Fairness in Distributive Justice by 3- and 5-Year-Olds Across Seven Cultures

This research investigates 3- and 5-year-olds' relative fairness in distributing small collections of even or odd numbers of more or less desirable candies, either with an adult experimenter or between two dolls. The authors compare more than 200 children from around the world, growing up in seven highly contrasted cultural and economic contexts, from rich and poor urban areas, to small-scale traditional and rural communities. Across cultures, young children tend to optimize their own gain, not showing many signs of self-sacrifice or generosity. Already by 3 years of age, self-optimizing in distributive justice is based on perspective taking and rudiments of mind reading. By 5 years, overall, children tend to show more fairness in sharing. What varies across cultures is the magnitude of young children's self-interest. More fairness (less self-interest) in distributive justice is evident by children growing up in small-scale urban and traditional societies thought to promote more collective values

Posttraumatic stress disorder and accelerated aging: PTSD and leukocyte telomere length in a sample of civilian women.

BACKGROUND: Studies in male combat veterans have suggested posttraumatic stress disorder (PTSD) is associated with shorter telomere length (TL). We examined the cross-sectional association of PTSD with TL in women exposed to traumas common in civilian life. METHODS: Data are from a substudy of the Nurses' Health Study II (N = 116). PTSD and subclinical PTSD were assessed in trauma-exposed women using diagnostic interviews. An array of health behaviors and conditions were assessed. DNA was extracted from peripheral blood leukocytes (collected 1996-1999). Telomere repeat copy number to single gene copy number (T/S) was determined by quantitative real-time PCR telomere assay. We used linear regression models to assess associations and examine whether a range of important health behaviors (e.g., cigarette smoking) and medical conditions (e.g., hypertension) previously associated with TL might explain a PTSD-TL association. We further examined whether type of trauma exposure (e.g., interpersonal violence) was associated with TL and whether trauma type might explain a PTSD-TL association. RESULTS: Relative to not having PTSD, women with a PTSD diagnosis had shorter log-transformed TL (β = -.112, 95% confidence interval (CI) = -0.196, -0.028). Adjustment for health behaviors and medical conditions did not attenuate this association. Trauma type was not associated with TL and did not account for the association of PTSD with TL. CONCLUSIONS: Our results add to growing evidence that PTSD may be associated with more rapid cellular aging as measured by telomere erosion. Moreover, the association could not be explained by health behaviors and medical conditions assessed in this study, nor by type of trauma exposure

Variability Modifies Life Satisfaction\u27s Association With Mortality Risk In Older Adults

Greater life satisfaction is associated with greater longevity, but its variability across time has not been examined relative to longevity. We investigated whether mean life satisfaction across time, variability in life satisfaction across time, and their interaction were associated with mortality over 9 years of follow-up. Participants were 4,458 Australians initially at least 50 years old. During the follow-up, 546 people died. After we adjusted for age, greater mean life satisfaction was associated with a reduction in mortality risk, and greater variability in life satisfaction was associated with an increase in mortality risk. These findings were qualified by a significant interaction such that individuals with low mean satisfaction and high variability in satisfaction had the greatest risk of mortality over the follow-up period. In combination with mean life satisfaction, variability in life satisfaction is relevant for mortality risk among older adults. Considering intraindividual variability provides additional insight into associations between psychological characteristics and health

Post-traumatic stress disorder symptom duration and remission in relation to cardiovascular disease risk among a large cohort of women

Prior studies suggest that post-traumatic stress disorder (PTSD) is associated with elevated cardiovascular disease (CVD) risk, but effects of duration and remission of PTSD symptoms have rarely been evaluated. We examined the association of time-updated PTSD symptom severity, remission and duration with incident CVD risk (552 confirmed myocardial infarctions or strokes) over 20 years in 49 859 women in the Nurses’ Health Study II. Among women who reported trauma on the Brief Trauma Questionnaire, PTSD symptoms, assessed by a screener, were classified by symptom severity and chronicity: (a) no symptoms, (b) 1–3 ongoing, (c) 4–5 ongoing, (d) 6–7 ongoing, (e) 1–3 remitted, (f) 4–7 remitted symptoms. Inverse probability weighting was used to estimate marginal structural logistic regression models, adjusting for time-varying and time-invariant confounders. Compared with women with no trauma exposure, women with trauma/no PTSD [odds ratio (OR) 1.30, 95% confidence interval (CI) 1.03–1.65] and women with trauma/6–7 symptoms (OR 1.69, 95% CI 1.08–2.63) had elevated risk of CVD; women with remitted symptoms did not have elevated CVD risk. Among women exposed to trauma, every 5 additional years of PTSD symptomology was associated with 9% higher CVD incidence compared with women with trauma/no PTSD. The findings suggest that alleviating PTSD symptoms shortly after onset may attenuate CVD risk

Post-traumatic Stress Disorder and 20-Year Physical Activity Trends Among Women

Introduction: Post-traumatic stress disorder (PTSD) may be associated with physical inactivity, a modifiable lifestyle factor that contributes to risk of cardiovascular and other chronic diseases; however, no study has evaluated the association between PTSD onset and subsequent physical activity (PA) changes. Method: Analyses were conducted between October 2014 and April 2016, using data from the ongoing Nurses’ Health Study II (N=50,327). Trauma exposure and PTSD symptoms were assessed using two previously validated measures, the Brief Trauma Questionnaire and Short Screening Scale for DSM-IV PTSD. Average PA (hours/week) was assessed using self-report measures at six time points across 20 years (1989–2009). Linear mixed models with time-updated PTSD assessed differences in PA trajectories by trauma/PTSD status. Among a subsample of women whose trauma/PTSD onset during follow-up, group differences in PA patterns before and after onset were assessed using linear spline models. Results: PA decreased more steeply over time among trauma-exposed women reporting four or five (β= –2.5E–3, SE=1.0E–3, p=0.007) or six or seven PTSD symptoms (β= –6.7E–3, SE=1.1E–3, p<0.001) versus women without trauma exposure, adjusting for potential confounders. Among a subsample of women whose trauma/PTSD symptoms onset during follow-up, no differences in PA were observed prior to onset; after onset, women with six or seven PTSD symptoms had a steeper decline (β= –17.1E–3, SE=4.2E–3, p<0.001) in PA over time than trauma-exposed women without PTSD. Conclusions: Decreases in PA associated with PTSD symptoms may be a pathway through which PTSD influences cardiovascular and other chronic diseases

