Biopsychosocial contexts influence adult cognitive function concurrently and longitudinally.

Background: Cognitive aging is a complex process that impacts human behavior. Identifying the factors that preserve cognitive functioning is a public health priority, given that 20% of the US population will be at least 65 years old in the next decade. Biopsychosocial determinants of cognitive decline across the lifespan are often examined as ecological factors that independently moderate cognitive aging, despite the known complexity surrounding these relationships. Objective: We aimed to address this gap by exploring the synergistic and simultaneous relationship between risk and protective factors on cognitive functioning. Method: Using the MIDUS study datasets, we examined the relationships among physiological markers, friendship quality, and global cognition functioning, concurrently and longitudinally over ten years. Our participants included 929 healthy (417 men, 512 women) adults (average age at Time 1: 54.6 ± 11.6 years). Exploratory analyses examining the effects of racial minority status were also conducted. Results: Cross-sectionally, age, and friendship quality moderated the relationship between vagally-mediated heart rate variability (vm-HRV) and cognition such that younger adults with greater friendship quality had a negative relationship between vm-HRV and cognitive performance; our unexpected finding suggests the heart-brain relationship is sensitive to the biopsychosocial environment. Longitudinally, higher IL-6 levels at Time 1 predicted poorer cognitive performance a decade later, but only among those with greater levels of friendship quality, especially for white-identifying individuals. Conclusions: The relationships among physiological risk factors, social protective factors and cognitive functioning appear to be temporally different during mid-adulthood. Given many of the whole sample findings were not replicated within the racial minority subgroup, we suggest that these relationships should be examined in a larger and more diverse racial minority sample to determine whether this study lacked the power necessary to detect a relationship or if the relationships are in fact different by racial minority sub-group. In addition, future research should overcome the study's reliance on healthy adults and self-report measures of friendship quality by including adults with pre-existing cognitive impairments, and employing more real-time measures of friendship quality, such as daily diary or ecological momentary assessment.

Depression, Inflammation, and Intestinal Permeability: Associations with Subjective and Objective Cognitive Functioning throughout Breast Cancer Survivorship.

About one-in-three breast cancer survivors have lingering cognitive complaints and objective cognitive impairment. Chronic inflammation and intestinal permeability (i.e., leaky gut), two risk factors for cognitive decline, can also fuel depression-another vulnerability for cognitive decline. The current study tested whether depression accompanied by high levels of inflammation or intestinal permeability predicted lower subjective and objective cognitive function in breast cancer survivors. We combined data from four breast cancer survivor studies (n = 613); some had repeated measurements for a total of 1015 study visits. All participants had a blood draw to obtain baseline measures of lipopolysaccharide binding protein-a measure of intestinal permeability, as well as three inflammatory markers that were incorporated into an inflammatory index: C-reactive protein, interleukin-6, and tumor necrosis factor-α. They reported depressive symptoms on the Center for Epidemiological Studies depression scale (CES-D), and a binary variable indicated clinically significant depressive symptoms (CES-D ≥ 16). The Kohli (749 observations) and the Breast Cancer Prevention Trial (591 observations) scales assessed subjective cognitive function. Objective cognitive function tests included the trail-making test, Hopkins verbal learning test, Conners continuous performance test, n-back test, FAS test, and animal-naming test (239-246 observations). Adjusting for education, age, BMI, cancer treatment type, time since treatment, study visit, and fatigue, women who had clinically elevated depressive symptoms accompanied by heightened inflammation or intestinal permeability reported poorer focus and marginally poorer memory. However, poorer performance across objective cognitive measures was not specific to inflammation-associated depression. Rather, there was some evidence of lower verbal fluency; poorer attention, verbal learning and memory, and working memory; and difficulties with visuospatial search among depressed survivors, regardless of inflammation. By themselves, inflammation and intestinal permeability less consistently predicted subjective or objective cognitive function. Breast cancer survivors with clinically significant depressive symptoms accompanied by either elevated inflammation or intestinal permeability may perceive greater cognitive difficulty, even though depression-related objective cognitive deficits may not be specific to inflammation- or leaky-gut-associated depression.

