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BackgroundElderly people are particularly affected by rising systolic blood pressure (SBP). We hypothesized that resting blood pressure (RBP)-reducing isometric exercise training (IET) can be delivered in a group setting with older adults.MethodsParticipants (63–88 years; N = 19) completed IET at 30% maximum voluntary contraction, 3 days a week for 12 weeks. RBP was measured weekly throughout, plus 6 weeks posttraining. Control participants did not engage in IET (N = 5). Changes in RBP were assessed using a 2-way repeated-measures analysis of variance.ResultsIET induced significant reductions in SBP (−10.5 mmHg; P < 0.05), but SBP also declined unexpectedly in the control group (−4.5 mmHg; P < 0.05). Diastolic blood pressure declined in the IET group only (−4.7 mmHg; P < 0.05). There were no significant differences between groups for SBP or diastolic blood pressure (P > 0.05). At 6 weeks posttraining, SBP was still 9.4 mmHg below baseline in the IET group only. A unique finding was that the clinically significant RBP reductions persisted for 6 weeks after IET.ConclusionsHandgrip IET may be an effective antihypertensive intervention, which persists for several weeks in older adults, even when training ceases.

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) 2022 APA, all rights reserved).

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.

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.

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; M age = 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.

Background Chronic stress plays a critical role in many of today's diseases and causes of death. Tobacco use reliably increases the likelihood of chronic disease development and premature death. In addition, habitual tobacco use elevates risk of chronic inflammatory diseases, and glucocorticoid therapy is often less effective in smokers compared with nonsmokers. Taken together, smokers may develop glucocorticoid insensitivity, thereby removing the body's greatest anti-inflammatory mechanism. Purpose The purpose of this study was to examine glucocorticoid sensitivity among 24 smokers and 24 age-, sex-, and body mass index-matched never smokers who were clinically healthy individuals (i.e., no diagnosis or medication use for chronic diseases and normotensive). Method Participants visited the lab after a 12 hr fast, provided a blood sample, and completed a series of psychosocial questionnaires. Smokers continued smoking ad libitum before the lab visit. Group differences in glucocorticoid sensitivity were examined using ANCOVA and repeated with linear mixed model to account for possible dependence among immune outcomes that matching participants on age, sex, and body mass index may have introduced. Results Prior to clinical disease onset, smokers' peripheral blood mononuclear cells (PBMCs) exhibited reduced glucocorticoid sensitivity as well as a diminished inflammatory response to lipopolysaccharide compared with never smokers' PBMCs; results were identical regardless of statistical modeling used. Conclusions Cigarette smoking, a self-initiated pharmacological chronic stressor, may provide a unique opportunity to examine early wear and tear on physiological functioning that may lead to chronic disease development. Additional research into PBMCs' intracellular changes must be examined as well as repeating this study in a larger, more heterogeneous population.

The purpose of this review was to discuss the psychological and physiological effects of caregiving stress in the general population as well as among cancer caregivers. Although caregiving for a loved one with cancer may be shorter in duration (i.e., number of months), it is often more intense (i.e., number hours per day) than caring for individuals with other chronic illnesses because cancer treatment has shifted toward outpatient therapy and placed a significant burden of informal caregiving on families, especially spouses/partners. Informal caregiving psychologically and physiologically taxes the caregiver and may negatively influence the caregiver’s health and well-being, regardless of chronic disease population. Unique to breast cancer and other female cancer populations, males often find themselves in the caregiving role. In addition, a paucity of research examining the role of caregiving among the cancer survivorship population exists, despite it being a very real possibility that survivors may find themselves in this position, given advancements in cancer treatment.

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

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.

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.

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.

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.

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.

Tobacco use reliably increases the likelihood of chronic disease development and premature death. However, the initiation of tobacco use does not immediately result in clinical disease manifestation. We recruited 24 healthy smokers and 24 age-, sex-, and BMI-matched never smokers to examine changes in immune function prior to clinical disease manifestations (e.g., no diagnosis or drug treatment for chronic health conditions). In addition to immune cell reactivity to lipopolysaccharide (LPS) and dexamethasone (DEX), we collected psychosocial and physical and mental health data. Smokers were moderately addicted to nicotine and had been smoking for an average of 6.6 years (standard error of mean [SEM] = 1.4) and had 9.4 pack years (SEM 1.9) of tobacco exposure. Smokers endorsed poorer sleep as well as greater psychological distress including anxiety, depression, and loneliness, compared to never smokers. In addition, smokers’ immune cells were less reactive to LPS than never smokers’. Thus, smokers exhibit poorer mental and physical health and modulation of their immune response compared to never smokers, indicating that the term “healthy smoker” is an oxymoron. However, the reduction of immune function observed in smokers was also found in never smokers who had higher levels of loneliness. Hence, loneliness may be as immuno-dysregulating as smoking. Upon further investigation, replacing smoking status with self-rated health explained more of the variability in immune cell responses. Overall, these findings caution the use of one facet, like smoking, as a definitive factor driving health status. When determining global health functioning, we must factor in as many facets as possible, as a long-term or trait-like negative emotion can be just a “unhealthy” as a negative health behavior. In this sample, individuals appear to be aware of their “healthiness,” and it was linked to immune dysregulation.

