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STANDFIRST:: Hopelessness and despair threaten health and longevity. We urgently need strategies to counteract these effects and improve population health. Prosociality contributes to better mental and physical health for individuals, and for the communities in which they live. We propose that prosociality should be a public health priority. COMMENT:: The COVID-19 pandemic produced high levels of stress, loneliness, and mental health problems, magnifying global trends in health disparities. Hopelessness and despair are growing problems particularly in the U.S. The sharp increase in rates of poor mental health is problematic in its own right, but poor mental health also contributes to greater morbidity and mortality. Without action, we will see steep declines in global population health and related costs to society. An approach that is “more of the same” is insufficient to stem the cascading effects of emotional ill-being. Something new is desperately needed. To this point, recent work called on the discipline of psychiatry to contribute more meaningfully to the deaths of despair framework (i.e., conceptualizing rises in suicide, drug poisoning and alcoholic liver disease as due to misery of difficult social and economic circumstances). Recognizing that simply expanding mental health services cannot address the problem, the authors noted the importance of population-level prevention and targeting macro-level causes for intervention. This requires identifying upstream factors causally related to these deaths. However, factors explaining population health trends are poorly delineated and focus on risks and deficits (e.g., adverse childhood experiences, unemployment). A ‘deficit-based’ approach has limits as the absence of a risk factor does not inevitably indicate presence of a protective asset; we also need an ‘asset-based’ approach to understanding more comprehensively the forces that shape good health and buffer harmful effects of stress and adversity.

This study examined effects of experimentally-induced optimism on physical activity and stress reactivity with community volunteers. Using an intervention to induce short-term optimism, we conducted two harmonized randomized experiments, performed simultaneously at separate academic institutions. All participants were randomized to either the induced optimism intervention or to a neutral control activity using essay-writing tasks. Physical activity tasks (Study 1) and stress-related physiologic responses (Study 2) were assessed during lab visits. Essays were coded for intensity of optimism. A total of 324 participants (207 women, 117 men) completed Study 1, and 118 participants (67 women, 47 men, 4 other) completed Study 2. In both studies, the optimism intervention led to greater increases in short-term optimism and positive affect relative to the control group. Although the intervention had limited effects on physical activity and stress reactivity, more optimistic language in the essays predicted increased physical activity and decreased stress reactivity.

Psychological well-being, characterized by feelings, cognitions, and strategies that are associated with positive functioning (including hedonic and eudaimonic well-being), has been linked with better physical health and greater longevity. Importantly, psychological well-being can be strengthened with interventions, providing a strategy for improving population health. But are the effects of well-being interventions meaningful, durable, and scalable enough to improve health at a population-level? To assess this possibility, a cross-disciplinary group of scholars convened to review current knowledge and develop a research agenda. Here we summarize and build on the key insights from this convening, which were: (1) existing interventions should continue to be adapted to achieve a large-enough effect to result in downstream improvements in psychological functioning and health, (2) research should determine the durability of interventions needed to drive population-level and lasting changes, (3) a shift from individual-level care and treatment to a public-health model of population-level prevention is needed and will require new infrastructure that can deliver interventions at scale, (4) interventions should be accessible and effective in racially, ethnically, and geographically diverse samples. A discussion examining the key future research questions follows.