Perspectives of (/memorandum for) systems thinking on COVID-19 pandemic and pathology.

Is data-driven analysis sufficient for understanding the COVID-19 pandemic and for justifying public health regulations? In this paper, we argue that such analysis is insufficient. Rather what is needed is the identification and implementation of over-arching hypothesis-related and/or theory-based rationales to conduct effective SARS-CoV2/COVID-19 (Corona) research. To that end, we analyse and compare several published recommendations for conceptual and methodological frameworks in medical research (e.g., public health, preventive medicine and health promotion) to current research approaches in medical Corona research. Although there were several efforts published in the literature to develop integrative conceptual frameworks before the COVID-19 pandemic, such as social ecology for public health issues and systems thinking in health care, only a few attempts to utilize these concepts can be found in medical Corona research. For this reason, we propose nested and integrative systemic modelling approaches to understand Corona pandemic and Corona pathology. We conclude that institutional efforts for knowledge integration and systemic thinking, but also for integrated science, are urgently needed to avoid or mitigate future pandemics and to resolve infection pathology.

Reappraisal and health: How habitual reappraisal and reappraisal ability interact to protect against life stress in young adults.

Inadequate emotion regulation may underlie the development of psychopathology as well as worsened physical health, particularly in the context of life stress. Cognitive reappraisal is typically considered an adaptive strategy to manage negative emotions. However, the extent to which reappraisal is beneficial may hinge upon contextual and individual differences. Specifically, it is unclear whether and how the ability to reappraise effectively (i.e., reappraisal ability) and exposure to stressful life events moderate the association between habitual reappraisal and health. Using a series of questionnaires and an experimental task designed to measure the ability to effectively down-regulate sad emotions using reappraisal, the present study examined the interactive effects of habitual reappraisal, reappraisal ability, and exposure to stressful life events on depressive and anxiety symptoms as well as self-reported physical health in 400 young adults (62.5% women; mean age = 19.8 ± 2.5). Results indicated that habitual reappraisal may protect against elevated depressive symptoms and worsened self-reported physical health for people exposed to more stressful life events. Moreover, reappraising often appeared to be particularly beneficial for those who were less effective in their attempts. Results for anxiety symptoms were not significant, although habitual reappraisal remained significantly associated with anxiety symptoms as a lower-order term. These findings provide novel contributions to the field of emotion regulation and health by clarifying that exposure to stressful life events is a key moderator in the association between reappraisal and some areas of health and by elucidating the important roles of both habitual reappraisal and reappraisal ability. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Childhood ADHD, Going Beyond the Brain: A Meta-Analysis on Peripheral Physiological Markers of the Heart and the Gut.

Attention-Deficit/Hyperactivity Disorder (ADHD) is the most common neurodevelopmental disorder diagnosed in children. Questions regarding its increased diagnostic rates and pharmacological treatments in developing children have led to a more holistic review of the multi-system pathophysiology observed in ADHD. The dopaminergic neurotransmitter system, known for its influence on reward-motivated behaviors and motor control, and the frontostriatal systems, that mediate motor, cognition, and behavior, are associated with ADHD's development. However, studies have shown that these neural systems do not wholly account for ADHD's multilayered and heterogeneous symptom presentation. For instance, the literature suggests that emotional dysregulation, the inability to regulate one's emotional responses to provoking stimuli, is associated with increased risk for social impairment in ADHD. A broader examination of physiological systems in children with ADHD has found potential markers in the heart-brain and gut-brain axes that correspond with certain behaviors associated with emotional dysregulation in recent studies. Hence, the purpose of this meta-analysis is to aggregate ten applicable published case studies and analyze task-related heart rate reactivity (HRR; n = 5 studies) and gut microbiota (n = 5 studies) data in children with and without ADHD. Data from a total of 531 youth with ADHD and 603 youth without ADHD revealed significant small and medium effect sizes for higher Chao1 levels and Actinobacteria levels in the ADHD group, respectively, but no evidence of altered task-related HRR. Thus, further research into multi-system psychophysiological measures of emotional dysregulation and ADHD is warranted. The clinical, empirical, and educational implications of these findings are discussed. Systematic Review Registration: https://www.crd.york.ac.uk/prospero/, identifier PROSPERO (CRD42021236819).

