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Meta-analyses indicate that positive psychological interventions are effective at increasing positive affect, as well as reducing anxiety and depression; however, it is unclear how well these effects generalize during periods of high stress. Therefore, the current study tested whether a 2-week online positive psychological intervention delivered during the COVID-19 pandemic, a naturalistic stressor, (1) increased positive affect; (2) improved psychological well-being, optimism, life satisfaction, perceived social support, and loneliness; (3) and reduced negative affect in college students, a group known to have high pandemic distress. Participants (N = 250; 76.9% female) ages 18-45 were recruited from the University of Pittsburgh undergraduate subject pool between September and November of 2020. Participants were randomized to the online positive psychological intervention or active control condition and stratified by trait positive affect, sex, and year in college. Participants in both conditions completed one writing activity every other day for two consecutive weeks. Control participants documented their activities for that day (e.g., meals, going to gym). Intervention participants chose from six positive psychology activities. All outcome variables were assessed pre- and post-intervention by validated questionnaires. Across both conditions, positive and negative affect decreased from pre- to post-intervention. No other psychological factor differed by condition, time, or their interaction. The current null findings are in line with a more recent meta-analysis indicating that positive psychological interventions may have smaller effects on psychological well-being and depressive symptoms than was reported pre-pandemic. Study findings may suggest reduced efficacy of virtual positive psychological interventions under highly stressful circumstances.Supplementary informationThe online version contains supplementary material available at 10.1007/s42761-022-00148-z.

A reliable finding from the physical pain literature is that individuals with higher resting (i.e., tonic) blood pressure experience relatively less pain in response to nociceptive stimuli. Converging lines of evidence suggest that biological factors that influence the experience of physical pain may also relate to social pain. An open question, however, is whether higher blood pressure per se is a biological factor associated with lower sensitivity to social pain. This possible association was tested in three studies. Consistent with prior findings on physical pain, higher resting blood pressure was associated with lower self-reported sensitivity to social pain across individuals (Study 1 r = -.303, Study 2 r = -.262, -.246), even after adjusting for confounding factors related to blood pressure (Study 3 r = -.222). Findings suggest a previously unknown biological correlate of sensitivity to social pain, providing further evidence for possible shared substrates for physical and social pain.

This Committee Report provides methodological, interpretive, and reporting guidance for researchers who use measures of heart rate (HR) and heart rate variability (HRV) in psychophysiological research. We provide brief summaries of best practices in measuring HR and HRV via electrocardiographic and photoplethysmographic signals in laboratory, field (ambulatory), and brain‐imaging contexts to address research questions incorporating measures of HR and HRV. The Report emphasizes evidence for the strengths and weaknesses of different recording and derivation methods for measures of HR and HRV. Along with this guidance, the Report reviews what is known about the origin of the heartbeat and its neural control, including factors that produce and influence HRV metrics. The Report concludes with checklists to guide authors in study design and analysis considerations, as well as guidance on the reporting of key methodological details and characteristics of the samples under study. It is expected that rigorous and transparent recording and reporting of HR and HRV measures will strengthen inferences across the many applications of these metrics in psychophysiology. The prior Committee Reports on HR and HRV are several decades old. Since their appearance, technologies for human cardiac and vascular monitoring in laboratory and daily life (i.e., ambulatory) contexts have greatly expanded. This Committee Report was prepared for the Society for Psychophysiological Research to provide updated methodological and interpretive guidance, as well as to summarize best practices for reporting HR and HRV studies in humans. [ABSTRACT FROM AUTHOR]

Neighborhood socioeconomic status (NSES) is associated with cognitive function, independently of individual demographic, health, and socioeconomic characteristics. However, research has been largely cross-sectional, and mechanisms of the association are unknown. In 1992-1993, Cardiovascular Health Study participants (n = 3,595; mean age = 74.8 years; 15.7% black) underwent cognitive testing and magnetic resonance imaging of white matter hyperintensities (WMH), and their addresses were geocoded. NSES was calculated using 1990 US Census data (block groups; 6 measures of wealth, education, and occupation). The Modified Mini-Mental State Examination (3MS) was used to assess general cognition, and the Digit Symbol Substitution Test (DSST) was used to assess speed of processing annually for 6 years. Associations of race-specific NSES tertiles with 3MS, DSST, and WMH were estimated using linear mixed-effects models accounting for geographic clustering, stratified by race, and adjusted for demographic, health, and individual socioeconomic status (education, income, lifetime occupational status) variables. In fully adjusted models, higher NSES was associated with higher 3MS scores in blacks (mean difference between highest and lowest NSES = 2.4 points; P = 0.004) and whites (mean difference = 0.7 points; P = 0.02) at baseline but not with changes in 3MS over time. NSES was marginally associated with DSST and was not associated with WMH. Adjustment for WMH did not attenuate NSES-3MS associations. Associations of NSES with cognition in late adulthood differ by race, are not explained by WMH, and are evident only at baseline.

We aimed to investigate if trajectory components (baseline level, slope, and variability) of peripheral interleukin-6 (IL-6) over time were related to cognitive impairment and smaller hippocampal volume and if hippocampal volume explained the associations between IL-6 and cognitive impairment. Multivariable regression models were used to test the association between IL-6 trajectory components with change in neuroimaging measures of the hippocampus and with cognitive impairment among 135 older adults (70-79 years at baseline) from the Healthy Brain Project over 14 years. IL-6 variability was positively associated with cognitive impairment (odds ratio [OR] = 5.86, 95% confidence interval [CI]: 1.24, 27.61) and with greater decrease per year of gray matter volume of the hippocampus (β = -0.008, standard error = 0.004, p = 0.03). After adjustment for hippocampal volume, the OR of cognitive impairment decreased for each unit of IL-6 variability and CIs widened (OR = 4.36, 95% CI: 0.67, 28.29). Neither baseline levels nor slopes of IL-6 were related to cognitive impairment or hippocampal volume. We believe this has potential clinical and public health implications by suggesting adults with stable levels of peripheral IL-6 may be better targets for intervention studies for slowing or preventing cognitive decline.