ObjectiveTo understand the association between psychosocial stressors and cardiovascular health by evaluating: (a) lifespan patterns of childhood and adulthood stressors in relation to hemodynamic acute stress reactivity and recovery and (b) the role of optimism in these associations.MethodParticipants (n = 1,092, 56% women, 21% racial/ethnic minority, Mage = 56.2) were from the Midlife in the United States Study II Biomarker Project. Lifespan profiles of psychosocial stressor exposure (low lifespan exposure, high childhood only, high adulthood only, persistent exposure) were constructed from responses to the Childhood Trauma Questionnaire and a life events inventory. Optimism was measured with the Life Orientation Test-Revised. Hemodynamic acute stress reactivity to and recovery from cognitive stressors were assessed using a standardized laboratory protocol involving continuous measurements of systolic and diastolic blood pressure (BP) and baroreflex sensitivity (BRS).ResultsCompared with the low lifespan exposure group, the high childhood- and persistent-exposure groups showed lower BP reactivity, and to a lesser extent, slower BP recovery. Persistent exposure was also associated with slower BRS recovery. Optimism did not modify the association between stressor exposure and any hemodynamic acute stress responses. However, in exploratory analyses, greater stressor exposure across all developmental periods was indirectly associated with reduced BP acute stress reactivity and slower recovery via lower optimism levels.ConclusionsFindings support childhood as a unique developmental period wherein high adversity exposure may exert an enduring influence on adulthood cardiovascular health by limiting individuals' capacity to cultivate psychosocial resources and altering hemodynamic responses to acute stressors. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

BackgroundMany studies have evaluated the stress-cognition association, but few have captured the cumulative nature of stress or distinguished the influences of stressors occurring in childhood versus adulthood. Using a lifecourse approach, we investigated whether cumulative stress exposures are associated with poorer cognitive function and faster cognitive decline.MethodsWe used data from the Midlife Development in the United States Study (N = 3,954, mean baseline age: 56 years). We fit marginal structural generalized estimating equations models to estimate the difference in baseline cognitive function per SD increment in the continuous stressor score, and, separately, between persons in each life course stressor profile and those who did not experience high stress in either childhood or adulthood. We also characterized differences in cognitive decline across levels of stress exposures.ResultsHigher cumulative stress exposure was associated with lower executive function (difference per SD in continuous stressor score = -0.12 SD units, 95% CI = -0.16, -0.08) and episodic memory (difference = -0.09 SD units, 95% CI = -0.13, -0.05). Baseline executive function and episodic memory were lower among those with high stress only in childhood, only in adulthood, and both, than among those without high stress in childhood or adulthood. There was little evidence that rate of change in executive function and episodic memory differed across levels of cumulative stress exposures.ConclusionsThese findings offer support to the hypothesis that stress exposures, accumulated over the life course, worsen cognitive performance, but limited support for the hypothesis that these exposures promote cognitive decline.

BackgroundResearch has suggested optimism is associated with healthy aging and exceptional longevity, but most studies were conducted among non-Hispanic White populations. We examined associations of optimism to longevity across racial and ethnic groups and assessed healthy lifestyle as a possible mediating pathway.MethodsParticipants from the Women's Health Initiative (N = 159,255) completed a validated measure of optimism and provided other demographic and health data at baseline. We evaluated associations of optimism with increments in lifespan using accelerated failure time models, and with likelihood of exceptional longevity (survival to age ≥90) using Poisson regression models. Causal mediation analysis explored whether lifestyle-related factors mediated optimism-lifespan associations.ResultsAfter covariate adjustment, the highest versus lowest optimism quartile was associated with 5.4% (95% confidence interval [CI] = 4.5, 6.4%) longer lifespan. Within racial and ethnic subgroups, these estimates were 5.1% (95%CI = 4.0, 6.1%) in non-Hispanic White, 7.6% (95%CI = 3.6, 11.7%) in Black, 5.4% (95%CI = -0.1, 11.2%) in Hispanic/Latina, and 1.5% (95% CI = -5.0, 8.5) in Asian women. A high proportion (53%) of the women achieved exceptional longevity. Participants in the highest versus lowest optimism quartile had greater likelihood of achieving exceptional longevity (e.g., full sample risk ratio = 1.1, 95%CI = 1.1, 1.1). Lifestyle mediated 24% of the optimism-lifespan association in the full sample, 25% in non-Hispanic White, 10% in Black, 24% in Hispanic/Latina, and 43% in Asian women.ConclusionsHigher optimism was associated with longer lifespan and a greater likelihood of achieving exceptional longevity overall and across racial and ethnic groups. The contribution of lifestyle to these associations was modest. Optimism may promote health and longevity in diverse racial and ethnic groups. Future research should investigate these associations in less long-lived populations.