Distress disorder histories predict HRV trajectories during and after stress.

BACKGROUND: Breast cancer survivors face a number of physical health threats including cardiovascular disease, the leading cause of death among breast cancer survivors. Low heart rate variability (HRV) represents one well-established risk factor for poor cardiovascular health. Among physically healthy adults and breast cancer survivors, distress disorders may contribute to lower HRV, enhancing morbidity and mortality. This study examined how a distress disorder history altered survivors' HRV trajectories during and after an experimental stressor. METHODS: Breast cancer survivors (n = 178; mean age = 51.22) who finished treatment for stages 0-IIIa cancer within the past two years completed a diagnostic interview assessing lifetime presence of psychological disorders. They also participated in a Trier Social Stress Test (TSST). HRV data provided information on survivors' cardiovascular responses at baseline, during the TSST, and during recovery. HRV recovery data at 45 min and 120 min post-TSST was also collected. Survivors also completed questionnaires before and after the TSST assessing task performance, stress levels, ability to cope, and hopelessness. Covariates included body mass index, age, cancer stage, cardiovascular medications, exercise, menopause status, fatigue, current depressive and anxiety symptoms, and physical comorbidities. RESULTS: Women with a distress disorder history had significantly lower HRV before, during, and after the TSST compared to women without such a history. Survivors with distress disorders found the TSST to be more threatening, and reported feeling less control over their performance than those without distress disorders. CONCLUSIONS: Breast cancer survivors with a distress disorder history may have lower autonomic flexibility before, during, and after stress exposure. Distress disorder histories also heighten several stress-related risk perceptions leading up to and following the TSST. These findings highlight distress disorder histories as a unique correlate of poorer cardiovascular function among survivors.

Frequent Interpersonal Stress and Inflammatory Reactivity Predict Depressive-Symptom Increases: Two Tests of the Social-Signal-Transduction Theory of Depression.

The social-signal-transduction theory of depression asserts that people who experience ongoing interpersonal stressors and mount a greater inflammatory response to social stress are at higher risk for depression. The current study tested this theory in two adult samples. In Study 1, physically healthy adults (N = 76) who reported more frequent interpersonal tension had heightened depressive symptoms at Visit 2, but only if they had greater inflammatory reactivity to a marital conflict at Visit 1. Similarly, in Study 2, depressive symptoms increased among lonelier and less socially supported breast-cancer survivors (N = 79). This effect was most pronounced among participants with higher inflammatory reactivity to a social-evaluative stressor at Visit 1. In both studies, noninterpersonal stress did not interact with inflammatory reactivity to predict later depressive symptoms.

Low-Dose Metformin Treatment Reduces In Vitro Growth of the LL/2 Non-small Cell Lung Cancer Cell Line.