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 ± 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.

Objectives: Cancersurvivorsoftenreportcognitiveproblems.Furthermore,decreasesinphysicalactivity typically occur over the course of cancer treatment. Although physical activity benefits cognitive function in noncancer populations, evidence linking physical activity to cognitive function in cancer survivors is limited. In our recent randomized controlled trial, breast cancer survivors who received a yoga intervention had lower fatigue and inflammation following the trial compared with a wait list control group. This secondary analysis of the parent trial addressed yoga’s impact on cognitive complaints. Methods: Posttreatment stage 0–IIIA breast cancer survivors (n=200) were randomized to a 12-week, twice-weekly Hatha yoga intervention or a wait list control group. Participants reported cognitive complaints using the Breast Cancer Prevention Trial Cognitive Problems Scale at baseline, immediately postintervention, and 3-month follow-up. Results: Cognitive complaints did not differ significantly between groups immediately postintervention (p=0.250). However, at 3-month follow-up, yoga participants’ Breast Cancer Prevention Trial Cognitive Problems Scale scores were an average of 23% lower than wait list participants’ scores (p=0.003). These group differences in cognitive complaints remained after controlling for psychological distress, fatigue, and sleep quality. Consistent with the primary results, those who practiced yoga more frequently reported significantly fewer cognitive problems at 3-month follow-up than those who practiced less frequently (p

Summary Objective: The pain, depression, and fatigue symptom cluster is an important health concern. Loneliness is a common risk factor for these symptoms. Little is known about the physiological mechanisms linking loneliness to the symptom cluster; immune dysregulation is a promising candidate. Latent herpesvirus reactivation, which is reflected by elevated herpesvirus antibody titers, provides a window into immune dysregulation. Cytomegalovirus (CMV) and Epstein—Barr virus (EBV) are two common herpesviruses. Methods: Participants were 200 breast cancer survivors who were 2 months to 3 years posttreatment at the time of the study. They completed questionnaires and provided a blood sample that was assayed for CMV and EBV antibody titers. Results: Lonelier participants experienced more pain, depression, and fatigue than those who felt more socially connected. Lonelier participants also had higher CMV antibody titers which, in turn, were associated with higher levels of the pain, depression, and fatigue symptom cluster. Contrary to expectations, EBVantibody titers were not associated with either loneliness or the symptom cluster. Conclusions: The pain, depression, and fatigue symptom cluster is a notable clinical problem, especially among cancer survivors. Accordingly, understanding the risk factors for these symptoms is important. The current study suggests that loneliness enhances risk for immune dysregulation and the pain, depression, and fatigue symptom cluster. The present data also provide a glimpse into the pathways through which loneliness may impact health.

The connection between caffeine and its potentially detrimental effects on blood markers of cardiovascular disease (CVD) are controversial. Most studies have focused on cholesterol as a putative mediator of the caffeine–CVD relationship. Other blood markers such as C-reactive protein (CRP) and fibrinogen have been understudied. We examined the effects of caffeine and psychological stress on these CVD markers in healthy, young men and women with a confirmed family history of hypertension. A total of 52 normotensive, healthy adults (26 men and 26 women) aged 18–29 years (21.4 ± 0.3) participated in a laboratory session to examine stress reactivity following caffeine consumption. All participants had normal cholesterol levels. Blood pressure (BP), heart rate, serum cortisol and CRP and plasma fibrinogen were collected. Men and women administered caffeine displayed an additional increase in systolic BP and cortisol response to the stressor (p

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.

