cortisol data reliability in original studies. Moreover, the CoAL can be used to evaluate data quality in meta research. The items representing strategies to obtain reliable cortisol data can be weighted to indicate which are absolutely necessary to consider and which could be applied less restrictively in order to balance data quality and feasibility. In this paper, the construction process of the CoAL is described. Methods: Item synthesis of the CoAL included a literature search to extract empirically based suggestions regarding the reliable assessment of cortisol. Estimates for the item weighting system were obtained by inviting experts in the field to participate in an online survey (n = 25). Inter-rater reliability (IRR) of the CoAL, was determined by letting independent raters use the CoAL to evaluate a set of randomly selected original studies (k = 90). Results: The CoAL was divided into four subscales related to the reporting of sampling procedures, the consideration of state covariates, trait covariates and exclusion criteria. Survey results indicated high agreement among experts for most items (89%) with approximately half of the items in the CoAL being classified as necessary (Cortisol Awakening Response (CAR): 52%; basal cortisol: 52%; reactive cortisol: 44%) in order to obtain reliable cortisol data. Inter-rater agreement was very high (Cohen's Kappa = .98 - 0.99), indicating sufficient psychometric quality of the CoAL. Discussion: The CoAL is the first tool to systematically plan, document and evaluate cortisol assessment. The survey results indicate that the majority of respondents are aware of essential requirements to increase data reliability. However, results were heterogeneous for some items, highlighting the need to start a process of developing a broad scientific consensus regarding reliable cortisol assessment. The implementation of the CoAL could be a first step in this direction. In conclusion, the CoAL reflects empirical evidence and expert knowledge regarding cortisol assessment and can be used as a flexible tool to plan and document empirical studies or evaluate cortisol data quality in meta research.
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Differential HPA axis function has been proposed to underlie sex-differences in mental disorders; however, the impact of fluctuating sex hormones across the menstrual cycle on HPA axis activity is still unclear. This meta-analysis investigated basal cortisol concentrations as a marker for HPA axis activity across the menstrual cycle. Through a systematic literature search of five databases, 121 longitudinal studies were included, summarizing data of 2641 healthy, cycling participants between the ages of 18 and 45. The meta-analysis showed higher cortisol concentrations in the follicular vs. luteal phase (dSMC = 0.12, p =.004, [0.04 - 0.20]). Comparisons between more precise cycle phases were mostly insignificant, aside from higher concentrations in the menstrual vs. premenstrual phase (dSMC = 0.17, [0.02 - 0.33], p =.03). In all included studies, nine samples used established cortisol parameters to indicate HPA axis function, specifically diurnal profiles (k = 4) and the cortisol awakening response (CAR) (k = 5). Therefore, the meta-analysis highlights the need for more rigorous investigation of HPA axis activity and menstrual cycle phase.
Subject(s)
Hydrocortisone , Hypothalamo-Hypophyseal System , Adolescent , Adult , Female , Humans , Hydrocortisone/analysis , Hypothalamo-Hypophyseal System/physiology , Menstrual Cycle/physiology , Middle Aged , Pituitary-Adrenal System/physiology , Saliva/chemistry , Young AdultABSTRACT
Dysregulated hypothalamic-pituitary-adrenal (HPA) axis functioning has been associated with posttraumatic stress disorder (PTSD). The current literature is inconsistent regarding this association, possibly due to confounding influences. Hair cortisol concentrations (HCC) allow for retrospective assessment of cumulative HPA axis secretion over several weeks and are considered a trait-like marker of HPA axis activity. Three groups of active and former German Armed Forces service members, comprising PTSD patients (n = 19), healthy controls with deployment-related trauma exposure (n = 10), and non-deployed healthy controls (n = 10) provided samples for HCC analysis. We observed significantly higher HCC in the PTSD and the deployed compared to the non-deployed group. HCC was neither significantly correlated with perceived chronic stress, nor with PTSD severity within patients. The results suggest a differential impact of trauma exposure on HPA axis activity and highlight the notion of cumulative, retrospective cortisol secretion as a psychobiological indicator of trauma exposure. TRIAL REGISTRATION: Australian Clinical Trials Registry (ACTRN12616000956404).
Subject(s)
Military Personnel , Stress Disorders, Post-Traumatic , Australia , Hair/chemistry , Humans , Hydrocortisone , Hypothalamo-Hypophyseal System , Pituitary-Adrenal System , Retrospective StudiesABSTRACT
BACKGROUND AND OBJECTIVES: Most eye tracking based paradigms evidence patterns of sustained attention on threat coupled with low evidence for vigilance to or avoidance of threat in posttraumatic stress symptoms (PTSS). Still, eye tracking data on attention bias is particularly limited for military population. This eye tracking study investigated attentional bias in PTSS in a sample of German Armed Forces veterans. METHODS: Veterans with deployment-related PTSS (N = 24), veterans with deployment-related traumatization without PTSS (N = 28), and never-deployed healthy veterans (N = 18) were presented with pairs of combat and neutral pictures, pairs of general threat and neutral pictures, and pairs of emotional and neutral faces. Their eye gazes were tracked during a free viewing task. 3 x 3 x 2 mixed general linear model analyses were conducted. Internal consistency of attention bias indicators was calculated for the entire sample and within groups. RESULTS: Veterans with PTSS dwelled longer on general threat AOIs in contrast to non-exposed controls and shorter on general threat and combat associated neutral AOIs in contrast to both control groups. Veterans with PTSS entered faster to general threat AOIs than non-exposed controls. Veterans with PTSS showed circumscribed higher attention fluctuation in contrast to controls. Internal consistency varied across attention bias indicators. LIMITATIONS: Statistical power was reduced due to recruitment difficulties. CONCLUSIONS: Evidence is provided for the maintenance hypothesis in PTSS. No robust evidence is provided for hypervigilant behavior in PTSS. Findings on attention bias variability remain unclear, calling for more investigations in this field.