Lung cancer maintains a relatively small survival rate (~19%) over a 5-year period and up to 80-85% of all lung cancer diagnoses are Non-Small Cell Lung Cancer (NSCLC). To determine whether metformin reduces non-small cell lung cancer (NSCLC) LL/2 cell growth, cells were grown in vitro and treated with metformin for 48 h. qPCR was used to assess genes related to cell cycle regulation and pro-apoptotic markers, namely Cyclin D, CDK4, p27, p21, and HES1. Treatment with 10 mM metformin significantly reduced HES1 expression (p = 0.011). Furthermore, 10 mM metformin treatment significantly decreased REDD1 (p = 0.0082) and increased p-mTOR Ser2448 (p = 0.003) protein expression. Control cells showed significant reductions in phosphorylated p53 protein expression (p = 0.0367), whereas metformin treated cells exhibited reduced total p53 protein expression (p = 0.0078). There were no significant reductions in AMPK, PKB/AKT, or STAT3. In addition, NSCLC cells were treated for 48 h. with 10 mM metformin, 4 µM gamma-secretase inhibitor (GSI), or the combination of metformin (10 mM) and GSI (4 µM) to determine the contribution of respective signaling pathways. Metformin treatment significantly reduced total nucleus expression of the proliferation maker Ki-67 with an above 65% reduction in Ki-67 expression between control and metformin-treated cells (p = 0.0021). GSI (4 µM) treatment significantly reduced Ki-67 expression by ~20% over 48 h (p = 0.0028). Combination treatment (10 mM metformin and 4 µM GSI) significantly reduced Ki-67 expression by more than 50% over 48 h (p = 0.0245). As such, direct administration of metformin (10 mM for 48 h) proved to be an effective pharmaceutical agent in reducing the proliferation of cultured non-small cell cancer cells. These intriguing in vitro results, therefore, support the further study of metformin in appropriate in vivo models as an anti-oncogenic agent and/or an adjunctive therapy.

Low-Dose Metformin as a Monotherapy Does Not Reduce Non-Small-Cell Lung Cancer Tumor Burden in Mice.

Non-small-cell lung cancer (NSCLC) makes up 80-85% of lung cancer diagnoses. Lung cancer patients undergo surgical procedures, chemotherapy, and/or radiation. Chemotherapy and radiation can induce deleterious systemic side effects, particularly within skeletal muscle. To determine whether metformin reduces NSCLC tumor burden while maintaining skeletal muscle health, C57BL/6J mice were injected with Lewis lung cancer (LL/2), containing a bioluminescent reporter for in vivo tracking, into the left lung. Control and metformin (250 mg/kg) groups received treatments twice weekly. Skeletal muscle was analyzed for changes in genes and proteins related to inflammation, muscle mass, and metabolism. The LL/2 model effectively mimics lung cancer growth and tumor burden. The in vivo data indicate that metformin as administered was not associated with significant improvement in tumor burden in this immunocompetent NSCLC model. Additionally, metformin was not associated with significant changes in key tumor cell division and inflammation markers, or improved skeletal muscle health. Metformin treatment, while exhibiting anti-neoplastic characteristics in many cancers, appears not to be an appropriate monotherapy for NSCLC tumor growth in vivo. Future studies should pursue co-treatment modalities, with metformin as a potentially supportive drug rather than a monotherapy to mitigate cancer progression.

Mental health is the health of the whole body: How psychoneuroimmunology & health psychology can inform & improve treatment.

BACKGROUND: Converging and accumulating evidence for the cross-communication among the nervous, immune, and endocrine systems, a field of study known as psychoneuroimmunology, implicates immunological dysfunction as a shared and common mechanism of both mental and physical illness. For example, psychiatric disorders like schizophrenia, bipolar disorder, major depression, and anxiety disorders have higher prevalence rates across a spectrum of autoimmune conditions compared to the general population. Additionally, subclinical immunological abnormalities are observed in a variety of psychiatric conditions, with chronic inflammation most extensively studied in the pathophysiology of depression. These observations blur the historical distinctions between mental and physical illness, yet clinical practice remains fragmented and primarily focused on differentially treating individual symptoms. PROPOSED THESIS: Therapeutically targeting inflammation offers translational opportunities for integrating mental and physical healthcare, a key niche of the interdisciplinary field of health psychology. CONCLUSION: Utilizing a psychoneuroimmunological lens, health psychologists and clinicians can reconceptualize healthcare through integrative treatment approaches and advocacy for comprehensive policy-level reform at both the individual-level of care as well as community-wide prevention approaches.

