Discrimination on the basis of race, gender identity, and age, among others, has been associated with negative cognitive outcomes. However, the mechanisms by which perceived discrimination impacts cognition are not yet well understood. Discrimination can lead to chronic stress, which disrupts glucocorticoid pathways and induces susceptibility to metabolic dysregulation. On the basis of this prior work, and the known associations between metabolic syndrome and cognition, the current study examined the hypothesis that metabolic syndrome mediates the relationship between discrimination and cognition.

1,063 adults (Mean age = 54.92 years, SD = 11.68) who participated in the Midlife in the United States project were included. Confirmatory factor analysis was used to examine the acceptability of a bifactor model of metabolic syndrome using four subfactors (insulin resistance, adiposity, dyslipidemia, and blood pressure). The mediating effect of the metabolic syndrome latent factor on the association between discrimination and cognition was tested using PROCESS (Hayes, 2013). Exploratory analyses were conducted to examine which cognitive domains and which metabolic syndrome subfactors were driving these relationships. Mediation analyses adjusted for age, race, sex, and education.

The three most frequently reported reasons for discrimination were gender (n = 209), age (n = 174), and race (n = 129). The CFA of metabolic symptoms was deemed acceptable based on previously outlined goodness of fit criteria (CFI = 0.986, TLI = 0.976, RMSEA = 0.040, SRMR = 0.034). Results of the mediation analysis indicated a significant indirect effect of major events discrimination on the total cognition composite through the general metabolic syndrome factor (B = -0.0029, 95% CI [-0.0016, -0.0066]). Further examination revealed that this relationship was driven through an indirect path of metabolic syndrome on the relationship between discrimination and executive functioning (B = -0.0024, 95% CI -0.0059, -0.0001]). We examined which subfactors were driving these relationships and found that there were significant indirect effects of major events discrimination on total cognition through the insulin resistance (B = -0.0028, 95% CI -0.0065, -0.0003]) and dyslipidemia factors (B = -0.0026, 95% CI -0.0064, -0.0002]).

Our findings provide evidence that metabolic syndrome can help explain differences in cognitive functioning based on experiences of discrimination, even after adjusting for relevant demographic factors. Results from this study suggest that understanding the impact of perceived discrimination on metabolic syndrome and developing lifestyle interventions that can improve metabolic syndrome may be helpful in reducing stress-related cognitive disparities.

Finding effective, innovative, and accessible methods of coping with and mitigating stress has been increasingly relevant in the midst of the COVID-19 pandemic. To do so, it is important to understand the impact of acute stress responses on cognition, behavior, and emotional functioning. The young adult population in particular has been known to show higher levels of stress. Studies have shown that deep breathing interventions are associated with improved affect, decreased stress levels, and improved cognitive functioning. The autonomic nervous system, particularly the functioning of the vagus nerve, has been thought to be a key mechanism in the effect of breathing on stress and mood. Most studies to date investigating the efficacy of breathing practices in stress reduction and mood improvement have lacked appropriate methodology, including adequate control groups, randomization, and cross-sectional designs. This single-blind, randomized, waitlist-controlled study investigated the feasibility of using a mobile application to train in resonance frequency breathing and its efficacy in reducing stress and improving cognitive functioning in a non-clinical sample of young adults with elevated stress.

80 healthy young adults with elevated stress levels were recruited from the NY/NJ community and the Queens College undergraduate research subject pool. Inclusion criteria: ages 18-29, Perceived Stress Scale score >13. Exclusion criteria: regular (at least 3 times per week) practice of any form of meditation, yoga, or breathing exercise; severe medical or psychiatric disorder; active suicidal ideation; drug or alcohol abuse within the past year; use of medication with a known negative impact on cognition or autonomic nervous system (ANS) arousal. Participants were randomized to a waitlist control group or breathing group. Participants in the breathing group were instructed to complete 10-minute breathing sessions using the free mobile application “The Breathing App” twice a day for five days per week for four weeks. Cognitive assessments were administered over the phone (pre and post-treatment) and self-report measures were completed online due to quarantine restrictions.

There were no significant main effects of group across any of the neuropsychological variables, including verbal memory, letter fluency, category fluency, cognitive flexibility, processing speed, basic attention span, and working memory. This indicated that breathing training did not significantly impact neuropsychological performance. Mediation analysis also demonstrated that breathing training did not indirectly lead to improvement in basic attention, processing speed, working memory, set-shifting, verbal fluency, category fluency, or cognitive flexibility, through its effects on stress reduction.