Background: Chronic exposure to air pollution may prime the immune system to be reactive, increasing inflammatory responses to immune stimulation and providing a pathway to increased risk for inflammatory diseases, including asthma and cardiovascular disease. Although long-term exposure to ambient air pollution has been associated with increased circulating markers of inflammation, it is unknown whether it also relates to the magnitude of inflammatory response. Objectives: The aim of this study was to examine associations between chronic ambient pollution exposures and circulating and stimulated levels of inflammatory mediators in a cohort of healthy adults. Methods: Circulating interleukin (IL)-6, C-reactive protein (CRP) (n = 392), and lipopolysaccharide stimulated production of IL-1[beta], IL-6, and tumor necrosis factor (TNF)-[alpha] (n = 379) were measured in the Adult Health and Behavior II cohort. Fine particulate matter [particulate matter with aerodynamic diameter less than or equal to 2.5 [micro]m ([PM.sub.2.5])] and constituents [black carbon (BC), and lead (Pb), manganese (Mn), zinc (Zn), and iron (Fe)] were estimated for each residential address using hybrid dispersion land use regression models. Associations between pollutant exposures and inflammatory measures were examined using linear regression; models were adjusted for age, sex, race, education, smoking, body mass index, and month of blood draw. Results: There were no significant correlations between circulating and stimulated measures of inflammation. Significant positive associations were found between exposure to [PM.sub.2.5] and BC with stimulated production of IL-6, IL-1[beta], and TNF-[alpha]. Pb, Mn, Fe, and Zn exposures were positively associated with stimulated production of IL-1[beta] and TNF-[alpha]. No pollutants were associated with circulating IL-6 or CRP levels. Discussion: Exposure to [PM.sub.2.5], BC, Pb, Mn, Fe, and Zn was associated with increased production of inflammatory mediators by stimulated immune cells. In contrast, pollutant exposure was not related to circulating markers of inflammation. These results suggest that chronic exposure to some pollutants may prime immune cells to mount larger inflammatory responses, possibly contributing to increased risk for inflammatory disease. https://doi.org/10.1289/EHP7089, Introduction Exposure to airborne fine particulate matter [particulate matter with aerodynamic diameter less than or equal to 2.5 [micro]m ([PM.sub.2.5])] has been associated with increased risk of cardiopulmonary diseases, and [...]

Childhood trauma may confer risk for poorer adult health through changes in systemic inflammation. Emotion regulation may plausibly moderate associations between childhood trauma and adult psychological well‐being, but it remains unclear whether moderation effects extend to differences in systemic inflammation. To examine whether childhood trauma and emotion regulation separately and interactively predict prospective changes in C‐reactive protein (CRP) and interleukin‐6 (IL‐6) and whether biopsychosocial factors account for observed associations. Healthy midlife adults (N = 331) retrospectively reported on childhood trauma, current trait‐level cognitive reappraisal and expressive suppression, and had their blood drawn. At baseline and then a median of 2.85 years later, 279 of the 331 participants had their blood drawn, body mass index calculated, and reported on health behaviours (smoking, sleep), psychological distress (perceived stress, depressive symptoms), and years of education. Childhood trauma predicted prospective increases in CRP (B = 0.004, p = 0.049), which were partially accounted for by differences in adiposity, psychological distress, and health behaviours. In contrast, cognitive reappraisal predicted prospective decreases in IL‐6 (B = −0.007, p = 0.006), which were independent of biopsychosocial influences. Cognitive reappraisal further moderated the association between childhood trauma and prospective changes in IL‐6 (B = −0.001, p = 0.012) such that childhood trauma predicted greater IL‐6 increases but only among adults lower in cognitive reappraisal (B = 0.006, p = 0.007). There were no main or moderation effects of expressive suppression (ps > 0.05). Cognitive reappraisal may attenuate IL‐6 changes over time and may moderate the prospective association between childhood trauma and systemic inflammation in midlife. [ABSTRACT FROM AUTHOR]

Background: Several personality traits increase the risk for atherosclerotic cardiovascular disease. Because many of these traits are correlated, their associations with disease risk could reflect shared variance, rather than unique contributions of each trait. We examined a higher‐order personality trait of Stability as related to preclinical atherosclerosis and tested whether any such relationship might be explained by correlated variation in cardiometabolic risk factors. Method: Among 798 community volunteers, lower‐order traits of Neuroticism, Agreeableness, and Conscientiousness were modeled as latent variables (from self‐ and informant ratings) and used to estimate the second‐order factor, Stability. Cardiometabolic risk was similarly modeled from indicators of glycemic control, blood pressure, adiposity, and lipids. Carotid artery atherosclerosis was measured as intima‐media thickness (IMT) by duplex ultrasonography. Result: A structural equation model incorporating direct and indirect effects showed lower Stability associated with greater IMT, and this relationship was accounted for by the indirect pathway via cardiometabolic risk. Secondary analyses showed that: (1) Neuroticism, Agreeableness, and Conscientiousness were unrelated to IMT independent of Stability; and (2) Stability predicted variation in IMT when estimated from informant‐, but not self‐rated, traits. Conclusion: Personality traits may associate with atherosclerotic burden through their shared, rather than unique, variance, as reflected in Stability. [ABSTRACT FROM AUTHOR]