"Get a Grip on Hypertension": EXPLORING THE USE OF ISOMETRIC HANDGRIP TRAINING IN CARDIOPULMONARY REHABILITATION PATIENTS.

PURPOSE: Isometric handgrip (IHG) training lowers systolic and diastolic blood pressure (SBP and DBP, respectively), but the efficacy of IHG training in cardiopulmonary rehabilitation patients is unknown. The purpose of this study was to determine if IHG decreases blood pressure in cardiopulmonary rehabilitation patients. METHODS: Cardiopulmonary rehabilitation program participants (n = 11; 50-80 yr old) were randomized to IHG (n = 6) or control (CON; no treatment; n = 5) groups. IHG participants completed an IHG training program at 30% maximal voluntary contraction, 3 d/wk for 6 wk. Resting SBP, DBP, and heart rate were assessed weekly. RESULTS: Mean regression for SBP following IHG was negative (-1.04 ± 0.80). Mean regression in the CON group was positive (0.50 ± 0.88), but there was no significant difference between groups. Separate analysis of weeks 1 to 7 yielded a negative mean regression (-1.12 ± 0.54) in the IHG group, but positive (1.2 ± 0.60) in the CON group. A Wilcoxon test of these differences yielded significance for SBP (P = .009). In 3 of 6 IHG participants, SBP was lower (mean ± SD: -16 ± 11 mm Hg; P = .12), and in 2 IHG participants, DBP was lower (-9 ± 1 mm Hg; P = .06) compared with baseline. In 2 of 5 CON participants, SBP was not significantly lower (-11 ± 7 mm Hg) and, in 3 of 5 CON participants, DBP was lower (-7 ± 4 mm Hg; P = .04). CONCLUSIONS: Our data suggest that standard IHG training may be inadequate for blood pressure management immediately following a major cardiac or pulmonary event. Future work with a larger cohort and more developed training protocol to determine the efficacy of IHG training in patients with cardiopulmonary disease is warranted.

Post-traumatic stress and psychological health following infidelity in unmarried young adults.

Infidelity is often conceptualized as a traumatic event; however, little research has explored this topic empirically, particularly in unmarried adults. We determined the prevalence of infidelity-related post-traumatic stress disorder (PTSD) symptoms among unmarried adults who experienced a partner's infidelity and whether probable infidelity-related PTSD was associated with additional psychological health outcomes (i.e., depressive symptoms, perceived stress, and anxiety symptoms). We also investigated whether negative post-traumatic cognitions mediated the associations between infidelity-related PTSD symptoms and psychological health. This study included 73 adults (M age = 19.42, SE = 0.19 years) who experienced infidelity within a committed nonmarital relationship within the last 5 years. Controlling for gender, race, and exposure to Diagnostic and Statistical Manual of Psychiatric Disorders Criterion A traumas, 45.2% of our sample reported symptoms suggesting probable infidelity-related PTSD. Whether used as continuous or categorical predictor, infidelity-related PTSD symptoms were significantly associated with depressive symptoms, although results for perceived stress and anxiety symptoms were mixed. Post-traumatic cognitions acted as a partial mediator for depressive symptoms and full mediator for perceived stress and anxiety symptoms. This empirical evidence suggests that infidelity may produce PTSD symptoms at a relatively high rate, even in unmarried young adults, and may put individuals at risk for poorer psychological health, partially through post-traumatic cognitions.

Health and Disease-Emergent States Resulting From Adaptive Social and Biological Network Interactions.