BackgroundDespite evidence linking posttraumatic stress disorder (PTSD), depression, and head injury, separately, with worse cognitive performance, investigations of their combined effects on cognition are limited in civilian women.MethodsThe Cogstate Brief Battery assessment was administered in 10,681 women from the Nurses' Health Study II cohort, mean age 64.9 years (SD = 4.6). Psychological trauma, PTSD, depression, and head injury were assessed using online questionnaires. In this cross-sectional analysis, we used linear regression models to estimate mean differences in cognition by PTSD/depression status and stratified by history of head injury.ResultsHistory of head injury was prevalent (36%), and significantly more prevalent among women with PTSD and depression (57% of women with PTSD and depression, 21% of women with no psychological trauma or depression). Compared to having no psychological trauma or depression, having combined PTSD and depression was associated with worse performance on psychomotor speed/attention ( β  = -.15, p = .001) and learning/working memory ( β  = -.15, p

Cognitive function at middle age is of particular public health interest, as it strongly predicts later dementia. Children who have experienced abuse subsequently have worse cognitive function than those who have not. However, it remains unclear whether the association of abuse with cognitive function persists into middle age. In 2014-2016, 14,151 women ages 49-69 years who had previously responded to a childhood abuse questionnaire completed a cognitive battery. In models adjusted for childhood socioeconomic status and head trauma, combined physical, emotional, and sexual abuse was associated with lower scores on both Learning/Working Memory (severe abuse, lower scores similar to that observed in women 4.8 years older in our data) and Psychomotor Speed/Attention (severe abuse, lower scores similar to that observed in women to 2.9 years older in our data). Adjustment for adulthood socioeconomic status and health factors (e.g., smoking, hypertension) slightly attenuated associations. In exploratory analyses further adjusted for psychological distress, associations were attenuated. Women exposed versus unexposed to childhood abuse had poorer cognitive function at mid-life. Associations were particularly strong for learning and working memory and were not accounted for by adulthood health factors. Childhood abuse should be investigated as a potential risk factor for cognitive decline and dementia in old age.

BackgroundPosttraumatic stress disorder (PTSD) has been associated with increased cardiovascular risk, however, underlying mechanisms have not been fully specified. PTSD is associated with stress-related hormones, including dysregulated glucocorticoid activity. Dysregulation of aldosterone, a mineralocorticoid activated by psychological stress and implicated in cardiovascular damage, may be a relevant pathway linking PTSD and cardiovascular risk. Few studies to date have evaluated the association between PTSD and aldosterone, none with repeated measures of aldosterone. We examined if trauma and PTSD were associated with altered aldosterone levels relative to women unexposed to trauma.MethodsThe association of trauma exposure and chronic PTSD with plasma aldosterone levels was investigated in 521 middle-aged women in the Nurses' Health Study II. Aldosterone was assessed at two time points, 10-16 years apart, and trauma exposure and PTSD were also ascertained for both time points. Regarding exposure assessment, women were characterized based on a structured diagnostic interview as: having chronic PTSD (PTSD at both time points; n = 174); being trauma-exposed (trauma exposure at first time point but no PTSD; n = 174); and being unexposed (no trauma exposure at either time point; reference group for all analyses; n = 173). Linear mixed models examined associations of trauma and PTSD status with log-transformed aldosterone levels, adjusting for covariates and health-related variables that may confound or lie on the pathway between PTSD and altered aldosterone levels.ResultsAcross the sample, mean aldosterone concentration decreased over time. Adjusting for covariates, women with chronic PTSD had significantly lower aldosterone levels averaged over time, compared to women unexposed to trauma (β = - 0.08, p = 0.04). Interactions between trauma/PTSD group and time were not significant, indicating change in aldosterone over time did not differ by trauma/PTSD status. Post-hoc exploratory analyses suggested that menopausal status partially mediated the relationship between chronic PTSD status and aldosterone level, such that postmenopausal status explained 7% of the effect of PTSD on aldosterone.ConclusionsThese findings indicate that PTSD is associated with lower levels of aldosterone. Further work is needed to understand implications of this type of dysregulation in a key biological stress system for cardiovascular and other health outcomes previously linked with PTSD.