Post-traumatic stress disorder symptoms and risk of hypertension over 22 years in a large cohort of younger and middle-aged women

Background Posttraumatic stress disorder (PTSD) has been linked to hypertension, but most research on PTSD and hypertension is cross-sectional, and potential mediators have not been clearly identified. Moreover, PTSD is twice as common in women than in men, but understanding of the PTSD-hypertension relation in women is limited. We examined trauma exposure and PTSD symptoms in relation to incident hypertension over 22 years in 47,514 civilian women in the Nurses’ Health Study II. Methods We used proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for new-onset hypertension (N=15,837). Results PTSD symptoms assessed with a screen were modestly associated with incident hypertension in a dose-response fashion after adjusting for potential confounders. Compared to women with no trauma exposure, women with 6–7 PTSD symptoms had the highest risk of developing hypertension (HR=1.20 [95% CI, 1.12–1.30]), followed by women with 4–5 symptoms (HR=1.17 [95% CI, 1.10–1.25]), women with 1–3 symptoms (HR=1.12 [95% CI, 1.06–1.18]), and trauma-exposed women with no symptoms (HR=1.04 [95% CI, 1.00–1.09]). Findings were maintained, although attenuated, adjusting for hypertension-relevant medications, medical risk factors, and health behaviors. Higher body mass index and antidepressant use accounted for 30% and 21% of the PTSD symptom-hypertension association. Conclusions Screening for hypertension and reducing unhealthy lifestyle factors, particularly obesity, in women with PTSD may hold promise for offsetting cardiovascular risk

Associations of Trauma Exposure and Posttraumatic Stress Symptoms With Venous Thromboembolism Over 22 Years in Women

Background: Trauma exposure and posttraumatic stress disorder (PTSD) have been linked to myocardial infarction and stroke in women, with biological and behavioral mechanisms implicated in underlying risk. The third most common cardiovascular illness, venous thromboembolism (VTE), is a specific health risk for women. Given previous associations with other cardiovascular diseases, we hypothesized that high levels of trauma and PTSD symptoms would be associated with higher risk of incident VTE in younger and middle‐aged women. Methods and Results: We used proportional hazards models to estimate hazard ratios (HRs) and 95% CIs for new‐onset VTE (960 events) over 22 years in 49 296 women in the Nurses’ Health Study II. Compared to no trauma exposure, both trauma exposure and PTSD symptoms were significantly associated with increased risk of developing VTE, adjusting for demographics, family history, and childhood adiposity. Women with the most PTSD symptoms exhibited the greatest risk elevation: trauma/6 to 7 symptoms: HR=2.42 (95% CI, 1.83–3.20); trauma/4 to 5 symptoms: HR=2.00 (95% CI, 1.55–2.59); trauma/1 to 3 symptoms: HR=1.44 (95% CI, 1.12–1.84); trauma/no symptoms: HR=1.72 (95% CI, 1.43–2.08). Results were similar, although attenuated, when adjusting for VTE‐relevant medications, medical conditions, and health behaviors. Conclusions: Women with the highest PTSD symptom levels had nearly a 2‐fold increased risk of VTE compared to women without trauma exposure in fully adjusted models. Trauma exposure alone was also associated with elevated VTE risk. Trauma and PTSD symptoms may be associated with a hypercoagulable state. Treatment providers should be aware that women with trauma exposure and PTSD symptoms may be vulnerable to VTE

Post-traumatic stress disorder and cardiometabolic disease: improving causal inference to inform practice

Post-traumatic stress disorder (PTSD) has been declared 'a life sentence' based on evidence that the disorder leads to a host of physical health problems. Some of the strongest empirical research - in terms of methodology and findings - has shown that PTSD predicts higher risk of cardiometabolic diseases, specifically cardiovascular disease (CVD) and type 2 diabetes (T2D). Despite mounting evidence, PTSD is not currently acknowledged as a risk factor by cardiovascular or endocrinological medicine. This view is unlikely to change absent compelling evidence that PTSD causally contributes to cardiometabolic disease. This review suggests that with developments in methods for epidemiological research and the rapidly expanding knowledge of the behavioral and biological effects of PTSD the field is poised to provide more definitive answers to questions of causality. First, we discuss methods to improve causal inference using the observational data most often used in studies of PTSD and health, with particular reference to issues of temporality and confounding. Second, we consider recent work linking PTSD with specific behaviors and biological processes, and evaluate whether these may plausibly serve as mechanisms by which PTSD leads to cardiometabolic disease. Third, we evaluate how looking more comprehensively into the PTSD phenotype provides insight into whether specific aspects of PTSD phenomenology are particularly relevant to cardiometabolic disease. Finally, we discuss new areas of research that are feasible and could enhance understanding of the PTSD-cardiometabolic relationship, such as testing whether treatment of PTSD can halt or even reverse the cardiometabolic risk factors causally related to CVD and T2D