Optimizing military mental health and stress resilience training through the lens of trainee preferences: A conjoint analysis approach.

Effective mental health and stress resilience (MHSR) training is essential in military populations given their exposure to operational stressors. The scarcity of empirical evidence supporting the benefits of these programs emphasizes the need for research dedicated to program optimization. This paper aims to identify the relative importance of MHSR training attributes preferred by military members. Conjoint analysis (CA), an experimental method used to prioritize end-user preferences for product feature development, was conducted using an online survey with 567 Canadian Armed Forces (CAF) personnel. Participants made a series of choices between hypothetical MHSR training options that were systematically varied across seven training attributes. Each training attribute consisted of 3-4 variations in the nature of the attribute or its intensity. Participants also completed questions on health beliefs, mental health and previous MHSR training experiences, and demographics, to assess whether preferences varied by individual characteristics. CA demonstrated that instructor type, leadership buy-in, degree of skills practice, and content relevance/applicability were attributes of highest and relatively equal importance. This was followed by degree of accessible supplemental content. Lowest importance was placed on degree of behavioral nudging and demographic similarity between the trainee and trainer. Sociodemographic factors were not associated with MHSR training preferences. Programs that incorporate expert-led instruction, demonstrate leadership buy-in, embed practical applications within simulated stress environments, and provide a digitally-accessible platform to augment training may be well-received among military members. Understanding and accommodating personal preferences when designing MHSR training programs may increase relevance, foster acceptance and trust, and support sustained engagement.

Exposure to moral stressors and associated outcomes in healthcare workers: prevalence, correlates, and impact on job attrition.

Introduction: Healthcare workers (HCWs) often experience morally challenging situations in their workplaces that may contribute to job turnover and compromised well-being. This study aimed to characterize the nature and frequency of moral stressors experienced by HCWs during the COVID-19 pandemic, examine their influence on psychosocial-spiritual factors, and capture the impact of such factors and related moral stressors on HCWs' self-reported job attrition intentions.Methods: A sample of 1204 Canadian HCWs were included in the analysis through a web-based survey platform whereby work-related factors (e.g. years spent working as HCW, providing care to COVID-19 patients), moral distress (captured by MMD-HP), moral injury (captured by MIOS), mental health symptomatology, and job turnover due to moral distress were assessed.Results: Moral stressors with the highest reported frequency and distress ratings included patient care requirements that exceeded the capacity HCWs felt safe/comfortable managing, reported lack of resource availability, and belief that administration was not addressing issues that compromised patient care. Participants who considered leaving their jobs (44%; N = 517) demonstrated greater moral distress and injury scores. Logistic regression highlighted burnout (AOR = 1.59; p < .001), moral distress (AOR = 1.83; p < .001), and moral injury due to trust violation (AOR = 1.30; p = .022) as significant predictors of the intention to leave one's job.Conclusion: While it is impossible to fully eliminate moral stressors from healthcare, especially during exceptional and critical scenarios like a global pandemic, it is crucial to recognize the detrimental impacts on HCWs. This underscores the urgent need for additional research to identify protective factors that can mitigate the impact of these stressors.

This study explored the nature of moral stressors encountered by health care workers, along with impacts on moral injury and intentions to leave their jobs.Morally distressing encounters were common, with the most prevalent and distressing experiences being organizational or team-based in nature.Findings revealed that severity of moral injury, particularly related to trust violation or betrayal, was a key factor influencing healthcare workers' intentions to leave their jobs.

Childhood household dysfunction is associated with reduced left ventricular mass in young adulthood.