Depression is the second leading cause of disability worldwide with prevalence ranging from 2.5 to 20 % of the population dependent on the country. It can present as a single condition, but often it is co-morbid with chronic diseases. Medical professionals commonly treat depression as a neurotransmitter imbalance; yet, many effects ascribed to antidepressant medication, such as selective serotonin reuptake inhibitors, have also been explained by the placebo effect in patients with mild to moderate depression. Largely ignored research indicates that depression is caused by highly complex interactions of neuroendocrine and inflammatory mechanisms. In addition, culture/stigma, access to mental health services, and social instability play significant roles in perpetuating HPA and inflammatory pathways to maintain the disease and treatment resistance. The presented evidence highlights the need to appreciate depression through a multi-disciplinary lens to properly treat it and successfully reduce the debilitating effects on quality of life, co-morbidity and mortality, especially from suicide.

Fatigue is a notable clinical problem in cancer survivors, and understanding its pathophysiology is important. The current study sought to determine biomarkers of fatigue that exist before cancer treatment. Relationships between the expression of latent Epstein–Barr virus (EBV) and cytomegalovirus (CMV) and fatigue were examined in 158 women newly diagnosed with breast cancer or awaiting a positive diagnostic result. Higher CMV antibody titers, but not EBV antibody titers, were associated with a greater likelihood of being fatigued. Associations between fatigue and higher CMV antibody titers remained after controlling for alcohol use, smoking, comorbidities, depressive symptoms, age, BMI, cancer stage, and sleep problems. More sleep problems and higher levels of depressive symptoms were also associated with a greater likelihood of being fatigued. CMV antibody titers, but not EBV antibody titers, were associated with higher levels of C-reactive protein (CRP), but CRP was not associated with fatigue. When the cellular immune system is compromised, reactivation of latent herpesviruses may fuel chronic inflammatory responses. Prior work has suggested that fatigue may be related to inflammation and its associated sickness behaviors; accordingly, our findings may be tapping into this same physiological substrate.

Normal aging is marked by dysregulated immune function or immunosenescence. However, there is considerable variation in the degree to which adults are susceptible or resilient to immune dysregulation and disease. Stress is an important factor that can further alter the aging immune system. In this chapter, we review research that shows how stress can enhance age-related immune dysregulation in a variety of clinically relevant ways. We then explore what factors promote resilience to the negative immunological consequences of stress and aging. Finally, we take a lifespan perspective to examine evidence to suggest that some of the most important factors that augment or assuage an older adult’s capacity for resilience to age and stress-related immune dysregulation develop long before he or she reaches older adulthood. Humans are living longer than ever before. More than 12% of the U.S. population is older than the age of 65 years, and those who live at the age of 65 years can expect to live an additional two decades (Kung, Hoyert, Xu, & Murphy, 2008). Decreased infant mortality, better nutrition, and improved medical and environmental conditions are largely responsible for these dramatic increases. Accordingly, aging researchers have become increasingly interested in the notion of “successful aging.” Although there are many defi nitions for what constitutes

There are well documented links between close relationships and physical health, such that those who have supportive close relationships have lower rates of morbidity and mortality compared to those who do not. Inflammation is one mechanism that may help to explain this link. Chronically high levels of inflammation predict disease. Across the lifespan, people who have supportive close relationships have lower levels of systemic inflammation compared to people who have cold, unsupportive, and conflict-ridden relationships. Not only are current relationships associated with inflammation, but past relationships are as well. In this article, we will first review the literature linking current close relationships across the lifespan to inflammation. We will then explore recent work showing troubled past relationships also have lasting consequences for people’s inflammatory levels. Finally, we will explore developmental pathways that may explain these findings.

Glucocorticoid (GC) insensitivity coincides with several chronic diseases, including cardiovascular disease (CVD), type 2 diabetes (T2D), and major depressive disorder. Unfortunately, whether GC insensitivity is a cause or symptom of these diseases remains elusive. Cigarette smokers report greater depression and are at risk for developing CVD and T2D. Furthermore, cigarette smokers have elevated inflammation and dysregulated neuroendocrine function, suggesting GC insensitivity may exist. Thus, we recruited healthy smokers (e.g., no clinical diagnoses or current medication use) and age-, sex-, and BMI-matched never smokers to examine GC sensitivity. Following a 12-h fast, 48 adults (30.4 ± 7.7 yrs; 28 males) provided a blood sample and answered psychosocial questionnaires. Whole blood was diluted and treated with lipopolysaccharide (LPS), dexamethasone (DEX), LPS+DEX, or phosphate buffered saline (control). mRNA was isolated and analyzed for proinflammatory cytokine expression. ANOVA analyses controlling for depressive symptoms, smokers’ peripheral blood lymphocytes (PBLs) showed diminished GC suppression as indexed by percent change in expression of LPS to LPS+DEX for interleukin (IL)-6 ( p = 0.05) and IFN-gamma ( p