Health is an adaptive state unique to each person. This subjective state must be distinguished from the objective state of disease. The experience of health and illness (or poor health) can occur both in the absence and presence of objective disease. Given that the subjective experience of health, as well as the finding of objective disease in the community, follow a Pareto distribution, the following questions arise: What are the processes that allow the emergence of four observable states-(1) subjective health in the absence of objective disease, (2) subjective health in the presence of objective disease, (3) illness in the absence of objective disease, and (4) illness in the presence of objective disease? If we consider each individual as a unique biological system, these four health states must emerge from physiological network structures and personal behaviors. The underlying physiological mechanisms primarily arise from the dynamics of external environmental and internal patho/physiological stimuli, which activate regulatory systems including the hypothalamic-pituitary-adrenal axis and autonomic nervous system. Together with other systems, they enable feedback interactions between all of the person's system domains and impact on his system's entropy. These interactions affect individual behaviors, emotional, and cognitive responses, as well as molecular, cellular, and organ system level functions. This paper explores the hypothesis that health is an emergent state that arises from hierarchical network interactions between a person's external environment and internal physiology. As a result, the concept of health synthesizes available qualitative and quantitative evidence of interdependencies and constraints that indicate its top-down and bottom-up causative mechanisms. Thus, to provide effective care, we must use strategies that combine person-centeredness with the scientific approaches that address the molecular network physiology, which together underpin health and disease. Moreover, we propose that good health can also be promoted by strengthening resilience and self-efficacy at the personal and social level, and via cohesion at the population level. Understanding health as a state that is both individualized and that emerges from multi-scale interdependencies between microlevel physiological mechanisms of health and disease and macrolevel societal domains may provide the basis for a new public discourse for health service and health system redesign.

Higher trait reappraisal predicts stronger HPA axis habituation to repeated stress.

Undergoing stress can be advantageous when it leads to adaptation and growth; however, failure of the hypothalamic-pituitary-adrenal (HPA) axis to habituate (i.e., nonhabituation) involves continuing to become highly activated in response to repeated exposure of the same stimulus and is considered maladaptive. Although 50-75% of individuals assessed in a laboratory exhibit adaptive habituation to repeated stress, variability in habituation suggests psychological processes used in response to stress may play a role, such as emotion regulation (ER). Nonetheless, no research to date has investigated whether ER strategies affect HPA axis habituation. We investigated whether tendency to use two ER strategies, reappraisal and suppression, influenced HPA axis habituation among 84 healthy young adults (60.7% female; Mage = 24.8 years, SD = 6.0) exposed to a standardized experimental stress paradigm on two consecutive days. HPA axis stress responses were assessed using salivary cortisol concentrations. We also examined whether non-manipulated state ER strategies (i.e., those used by the participant during and following the stressor on the first day) modulated HPA axis habituation over and above trait-use in a subsample (N = 60). Trait, but not state, reappraisal was associated with stronger HPA axis habituation. Neither trait nor state suppression were significantly associated with HPA axis habituation. These findings expand our current understanding of how ER can affect stress-related health outcomes and suggest habitual reappraisal plays an important role in adaption of the HPA axis to stress.

Inflammation-Nature's Way to Efficiently Respond to All Types of Challenges: Implications for Understanding and Managing "the Epidemic" of Chronic Diseases.