The effect of adverse childhood experiences (ACEs) on left ventricular mass (LVM) and left ventricular function remains largely unknown across the lifespan. This study investigated the influence of ACEs on LVM and left ventricular function and whether inflammation influences this relationship. Two hundred forty-eight healthy young adults participated and a final sample of 217 (age, 22.6 ± 0.1 yr; females, 114) had complete data. Echocardiographic assessment of LVM was indexed to height2.7 (LVMHT) and body surface area (LVMBSA). Ejection fraction (EF) and fractional shortening were also assessed. Interleukin-6 (IL-6), C-reactive protein, tumor necrosis factor-α, and matrix metalloproteinase (MMP) 1-3 were measured and ACEs exposures were assessed based on exposure and nonexposure to childhood household dysfunction and maltreatment, and quantity of adversity, (i.e., <4 ACEs and ≥4 ACEs). Individuals who experienced household dysfunction demonstrated lower LVM, LVMHT, and LVMBSA (P < 0.01) and greater IL-6 (P < 0.05) than those who did not experience household dysfunction. Reduced MMP3 was present in individuals who experienced maltreatment (P < 0.05) and ≥4 ACEs (P < 0.01) compared with no maltreatment and <4 ACEs, respectively. After controlling for covariates (i.e., sex, recent life stress, height, body mass index, smoking, physical activity, and inflammation), a significant negative effect of household dysfunction on LVM, LVMHT, and LVMBSA persisted. Likewise, a negative effect on EF independent of covariates was observed in individuals who experienced ≥4 ACEs. As such, alterations in LVM and EF may be perpetuated through a toxic home environment, promoting left ventricular underdevelopment in young adulthood. The effect of which in midlife and beyond requires additional investigation.NEW & NOTEWORTHY This is the first study to investigate the influence of adverse childhood experiences (ACEs) on left ventricular mass (LVM) and function. We identified experiencing any childhood household dysfunction was associated with lower LVM in young adults independent of sex, recent life stress, BMI and height, smoking, physical activity, and inflammation. We speculate an inflection point in LVM occurs in midlife predisposing these individuals toward a hypertrophic profile and elevated risk of heart disease in later life, although this requires longitudinal investigation.

Adverse childhood experiences are associated with altered cardiovascular reactivity to head-up tilt in young adults.

Adverse childhood experiences (ACEs) are associated with greater prevalence of cardiovascular disease and altered acute stress reactivity. The current study investigated the effect of ACEs on hemodynamic and autonomic responses to orthostatic stress imposed by 60° head-up tilt (HUT) in young adults. Two-hundred twenty-six healthy young adults (age = 22.6 ± 1.5 yr; n = 116 females) without cardiovascular disease participated and had complete data. Participants underwent supine blood pressure (BP), R-R interval (RRI), cardiac output (CO), total peripheral resistance (TPR), and cardiovagal baroreflex sensitivity (cvBRS) testing followed by a transition to 60° HUT where measures were reassessed. Childhood adversity exposures were assessed based on categorical exposure and nonexposure to childhood household dysfunction and maltreatment, and <4 and ≥4 types of ACEs. Significantly greater increases in SBP (P < 0.05), DBP, MAP, and TPR (P < 0.01; all) following 60° HUT were observed in individuals with ≥4 compared with those with <4 types of ACEs. Attenuated decreases in RRI and cvBRS were observed in those with ≥4 types of ACEs (P < 0.05). Experiencing ≥4 types of ACEs was associated with augmented BP and TPR reactivity and a blunted decrease in cvBRS in response to 60° HUT in young adults. Results suggest that a reduced vagal response to orthostatic stress is present in those who have experienced ≥4 types of ACEs that may promote autonomic dysfunction. Future research examining the sympathetic and vagal baroreflex branches is warranted.

No Mediation Effect of Telomere Length or Mitochondrial DNA Copy Number on the Association Between Adverse Childhood Experiences (ACEs) and Central Arterial Stiffness.

Background Adverse childhood experiences (ACEs) have been linked to increased cardiovascular disease (CVD) risk. Previous reports have suggested that accelerated biological aging-indexed by telomere length (TL) and mitochondrial DNA copy number (mtDNAcn)-may contribute to associations between ACEs and cardiovascular health outcomes. Here, we examine the potential mediating effects of TL and mtDNAcn on the association between ACEs and central arterial stiffness-an intermediate cardiovascular health outcome-as a novel pathway linking ACEs to CVD risk among young adults. Methods and Results One hundred and eighty-five (n=102 women; mean age, 22.5±1.5 years) individuals provided information on ACEs. TL (kb per diploid cell) and mtDNAcn (copies per diploid cell) were quantified using quantitative polymerase chain reaction techniques. Central arterial stiffness was measured as carotid-femoral pulse wave velocity (cfPWV; m/s). Multiple linear regression analyses were used to examine the associations between ACEs, TL, mtDNAcn, and cfPWV. ACEs were positively associated with cfPWV (ß=0.147, P=0.035). TL (ß=-0.170, P=0.011) and mtDNAcn (ß=-0.159, P=0.019) were inversely associated with cfPWV. Neither TL (ß=-0.027, P=0.726) nor mtDNAcn (ß=0.038, P=0.620) was associated with ACEs. Neither marker mediated the association between ACEs and cfPWV. Conclusions An increasing number of ACEs were associated with a faster cfPWV and thus, a greater degree of central arterial stiffness. ACEs were not associated with either TL or mtDNAcn, suggesting that these markers do not represent a mediating pathway linking ACEs to central arterial stiffness.