Cancer survivors often report cognitive problems. Furthermore, decreases in physical activity typically occur over the course of cancer treatment. Although physical activity benefits cognitive function in noncancer populations, evidence linking physical activity to cognitive function in cancer survivors is limited. In our recent randomized controlled trial, breast cancer survivors who received a yoga intervention had lower fatigue and inflammation following the trial compared with a wait list control group. This secondary analysis of the parent trial addressed yoga's impact on cognitive complaints.Posttreatment stage 0-IIIA breast cancer survivors (n = 200) were randomized to a 12-week, twice-weekly Hatha yoga intervention or a wait list control group. Participants reported cognitive complaints using the Breast Cancer Prevention Trial Cognitive Problems Scale at baseline, immediately postintervention, and 3-month follow-up.Cognitive complaints did not differ significantly between groups immediately postintervention (p = 0.250). However, at 3-month follow-up, yoga participants' Breast Cancer Prevention Trial Cognitive Problems Scale scores were an average of 23% lower than wait list participants' scores (p = 0.003). These group differences in cognitive complaints remained after controlling for psychological distress, fatigue, and sleep quality. Consistent with the primary results, those who practiced yoga more frequently reported significantly fewer cognitive problems at 3-month follow-up than those who practiced less frequently (p 0.001).These findings suggest that yoga can effectively reduce breast cancer survivors' cognitive complaints and prompt further research on mind-body and physical activity interventions for improving cancer-related cognitive problems.

Purpose To evaluate yoga's impact on inflammation, mood, and fatigue. Patients and Methods A randomized controlled 3-month trial was conducted with two post-treatment assessments of 200 breast cancer survivors assigned to either 12 weeks of 90-minute twice per week hatha yoga classes or a wait-list control. The main outcome measures were lipopolysaccharide-stimulated production of proinflammatory cytokines interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and interleukin-1β (IL-1β), and scores on the Multidimensional Fatigue Symptom Inventory-Short Form (MFSI-SF), the vitality scale from the Medical Outcomes Study 36-item Short Form (SF-36), and the Center for Epidemiological Studies-Depression (CES-D) scale. Results Immediately post-treatment, fatigue was not lower (P > .05) but vitality was higher (P = .01) in the yoga group compared with the control group. At 3 months post-treatment, fatigue was lower in the yoga group (P = .002), vitality was higher (P = .01), and IL-6 (P = .027), TNF-α (P = .027), and IL-1β (P = .037) were lower for yoga participants compared with the control group. Groups did not differ on depression at either time (P > .2). Planned secondary analyses showed that the frequency of yoga practice had stronger associations with fatigue at both post-treatment visits (P = .019; P < .001), as well as vitality (P = .016; P = .0045), but not depression (P > .05) than simple group assignment; more frequent practice produced larger changes. At 3 months post-treatment, increasing yoga practice also led to a decrease in IL-6 (P = .01) and IL-1β (P = .03) production but not in TNF-α production (P > .05). Conclusion Chronic inflammation may fuel declines in physical function leading to frailty and disability. If yoga dampens or limits both fatigue and inflammation, then regular practice could have substantial health benefits.

Background To follow up on a recent report from our lab [Hum Psychopharmacol 25:359–367, 2010.] we examined the effects of caffeine on salivary α-amylase (sAA) activity in response to an engaging, non-stressful task in healthy young males (age 18–30 yrs) who consumed caffeine on a daily basis. Using a placebo-controlled, double-blind, between-subjects design, 45 men received either placebo, 200 mg or 400 mg of caffeine (Vivarin®). Participants then rested for 20 minutes, and performed a 20-minute computerized air traffic controller-like task that was cognitively engaging but not stressful. Saliva samples (assayed for sAA and cortisol), blood pressure, and heart rate were taken before (baseline) and 15 minutes after the computerized task. Results Systolic and diastolic blood pressure and sAA activity increased across the laboratory session (F’s > 9.20, p’s

Although evidence suggests that loneliness may increase risk for health problems, the mechanisms responsible are not well understood. Immune dysregulation is one potential pathway: Elevated proinflammatory cytokines such as interleukin-6 (IL-6) increase risk for health problems. In our first study ( N = 134), lonelier healthy adults exposed to acute stress exhibited greater synthesis of tumor necrosis factor-alpha (TNF-α) and IL-6 by peripheral blood mononuclear cells (PBMCs) stimulated with lipopolysaccharide (LPS) than their less lonely counterparts. Similarly, in the second study ( N = 144), lonelier posttreatment breast-cancer survivors exposed to acute stress exhibited greater synthesis of IL-6 and interleukin-1 beta (IL-1β) by LPS-stimulated PBMCs than their counterparts who felt more socially connected. However, loneliness was unrelated to TNF-α in Study 2, although the result was in the expected direction. Thus, two different populations demonstrated that lonelier participants had more stimulated cytokine production in response to stress than less lonely participants, which reflects a proinflammatory phenotype. These data provide a glimpse into the pathways through which loneliness may affect health.