Siloed or singular system approach to disease management is common practice, developing out of traditional medical school education. Textbooks of medicine describe a huge number of discrete diseases, usually in a systematic fashion following headings like etiology, pathology, investigations, differential diagnoses, and management. This approach suggests that the body has a multitude of ways to respond to harmful incidences. However, physiology and systems biology provide evidence that there is a simple mechanism behind this phenotypical variability. Regardless if an injury or change was caused by trauma, infection, non-communicable disease, autoimmune disorders, or stress, the typical physiological response is: an increase in blood supply to the area, an increase in white cells into the affected tissue, an increase in phagocytic activity to remove the offending agent, followed by a down-regulation of these mechanisms resulting in healing. The cascade of inflammation is the body's unique mechanism to maintain its integrity in response to macroscopic as well as microscopic injuries. We hypothesize that chronic disease development and progression are linked to uncontrolled or dysfunctional inflammation to injuries regardless of their nature, physical, environmental, or psychological. Thus, we aim to reframe the prevailing approach of management of individual diseases into a more integrated systemic approach of treating the "person as a whole," enhancing the patient experience, ability to a make necessary changes, and maximize overall health and well-being. The first part of the paper reviews the local immune cascades of pro- and anti-inflammatory regulation and the interconnected feedback loops with neural and psychological pathways. The second part emphasizes one of nature's principles at work-system design and efficiency. Continually overwhelming this finely tuned system will result in systemic inflammation allowing chronic diseases to emerge; the pathways of several common conditions are described in detail. The final part of the paper considers the implications of these understandings for clinical care and explore how this lens could shape the physician-patient encounter and health system redesign. We conclude that healthcare professionals must advocate for an anti-inflammatory lifestyle at the patient level as well as at the local and national levels to enhance population health and well-being.

Biopsychosocial approach to understanding resilience: Stress habituation and where to intervene.

BACKGROUND: Resilience in the face of adversity is a human experience that leads to better health, both mentally and physically. We briefly review its historical origins rooted in ecological biology and its adoption into health care. Resilience is the common response to adversity or potential traumatic events. Individual differences in emotion regulation and coping skills as well as social capital and one's physical environment influence a person's ability to achieve resilience. PROPOSED MECHANISM: One potential biopsychosocial measure of resilience includes stress habituation to repeated stress as demonstrated in the laboratory, possibly providing a tool to observe mastery of resilience training in the clinic. Evidence-based interventions at the individual and small group level (eg, family, classroom) have successfully shown development of resilient behaviours and improved mental and physical health outcomes. However, the role of social context and public policy clearly influence an individual's ability to be resilient. CONCLUSIONS: Despite the current limited evidence of the effectiveness of resilience building interventions, clinicians, researchers, and other health care professions have an obligation to become advocates for laws and policies that support the most vulnerable, and least resilient, in our society to attain resilience for their health. This salutary effect will enable them to become socially as well as economically productive members of the community at large. It is not possible to remove stress or adversity from life, but we can influence the development of regulatory flexibility and decrease the sociocultural factors linked to the nonresilient experience, thus mitigating adversity's long-term effects on health.

A comparison of blood pressure reductions following 12-weeks of isometric exercise training either in the laboratory or at home.

Isometric exercise training (IET)-induced reductions in resting blood pressure (RBP) have been achieved in laboratory environments, but data in support of IET outside the laboratory are scarce. The aim of this study was to compare 12 weeks of home-based (HOM) IET with laboratory-based, face-to-face (LAB) IET in hypertensive adults. Twenty-two hypertensive participants (24-60 years) were randomized to three conditions: HOM, LAB, or control (CON). IET involved isometric handgrip training (4 × 2 minutes at 30% maximum voluntary contraction, 3 days per week). RBP was measured every 6 weeks (0, 6, and 12 weeks) during training and 6 weeks after training (18 weeks). Clinically meaningful, but not statistically significant reductions in RBP were observed after 12 weeks of LAB IET (resting systolic blood pressure [SBP] -9.1 ± 4.1; resting diastolic blood pressure [DBP] -2.8 ± 2.1; P > .05), which was sustained for 6 weeks of detraining (SBP -8.2 ± 2.9; DBP -4 ± 2.9, P > .05). RBP was reduced in the HOM group after 12 weeks of training (SBP -9.7 ± 3.4; DBP -2.2 ± 2.0; P > .05), which was sustained for an additional 6 weeks of detraining (SBP -5.5 ± 3.4; DBP -4.6 ± 1.8; P > .05). Unsupervised home-based IET programs present an exciting opportunity for community-based strategies to combat hypertension, but additional work is needed if IET is to be used routinely outside the laboratory.

Stressful life events, relationship stressors, and cortisol reactivity: The moderating role of suppression.