BackgroundPosttraumatic stress disorder (PTSD) is associated with higher risk of certain chronic diseases, including ovarian cancer, but underlying mechanisms remain unclear. Although prior work has linked menopausal hormone therapy (MHT) use with elevated ovarian cancer risk, little research considers PTSD to likelihood of MHT use. We examined whether PTSD was prospectively associated with greater likelihood of initiating MHT use over 26 years.MethodsUsing data from the Nurses' Health Study II, with trauma and PTSD (symptoms and onset date) assessed by screener in 2008 and MHT assessed via biennial survey (from 1989), we performed Cox proportional regression models with women contributing person-years from age 36 years. Relevant covariates were assessed at biennial surveys. We considered potential effect modification by race/ethnicity, age at baseline, and period (1989-2002 vs. 2003-2015).ResultsOver follow-up, 22,352 of 43,025 women reported initiating MHT use. For example, compared with women with no trauma, the HR for initiating MHT was 1.18 for those with trauma/1-3 PTSD symptoms [95% confidence interval (CI), 1.13-1.22] and 1.31 for those with trauma/4-7 PTSD symptoms (95% CI, 1.25-1.36; P trend < 0.001), adjusting for sociodemographic factors. Associations were maintained when adjusting for reproductive factors and health conditions. We found evidence of effect modification by age at baseline.ConclusionsTrauma and number of PTSD symptoms were associated with greater likelihood of initiating MHT use in a dose-response manner.ImpactMHT may be a pathway linking PTSD to altered chronic disease risk. It is important to understand why women with PTSD initiate MHT use.

The rapid pace of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2; COVID-19) pandemic presents challenges to the real-time collection of population-scale data to inform near-term public health needs as well as future investigations. We established the COronavirus Pandemic Epidemiology (COPE) consortium to address this unprecedented crisis on behalf of the epidemiology research community. As a central component of this initiative, we have developed a COVID Symptom Study (previously known as the COVID Symptom Tracker) mobile application as a common data collection tool for epidemiologic cohort studies with active study participants. This mobile application collects information on risk factors, daily symptoms, and outcomes through a user-friendly interface that minimizes participant burden. Combined with our efforts within the general population, data collected from nearly 3 million participants in the United States and United Kingdom are being used to address critical needs in the emergency response, including identifying potential hot spots of disease and clinically actionable risk factors. The linkage of symptom data collected in the app with information and biospecimens already collected in epidemiology cohorts will position us to address key questions related to diet, lifestyle, environmental, and socioeconomic factors on susceptibility to COVID-19, clinical outcomes related to infection, and long-term physical, mental health, and financial sequalae. We call upon additional epidemiology cohorts to join this collective effort to strengthen our impact on the current health crisis and generate a new model for a collaborative and nimble research infrastructure that will lead to more rapid translation of our work for the betterment of public health.

Posttraumatic stress disorder (PTSD) has increasingly been linked to heightened systemic inflammation. It matters whether this association is causal (and either bidirectional or unidirectional) or correlational. Investigators have hypothesized that chronic systemic low-grade inflammation may contribute to greater risk of developing PTSD after experiencing trauma and/or serve as a mechanism linking PTSD to adverse physical health outcomes. However, if the PTSD-inflammation relation is correlational, it may not warrant further research aimed at understanding inflammation as a PTSD risk factor or as a pathway linking PTSD with poor health. In this review, we first assess the longitudinal evidence related to PTSD and inflammation to understand more clearly the directionality and causal nature of this relation. Overall, few longitudinal studies rigorously assess the direction of the PTSD-inflammation relation. Some of the evidence indicates that elevated inflammation assessed pretrauma or in the acute aftermath of trauma increases risk for developing PTSD. Fewer studies evaluate the influence of PTSD on subsequent inflammation levels, and findings are mixed. Sample characteristics and study designs, and also the type of inflammation-related measure, vary widely across studies. Based on current evidence, we then recommend several statistical and study design approaches that may help untangle issues of bidirectionality and aid in determining the direction of causality between PTSD and inflammation. Last, we conclude with future research directions and consider potential implications for interventions or treatment approaches based on this growing body of literature.

