<h4>Background and objectives</h4>Laboratory-based stress inductions are commonly used to elicit acute stress but vary widely in their procedures and effectiveness. We compared the effects of stress induction techniques on measures of two major biological stress systems: the early sympathetic-adrenal-medullary (SAM) and the delayed hypothalamic-pituitary-adrenal (HPA) axis response.<h4>Design</h4>A review and meta-analysis to examine the relationship between stress induction techniques on cardiorespiratory and salivary measures of SAM and HPA system activity.<h4>Methods</h4>A systematic literature search identified 245 reports and 700 effects.<h4>Results</h4>The overall effect of stress induction techniques on the stress response was moderate (Fisher's <i>z</i>_r = 0.44), inducing stronger SAM-related (<i>z</i>_r = 0.48) versus HPA-related (<i>z</i>_r = 0.37) responses. Three factors moderated these associations: the stress system examined (SAM vs HPA), the specific stress induction technique employed (e.g., Cold Pressor), the physiological sampling time relative to the stress induction, and participant sex. Loud music elicited the most robust SAM-related effects, whereas combined stress inductions elicited the most robust HPA-related effects. Men showed stronger stress responses than women.<h4>Conclusions</h4>Stress induction techniques variably elicit SAM - and HPA-related responses. Results recommend specific induction techniques for targeting stress systems, highlighting the importance of carefully selecting methodologies in laboratory contexts.

The health and life outcomes of individuals are intertwined with the context in which they grow and live. The totality of exposures one experiences affects health in the short term and throughout the life course. Environmental exposure to multiple contaminants can increase stress levels in individuals and neighborhoods with psychosocial stressors such as crime, drug and alcohol misuse, and violence also taking a toll on individual and neighborhood wellbeing. In addition, the availability, organization, and quality of local institutions and infrastructure all affect health in the short and long term. The role of these factors in endometrial cancer will be explored in this paper. In addition, policy implications regarding lead, chronic physiological stress, and endometrial cancer will be explored to ascertain the impact of these factors on at-risk women.

ABSTRACT Dysfunctioning of stress systems, i.e., the autonomic nervous system (ANS) and hypothalamic-pituitary-adrenal (HPA) axis, has been implicated in chronic pain. However, the exact interplay between (re)activity and recovery of stress and pain systems in chronic pain remains unclear. A systematic review and meta-analysis was pre-registered on PROSPERO (CRD42024495934). Six databases were searched to identify relevant literature. Risk of bias (RoB) was evaluated with the Newcastle-Ottawa Scale, and certainty of evidence (CoE) with GRADE. Clusters of interactions between physiological markers of stress and experimental outcomes of pain were formed based on the timing of the stress measurements. Fifty-two studies (5 cross-sectional, 47 case-control; n = 2,657) were included and scored on average 9/12 (range: 2-11) on RoB. Overall CoE was very low to moderate. Qualitative analyses showed significant correlations between lower mean arterial pressure and higher pain sensitivity at baseline in individuals with chronic primary pain, which was supported by a meta-analysis. Furthermore, meta-analyses showed that higher pain sensitivity was associated with higher cortisol levels at baseline, lower high-frequency heart rate variability during recovery, and higher heart rate at multiple timepoints of the stress system response. Other associations did not yield significance. Taken together, these findings suggest that dysfunction of the ANS and HPA axis is linked to heightened pain sensitivity in chronic primary pain populations. However, the level of evidence remains low due to methodological heterogeneity, highlighting the need for studies combining stress markers and pain measures to provide insights into underlying stress-pain mechanisms. HIGHLIGHTS – Sympathetic cardiovascular dominance appears to be associated with enhanced pain sensitivity in chronic primary pain – A dysregulation in baroreflex activity might be present in chronic primary pain – HPA axis dysfunctioning seems to be related to enhanced pain sensitivity in chronic primary pain – Need for more standardized and comprehensive mapping of stress-pain interactions to unravel underlying mechanisms

Chronic stress has emerged as a critical global public health threat, acting as a risk hub that mediates the onset and progression of diverse psychosomatic diseases (e.g., cardiovascular diseases, mental disorders, metabolic syndrome, and even cancer) through interconnected biological pathways. This review systematically elaborates on the core biological mechanisms underlying chronic stress-induced psychosomatic dysfunction, including hypothalamic-pituitary-adrenal (HPA) axis dysregulation, autonomic nervous system (ANS) imbalance, abnormal inflammatory responses, and excessive oxidative stress-with precise corrections to factual descriptions of neuroendocrine signaling. From a clinical nursing perspective, we critically evaluate existing evidence for each pathway, identify key gaps in current research, and strengthen the mechanistic link between targeted nursing interventions and biological pathway modulation. We also integrate recent advances in neuro-immuno-endocrinology (e.g., peripheral stress response in the skin) and photo-neuro-immuno-endocrinology, and supplement evidence for stress-cancer crosstalk. Additionally, we clarify the definition of the "risk hub" concept, add a brief literature selection methodology, and propose visualized pathway schematics to enhance clarity. This review provides a refined theoretical foundation for clinical nurses to conduct precise risk stratification, develop pathway-specific intervention plans, and implement personalized care, ultimately advancing early prevention and prognosis improvement of chronic stress-related psychosomatic diseases.

Research has demonstrated that stressors play a critical role in the development of generalized anxiety disorder (GAD), social anxiety disorder (SAD), and major depressive disorder (MDD). Separately, deficits in positive affect (PA) have been identified in GAD, SAD, and MDD. Whereas previous research has linked the buffering effects of PA in chronic illness, such effects have yet to be investigated for chronic stressors and emotional disorder–related symptom severity. The purpose of the present study was to examine PA as a moderator of chronic interpersonal and noninterpersonal stress on GAD,