Stressful life events (SLEs) are exceedingly common and have been associated with a range of psychological disorders, perhaps through dysregulation in the hypothalamic-pituitary-adrenal (HPA) axis. The use of certain emotion regulation strategies in response to stress, such as expressive suppression and cognitive reappraisal, has additionally been linked to heightened HPA axis reactivity to acute stress. However, it is unclear how emotion regulation may interact with SLEs to affect HPA axis reactivity, particularly concerning relationship stressors (RSs). Using cross-sectional data from 117 men and 85 women aged 18-55 years old (M = 39.9 ±â€¯10.7), we investigated whether trait use of suppression or reappraisal interacted with recent negatively perceived SLEs and relationship stressors to impact HPA axis response to an acute stressor. Separate area under the curve and linear mixed models revealed that trait suppression interacted with SLEs and RSs to predict cortisol response to stress, while reappraisal did not. Findings indicate higher trait expressive suppression may influence the cortisol response to acute stress after exposure to more recent stressful events, particularly when those stressful events include relationship stress.

Inflammation and positive affect: Examining the stress-buffering hypothesis with data from the National Longitudinal Study of Adolescent to Adult Health.

The present study examined the influence of positive affect (PA) on levels of inflammation within the context of Pressman and Cohen's (2005) stress-buffering model, which suggests that PA confers protective health benefits through its ability to mitigate the pathogenic influence of stress. We hypothesized that greater PA would buffer against the influence of perceived psychological stress (PPS) on systemic inflammation, operationalized as C-reactive protein (CRP, mg/L). Specifically, we predicted that PA would moderate the relationship between PPS and CRP. Cross-sectional data were drawn from Wave IV (2008-2009) of the National Longitudinal Study of Adolescent to Adult Health (Add Health). Participants (n=3093) ranged in age from 25 to 34years old (M=29.0±1.79). Using a moderated hierarchical regression analysis, PPS and PA significantly interacted to predict levels of CRP (p<0.05). Examination of the simple slopes revealed a disordinal interaction between PPS and PA, such that higher PA was protective against elevated CRP levels, but only when individuals also reported greater levels of PPS. Thus, the data partially support the stress-buffering model of PA and extend existing evidence regarding the complexity by which PPS and PA influence health. Findings also provide caution of future assumptions that relationships among PA, PPS, and physical health markers, such as CRP, are always positive (e.g., PA) or negative (e.g., PPS) in nature.

'Multimorbidity' as the manifestation of network disturbances.

We argue that 'multimorbidity' is the manifestation of interconnected physiological network processes within an individual in his or her socio-cultural environment. Networks include genomic, metabolomic, proteomic, neuroendocrine, immune and mitochondrial bioenergetic elements, as well as social, environmental and health care networks. Stress systems and other physiological mechanisms create feedback loops that integrate and regulate internal networks within the individual. Minor (e.g. daily hassles) and major (e.g. trauma) stressful life experiences perturb internal and social networks resulting in physiological instability with changes ranging from improved resilience to unhealthy adaptation and 'clinical disease'. Understanding 'multimorbidity' as a complex adaptive systems response to biobehavioural and socio-environmental networks is essential. Thus, designing integrative care delivery approaches that more adequately address the underlying disease processes as the manifestation of a state of physiological dysregulation is essential. This framework can shape care delivery approaches to meet the individual's care needs in the context of his or her underlying illness experience. It recognizes 'multimorbidity' and its symptoms as the end product of complex physiological processes, namely, stress activation and mitochondrial energetics, and suggests new opportunities for treatment and prevention. The future of 'multimorbidity' management might become much more discerning by combining the balancing of physiological dysregulation with targeted personalized biotechnology interventions such as small molecule therapeutics targeting specific cellular components of the stress response, with community-embedded interventions that involve addressing psycho-socio-cultural impediments that would aim to strengthen personal/social resilience and enhance social capital.