Cumulative stress exposure is extensively involved in carcinogenesis. However, cancer risk associated with allostatic load (AL), a valid measure of chronic stress, has not been comprehensively evaluated in large cohorts, and the combined effect of AL and personality trait on cancer risk remains unknown.

This prospective cohort study was conducted based on 245,683 participants from the UK Biobank, with a median follow-up of 13.5 years. The AL score was calculated based on 11 biomarkers. Personality traits were constructed and categorized into two clusters. Multivariable Cox regression model was used to assess the risk of incident cancer according to AL and personality clusters, and multiplicative and additive interactions were evaluated.

High AL was associated with an increased cancer risk compared to low AL (hazard ratio [HR] = 1.06, 95% confidence interval [CI]: 1.04–1.09), particularly for cancers of stomach, liver, kidney, esophageal, lung, colorectal, breast, and leukemia (HR ranged from 1.08 to 1.43). Personality clusters was associated with risk of lung cancer (HR = 1.14, 95% CI: 1.05–1.23), but not overall cancer. Significant synergistic interaction was observed between high AL and ‘nervous-dominant’ personality for overall cancer risk, with the strongest association observed for liver cancer (HR = 1.58, 95% CI: 1.24–2.02).

High AL was related to higher risks of overall cancer and site-specific cancers, particularly when combined with nervous-dominant personality, highlighting the interplay between chronic physiological stress and psychological factors in cancer development.

As the global shift towards autocracy continues and soft political repression rises, it is crucial to understand its long-term health implications. Typical tactics of soft political repression are surveillance, denunciation and harassment, operating beneath the threshold of criminal or violent persecution. Despite its prevalence, soft repression remains underexplored, particularly in terms of its psychobiological health consequences.

The current study investigates the long-term sequelae of soft political repression in the German Democratic Republic (GDR: 1949–1990), focusing on psychological distress, systemic inflammation and cellular ageing.

The cross-sectional laboratory study included 100 50–78 years old participants from the states of Thuringia and Saxony in Germany. Participants in the repression group (n = 49) had experienced at least two forms of state-organised soft repression in the GDR. The age, gender and origin matched control group reported no such experiences. Psychological measures included depressive, anxiety and trauma symptoms. Physiological health outcomes were measured through the inflammatory markers interleukin-6 and high sensitivity C-reactive protein (hs-CRP), as well as telomere length as a marker of cellular ageing. Resilience, social support and socioeconomic status were included in the analyses as potential buffers of repression effects.

Participants with repression experience (versus control group) scored significantly higher on all psychological distress variables. Furthermore, they exhibited higher levels of interleukin-6, indicating increased systemic inflammation. No group differences were found for hs-CRP or telomere length. However, in the repression group, lower social support was associated with shorter telomeres.

This study is the first to explore the psychobiological health consequences of soft political repression. Findings emphasise its long-term consequences on the psyche and immune system and highlight the potential role of social support in mitigating cellular ageing. As authoritarian tactics are becoming more prevalent worldwide, understanding the impact of soft repression on health is essential for supporting affected individuals.

Noradrenergic activation in the central and peripheral nervous systems is a putative mechanism explaining the link between hypertension and affective disorders.

We investigated whether these stress-sensitive comorbidities may be dependent on basal noradrenergic activity and whether vascular responses to centrally acting stimuli vary according to noradrenergic activity.

We examined the relation of affective disorders and stress-mediated vascular responses to plasma concentrations of normetanephrine, a measure of noradrenergic activity, in subjects with primary hypertension (n = 100, mean ± s.d. age 43 ± 11 years, 54% male). The questionnaires Patient Health Questionnaire-9 (PHQ-9), 16-item Quick Inventory of Depressive Symptomatology-Self Report (QIDSSR-16) and Generalized Anxiety Disorder-7 (GAD-7) were used for evaluation of symptoms of depression and anxiety. Forearm blood flow (strain gauge plethysmography) was used to assess vascular responses to mental stress and to device-guided breathing (DGB), interventions that respectively increase or decrease noradrenergic activity in the prefrontal cortex and locus coeruleus.

Low mood and high anxiety were two- to threefold higher for hypertensive subjects in the highest compared with the lowest normetanephrine tertiles (each P < 0.005). Forearm vasodilator responses to mental stress and vasoconstrictor responses to DGB were attenuated in those with high compared with low normetanephrine (28.3 ± 21% v. 47.1 ± 30% increases for mental stress and 3.7 ± 21% v. 18.6 ± 15% decreases for DGB for highest versus lowest tertiles of normetanephrine, each P ≤ 0.01).

A hyperadrenergic state in hypertension is associated with mood disturbance and impaired stress-modulated vasomotor responses. This association may be mediated by chronic stress impinging on pathways regulating central arousal and peripheral sympathetic nerve activity.

Stress leads to neurobiological changes, and failure to regulate these can contribute to chronic psychiatric issues. Despite considerable research, the relationship between neural alterations in acute stress and coping with chronic stress is unclear. This longitudinal study examined whole-brain network dynamics following induced acute stress and their role in predicting chronic stress vulnerability.

Sixty military pre-deployment soldiers underwent a lab-induced stress task where subjective stress and resting-state functional magnetic resonance imaging were acquired repeatedly (before stress, after stress, and at recovery, 90 min later). Baseline depression and post-traumatic stress symptoms were assessed, and again a year later during military deployment. We used the Leading Eigenvector Dynamic Analysis framework to characterize changes in whole-brain dynamics over time. Time spent in each state was compared across acute stress conditions and correlated with psychological outcomes.

Findings reveal significant changes at the network level from acute stress to recovery, where the frontoparietal and subcortical states decreased in dominance in favor of the default mode network, sensorimotor, and visual states. A significant normalization of the frontoparietal state activity was related to successful psychological recovery. Immediately after induced stress, a significant increase in the lifetimes of the frontoparietal state was associated with higher depression symptoms (r = 0.49, p < .02) and this association was also observed a year later following combat exposure (r = 0.49, p < .009).

This study revealed how acute stress-related neural alterations predict chronic stress vulnerability. Successful recovery from acute stress involves reducing cognitive–emotional states and enhancing self-awareness and sensory–perceptual states. Elevated frontoparietal activity is suggested as a neural marker of vulnerability to chronic stress.

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.