Serum MMP-3 and its association with central arterial stiffness among young adults is moderated by smoking and BMI.

Central arterial stiffness is an independent predictor of cardiovascular disease. It is characterized by a marked reduction in the elastin-collagen ratio of the arterial wall extracellular matrix (ECM), and is largely the result of degradation of various ECM components. Matrix metalloproteinase-3 (MMP-3) may contribute to central arterial stiffness via its involvement in ECM homeostasis and remodeling. This study examined the association between serum MMP-3 concentrations and central arterial stiffness and potential interactions of MMP-3 and traditional cardiovascular risk factors in a population of healthy young adults. A total of 206 participants (n = 109 females) aged 19-25 years were included in the current study. Central arterial stiffness was measured non-invasively as carotid-femoral pulse wave velocity (cfPWV) (m/s). MMP-3 concentrations (ng/ml) were measured using ELISA techniques. Regression analyses were used to examine the association between cfPWV and MMP-3, adjusting for age, sex, smoking status, body mass index (BMI), instantaneous mean arterial pressure (MAP) and heart rate, and serum C-reactive protein. Interactions between MMP-3 with smoking, BMI, sex, and MAP were analyzed in subsequent regression models. MMP-3 was an independent predictor of cfPWV (ß = 0.187, p = 0.007), and significant interactions between MMP-3 and regular smoking (ß = 0.291, p = 0.022), and MMP-3 and BMI (ß = 0.210, p = 0.013) were observed. Higher serum MMP-3 concentrations were associated with a faster cfPWV and thus, greater central arterial stiffness. Interactions between MMP-3 and smoking, and MMP-3 and BMI may, in part, drive the association between MMP-3 and central arterial stiffness.

Linking the hemodynamic consequences of adverse childhood experiences to an altered HPA axis and acute stress response.

Adverse childhood experiences (ACEs), such as maltreatment and severe household dysfunction, represent a significant threat to public health as ACEs are associated with increased prevalence of several chronic diseases. Biological embedding, believed to be rooted in dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis, is the prevailing theory by which chronic diseases become imprinted in individuals following childhood adversity. A shift towards HPA axis hypoactivity occurs in response to ACEs exposure and is proposed to contribute towards altered cortisol secretion, chronic low-grade inflammation, and dysregulated hemodynamic and autonomic function. This shift in HPA axis activity may be a long-term effect of glucocorticoid receptor methylation with downstream effects on hemodynamic and autonomic function. Emerging evidence suggests syncopal tendencies are increased among those with ACEs and coincides with altered neuroimmune function. Similarly, chronic low-grade inflammation may contribute towards arterial baroreceptor desensitization through increased arterial stiffness, negatively impacting autonomic regulation following posture change and increasing rates of syncope in later life, as has been previously highlighted in the literature. Although speculative, baroreceptor desensitization may be secondary to increased arterial stiffness and changes in expression of glucocorticoid receptors and arginine vasopressin, which are chronically altered by ACEs. Several research gaps and opportunities exist in this field and represent prospective areas for future investigation. Here, we synthesize current findings in the areas of acute psychosocial stress reactivity pertaining to HPA axis function, inflammation, and hemodynamic function while suggesting ideas for future research emphasizing systemic interactions and postural stress assessments among those with ACEs. This review aims to identify specific pathways which may contribute towards orthostatic intolerance in populations with history of childhood adversity.

Adverse Childhood Experiences (ACEs) Predict Increased Arterial Stiffness from Childhood to Early Adulthood: Pilot Analysis of the Niagara Longitudinal Heart Study.