BackgroundStudies have shown adverse effects of a disadvantaged childhood on adult health-promoting behaviors and related outcomes. Optimism and social support have been linked to greater likelihood of engaging in healthy behavior, but it is unclear whether these positive psychosocial factors may buffer harmful effects of early adversity. This study aims to determine if optimism and social support in adulthood can modify effects of childhood disadvantage on health behavior-related outcomes.MethodsLongitudinal data were analyzed from a subset of participants in a US birth cohort established in 1959-1966 (ns of 681-840, per outcome). An index of childhood social disadvantage was derived from adverse socioeconomic and family stability factors reported by mothers at child's birth and age 7 years. Health behavior-related outcomes were self-reported when participants were of mean age 47 years. Multivariable adjusted robust Poisson regressions were performed.ResultsRegardless of level of childhood social disadvantage, we found higher levels of optimism and social support were both associated with higher probabilities of being a non-smoker (relative risk [RR]optimism = 1.17, 95% confidence interval [CI] = 1.09-1.26; RRsocial support = 1.24, 95%CI = 1.11-1.39), having a healthy diet (RRoptimism = 1.25, 95%CI = 1.10-1.43; RRsocial support = 1.27, 95%CI = 1.04-1.56), and a healthy body mass index (RRoptimism = 1.18, 95%CI = 1.00-1.40; RRsocial support = 1.29, 95%CI = 1.00-1.66). Interactions link higher optimism or social support with lower risk of smoking among those with moderate childhood disadvantage.ConclusionsOverall, these findings are consistent with the possibility that positive psychosocial resources contribute to maintaining a healthy lifestyle in mid-adulthood and may buffer effects of childhood social disadvantage.

Measures of well-being have proliferated over the past decades. Very little guidance has been available as to which measures to use in what contexts. This paper provides a series of recommendations, based on the present state of knowledge and the existing measures available, of what measures might be preferred in which contexts. The recommendations came out of an interdisciplinary workshop on the measurement of well-being. The recommendations are shaped around the number of items that can be included in a survey, and also based on the differing potential contexts and purposes of data collection such as, for example, government surveys, or multi-use cohort studies, or studies specifically about psychological well-being. The recommendations are not intended to be definitive, but to stimulate discussion and refinement, and to provide guidance to those relatively new to the study of well-being.

ObjectiveMounting evidence suggests that higher optimism is associated with reduced risk of age-related morbidities and premature mortality. However, possible biological mechanisms underlying these associations remain understudied. One hypothesized mechanism is a slower rate of cellular aging, which in turn delays age-related declines in health.MethodsWe used data from two large cohort studies to test the hypothesis that higher optimism is associated with longer leukocyte telomere length. With cross-sectional data from the Health and Retirement Study (HRS; n = 6417; mean age = 70 years) and the Women's Health Initiative (WHI; N = 3582; mean age = 63 years), we used linear regression models to examine the association of optimism with relative telomere length (assessed in leukocytes from saliva [HRS] or plasma [WHI]). Models adjusted for sociodemographics, depression, health status, and health behaviors.ResultsConsidering both optimism and telomere length as continuous variables, we found consistently null associations in both cohorts, regardless of which covariates were included in the models. In models adjusting for demographics, depression, comorbidities, and health behaviors, optimism was not associated with mean relative telomere length (HRS: β = -0.002, 95% confidence interval = -0.014 to 0.011; WHI: β = -0.004, 95% confidence interval = -0.017 to 0.009).ConclusionsFindings do not support mean telomere length as a mechanism that explains observed relations of optimism with reduced risk of chronic disease in older adults. Future research is needed to evaluate other potential biological markers and pathways.