These results do not support literature suggesting that breathing at resonance frequency is associated with improved cognitive functioning such as greater cognitive flexibility, improved decision-making, stronger response inhibition, faster processing speed, and increased working memory. Future study designs should consider implementing active control groups (e.g., mindfulness meditation) and differential dosages of the breathing treatment.

Psychosocial stress has been associated with impaired cognition and risk for neurodegenerative disease. However, the intermediate pathways underlying this relationship are not yet well understood. Chronic exposure to stress causes endocrine and immune dysregulation that can lead to heightened systemic inflammation. Moreover, chronic, low-grade inflammation has been linked to neurodegeneration, impaired neurogenesis and cognitive decline. Given the strength of the individual links between stress, inflammation and cognition, the current study tested the hypothesis that inflammatory biomarkers would mediate the relationship between perceived stress and executive functions.

Data from the Midlife in the United States Study (MIDUS) (N=863; Mean age= 52.72) provided measures of perceived psychological stress, inflammatory biomarkers [C-reactive protein (CRP) and interleukin-6 (IL-6)] and executive functions. Structural equation modeling (SEM) was used to test for the mediating effect of inflammation on the relationship between perceived stress and executive functions. Exploratory analyses were conducted to investigate whether sex-differences were driving these relationships. Mediation analyses adjusted for age and history of smoking.

In the full sample of men and women, there was a significant indirect effect of perceived stress on executive functions through inflammation [ß=-0.021, z=-2.841, p=0.005]. Further examination revealed that this effect was present in women [B=-0.039, z=-2.680, p=0.007] but not men [ß=-0.003, z=-0.558, p=0.577]. While inflammation was negatively associated with executive functions in both men and women [ß=-0.126, z=-1.930, p=0.050; ß=-0.279, z=-0.558, p>0.001], pathways linking perceived stress to inflammation and executive functions were only significant in women [ß=0.014, z=-3.190, p=0.001; ß=-0.192, z=-3.355, p=0.001].

These findings suggest that inflammatory biomarkers are a viable pathway for explaining how experiencing stress can negatively affect executive functions. Results indicate that women may be particularly vulnerable to the inflammatory and cognitive consequences of stress. As such, psychosocial stress and associated inflammation may be important targets for improving cognitive health outcomes, particularly in women.

Intimate partner violence (IPV) alters women's neurobiological stress response systems. We propose that individual differences early in the attentional processing of threats are associated with these neurobiological mechanisms and contribute to mental illness in this population.

We assessed attentional bias in relation to threat (AB) in women survivors of IPV (n = 69) and controls (n = 36), and examined overall cortisol secretion using hair cortisol (HC), and stress responsiveness measuring salivary cortisol and α-amylase (sAA) before (T0), and after (T1, T2) an acute psychosocial stress task (Trier Social Stress Test). We used repeated-measures ANCOVAs to explore the associations between Group (IPV, control) and AB with acute stress response, and regression models to examine the associations with mental health symptoms.

There were no between-group differences in HC levels. An interaction between Group and AB was found regarding cortisol reactivity (p < 0.05). IPV women with threat avoidance AB showed a blunted cortisol response compared to controls and to IPV participants with threat vigilance AB. The association between sAA reactivity and the interaction between Group, AB, and time approached significance (p = 0.07), with a trend to lower sAA levels particularly in IPV women with threat avoidance AB. Group and cortisol reactivity were associated with symptoms of depression, generalized anxiety, and post-traumatic stress disorder (8–20% explained variance).

Threat avoidance AB is associated with blunted acute cortisol response among women exposed to chronic stress (IPV). Experiencing IPV and acute cortisol response appear to be clearly implicated in long-term mental health problems.

The 22q11.2 deletion (22q11Del) is among the strongest known genetic risk factors for psychosis. Stress, a known risk factor for psychosis in the general population, has seldom been studied in 22q11Del. We investigated how lifetime stressors related to symptomatic outcomes in patients with 22q11Del. We also explored this association in individuals with 22q11.2 duplications (22q11Dup), which may be potentially protective against psychosis.

One hundred individuals (46 with 22q11Del, 30 with 22q11Dup, and 24 healthy controls; Mage = 17.30 years±10.15) were included. Logistic models were used to examine cross-sectional associations between lifetime acute and chronic stressors (severity and count) and the presence (score ⩾3) of positive, negative, and general symptoms, assessed via the Structured Interview for Psychosis-risk Syndromes (SIPS).

The 22q11Dup group reported the greatest number and severity of acute lifetime stressors, but did not differ from 22q11Del in chronic stressor count or severity. Lifetime chronic and acute stressors were uniquely associated with positive symptoms in 22q11Del (chronic count: odds ratio [OR] = 2.35, p = 0.02; chronic severity: OR = 1.88, p = 0.03; acute count: OR = 1.78, p = 0.03), but not with negative or general symptoms (ps > 0.05).