An association among adults between adverse childhood experiences (ACEs) and arterial stiffness and between arterial stiffness and cardiovascular disease has been established. Recent cross-sectional evidence suggests that ACEs is linked to the development and progression of arterial stiffness, but it remains unclear when these changes begin to manifest. We examine the relationship between ACEs and changes in arterial stiffness from childhood into adulthood using population-based longitudinal data. The Niagara Longitudinal Heart Study (NLHS) pilot data included 76 young adults (females = 44), with an average age of 21 years (SD = 1), and had a follow-up period of 9 years. Mixed effects modeling was used to examine the effect of ACEs on changes in arterial stiffness over time adjusting for sex, changes in heart rate, systolic blood pressure, body mass index, and physical activity. Individuals with four or more ACEs have a greater increase in arterial stiffness over time from childhood into young adulthood. This increase was similar for both males and females and independent of the effects of change in heart rate, systolic blood pressure, body mass index, and physical activity. Exposure to ACEs is associated with greater increase in arterial stiffness, a marker for cardiovascular disease among adults. This suggests that interventions targeted at individuals with high exposure to ACEs early on in life could lower the risk of arterial stiffness and in turn the cascade of events leading to cardiovascular disease.

Adverse childhood experiences (ACEs) and cardiovascular development from childhood to early adulthood: study protocol of the Niagara Longitudinal Heart Study.

INTRODUCTION: Recent reviews have found substantial links between a toxic childhood environment including child abuse and severe household dysfunction and adult cardiovascular disease (CVD). Collectively referred to as adverse childhood experiences (ACEs), this toxic environment is prevalent among children, with recent Canadian estimates of child abuse at 27%-32%, and severe household dysfunction at 49%. Based on these prevalence rates, the potential effect of ACEs on CVD is more significant than previously thought. Yet, how ACEs amplify the risk for later CVD remains unclear. Lifestyle risk factors only partially account for this connection, instead directing attention to the interaction between psychosocial factors and physiological mechanisms such as inflammation. The Niagara Longitudinal Heart Study (NLHS) examines how ACEs influence cardiovascular health (CVH) from childhood to early adulthood. Integrating the stress process and biological embedding models, this study examines how psychosocial and physiological factors in addition to lifestyle factors explain the relationship between ACEs and CVH. METHODS: This follow-up study combines three baseline studies from 2007 to 2012 that collected CVH measures including child blood pressure, heart rate, left ventricular structure and function, arterial stiffness indices and baroreflex sensitivity on 564 children. Baseline data also include anthropometric, biological, lifestyle, behavioural, and psychosocial measures that varied across primary studies. Now over 18 years of age, we will recruit and retest as many participants from the baseline studies as possible collecting data on ACEs, CVH, anthropometric, lifestyle and psychosocial measures as well as blood, saliva and hair for physiological biostress markers. ETHICS AND DISSEMINATION: Ethics approval has been received for the NLHS follow-up. Written consent to participate in the follow-up study is obtained from each participant. Results testing all proposed hypotheses will be submitted for publication in peer-reviewed journals.

Role of aortic arch vascular mechanics in cardiovagal baroreflex sensitivity.

Cardiovagal baroreflex sensitivity (cvBRS) measures the efficiency of the cardiovagal baroreflex to modulate heart rate in response to increases or decreases in systolic blood pressure (SBP). Given that baroreceptors are located in the walls of the carotid sinuses (CS) and aortic arch (AA), the arterial mechanics of these sites are important contributors to cvBRS. However, the relative contribution of CS and AA mechanics to cvBRS remains unclear. This study employed sex differences as a model to test the hypothesis that differences in cvBRS between groups would be explained by the vascular mechanics of the AA but not the CS. Thirty-six young, healthy, normotensive individuals (18 females; 24 ± 2 yr) were recruited. cvBRS was measured using transfer function analysis of the low-frequency region (0.04-0.15 Hz). Ultrasonography was performed at the CS and AA to obtain arterial diameters for the measurement of distensibility. Local pulse pressure (PP) was taken at the CS using a hand-held tonometer, whereas AA PP was estimated using a transfer function of brachial PP. Both cvBRS (25 ± 11 vs. 19 ± 7 ms/mmHg, P = 0.04) and AA distensibility (16.5 ± 6.0 vs. 10.5 ± 3.8 mmHg(-1) × 10(-3), P = 0.02) were greater in females than males. Sex differences in cvBRS were eliminated after controlling for AA distensibility (P = 0.19). There were no sex differences in CS distensibility (5.32 ± 2.3 vs. 4.63 ± 1.3 mmHg(-1) × 10(-3), P = 0.32). The present data demonstrate that AA mechanics are an important contributor to differences in cvBRS.