Findings suggest that stress may play a role in psychotic symptoms in 22q1Del, while the 22q11Dup CNV appears protective against psychotic symptoms despite higher rates of stressors. Interventions that mitigate effects of stressors in 22qDel may reduce the odds of psychosis in this group. Prospective longitudinal research is needed to replicate these findings.

Although maternal stressor exposure has been associated with shorter telomere length (TL) in offspring, this literature is based largely on White samples. Furthermore, timing of maternal stressors has rarely been examined. Here, we examined how maternal stressors occurring during adolescence, pregnancy, and across the lifespan related to child TL in Black and White mothers.

Mothers (112 Black; 110 White; Mage = 39) and their youngest offspring (n = 222; Mage = 8) were part of a larger prospective cohort study, wherein mothers reported their stressors during adolescence (assessed twice during adolescence for the past year), pregnancy (assessed in midlife for most recent pregnancy), and across their lifespan (assessed in midlife). Mother and child provided saliva for TL measurement. Multiple linear regression models examined the interaction of maternal stressor exposure and race in relation to child TL, controlling for maternal TL and child gender and age. Race-stratified analyses were also conducted.

Neither maternal adolescence nor lifespan stressors interacted with race in relation to child TL. In contrast, greater maternal pregnancy stressors were associated with shorter child TL, but this effect was present for children of White but not Black mothers. Moreover, this effect was significant for financial but not social pregnancy stressors. Race-stratified models revealed that greater financial pregnancy stressors predicted shorter telomeres in offspring of White, but not Black mothers.

Race and maternal stressors interact and are related to biological aging across generations, but these effects are specific to certain races, stressors, and exposure time periods.

Higher inflammation has been linked to poor physical and mental health outcomes, and mortality, but few studies have rigorously examined whether changes in perceived stress and depressive symptoms are associated with increased inflammation within family caregivers and non-caregivers in a longitudinal design.

Longitudinal Study.

REasons for Geographic And Racial Differences in Stroke cohort study.

Participants included 239 individuals who were not caregivers at baseline but transitioned to providing substantial and sustained caregiving over time. They were initially matched to 241 non-caregiver comparisons on age, sex, race, education, marital status, self-rated health, and history of cardiovascular disease. Blood was drawn at baseline and approximately 9.3 years at follow-up for both groups.

Perceived Stress Scale, Center for Epidemiological Studies-Depression, inflammatory biomarkers, including high-sensitivity C-reactive protein, D dimer, tumor necrosis factor alpha receptor 1, interleukin (IL)-2, IL-6, and IL-10 taken at baseline and follow-up.

Although at follow-up, caregivers showed significantly greater worsening in perceived stress and depressive symptoms compared to non-caregivers, there were few significant associations between depressive symptoms or perceived stress on inflammation for either group. Inflammation, however, was associated with multiple demographic and health variables, including age, race, obesity, and use of medications for hypertension and diabetes for caregivers and non-caregivers.

These findings illustrate the complexity of studying the associations between stress, depressive symptoms, and inflammation in older adults, where these associations may depend on demographic, disease, and medication effects. Future studies should examine whether resilience factors may prevent increased inflammation in older caregivers.

The activity of military personnel is associated with risk and tension which can affect both physical and mental health. Hardiness reflects certain characteristics of a person that can motivate them to take an active part in overcoming difficult circumstances. Thou we considering Hardiness is a resource for the reliability of professional activity. The study was supported by the RFBR #19-013-00799.

Research of Hardiness as a military personnel professional reliability resource.

The research involved 315 participants, male. Average age 20.12 years (min – 18, max – 32). The participants completed 3 standardized questionnaires: The Occupational Stress Survey (Leonova, 2006), The 16 PF Questionnaire (rus. version, Kapustina (eds.), 2001), Hardiness Survey (rus. ver. by Leontiev, Rasskazova, 2006).

In our study Hardiness value was above-average (M = 101.3; SD = 15.96). Correlation analysis revealed a direct relationship between Hardiness and “Reliability of professional activity” (M = 0; SD = 1) – Chronic stress, Emotional Stability, Motivational Distortion, Apprehensiveness (p = 0.0001; r = 0.678). It also appeared that Hardiness is a predisposition factor of professional reliability activity (adj. R2=0.539). Correlation analysis also revealed an inverse correlation between Hardiness and Chronic stress (p = 0.0001; r = -0.730).

Thus Hardiness is a resource for the reliability of professional activity. These results can be used in practice for performing trainings to support specialists and help them develop resources for reliability of professional activity.

No significant relationships.