Caregiving for a spouse with dementia is highly distressing. On average, spouses serving as dementia caregivers spend more than 10 h per day providing care for over 5 years. During this time, they experience a type of “living bereavement” as they watch their partners slowly lose their personality and intellect.

Psychoneuroimmunology (PNI) is a field in which researchers investigate the intersections among behavior, the nervous system, and the immune system. Its development over the past 35 years followed the realization that the immune system does not function in isolation [1, 2]. The initial focus on biological mechanisms encouraged the use of animal models to uncover pathways through which the brain and behavior affect immune activity. Once biological pathways were established, researchers started replicating similar results in humans with broad applications in areas such as infectious diseases, cardiovascular disease, autoimmunity, and cancer. Today, the transdisciplinary field of PNI continues to unravel the complex connections among behavior, immune function, and health.

The connection between caffeine and its potentially detrimental effects on blood markers of cardiovascular disease (CVD) are controversial. Most studies have focused on cholesterol as a putative mediator of the caffeine-CVD relationship. Other blood markers such as C-reactive protein (CRP) and fibrinogen have been understudied. We examined the effects of caffeine and psychological stress on these CVD markers in healthy, young men and women with a confirmed family history of hypertension. A total of 52 normotensive, healthy adults (26 men and 26 women) aged 18-29 years (21.4 ± 0.3) participated in a laboratory session to examine stress reactivity following caffeine consumption. All participants had normal cholesterol levels. Blood pressure (BP), heart rate, serum cortisol and CRP and plasma fibrinogen were collected. Men and women administered caffeine displayed an additional increase in systolic BP and cortisol response to the stressor (p 0.05). Stress interacted with caffeine and sex to alter cortisol, fibrinogen and systolic BP but not CRP levels. These results may shed light on sex-specific pathways that associate caffeine with CVD.

Summary Cigarette smoking continues to be the most preventable cause of illness and death and has been linked to the development and prognosis of cancer. Current smokers have higher levels of inflammation than nonsmokers, and inflammation can remain elevated in former smokers even years following cessation. Inflammation can also be enhanced by stress. This study examined cortisol and inflammatory responses to a laboratory stressor in breast cancer survivors who formerly smoked compared to their counterparts who had never smoked. Participants included 89 women (age = 51.6 ± 8.9 years) who had completed treatment for stage 0–IIIA breast cancer within the past three years and were at least two months post surgery, radiation or chemotherapy, whichever occurred last. Cortisol and interleukin-6 (IL-6) were evaluated in response to a standardized laboratory speech and mental arithmetic stressor. Former (n = 25) and never (n = 64) smokers did not differ by cancer stage, cancer treatment, comorbidities, time since cancer treatment, depression, or stress. Despite having similar cortisol responses to the stressor, former smokers had exaggerated IL-6 responses two hours post-stressor compared to never smokers. This effect persisted after controlling for age, BMI, time since treatment, education, and antidepressant use. An exaggerated and prolonged inflammatory response to stress could be one mechanism underlying the persistent inflammation observed in former smokers.

Health disparities increase with each step down the socioeconomic status (SES) ladder (Adler & Rehkopf, 2008). Adults with lower incomes, less education, and less prestigious jobs are at greater risk for chronic disease, disability, and premature mortality (Stowe et al., 2010). Although income clearly limits health care access, the connection between lower SES and poor health still exists in countries with universal health care; thus, health care access is not the sole mechanism (Cohen, Doyle, & Baum, 2006). Understanding why SES-related health disparities exist could lead to improvements in health. Maladaptive alterations in immune function are central to SES health disparities. Research addressing pathogen burden has provided some of the strongest data in this regard, with the herpesviruses playing a pivotal role (Stowe, et al., 2010). Once a person has been infected with one of the herpesviruses, they will carry the virus for the rest of their life (Glaser & Kiecolt-Glaser, 1994). Herpesviruses create persistent latent infections, in which the virus remains “dormant” in latently infected cells. Under a variety of conditions, the virus may be triggered to reactivate in those cells and replicate, thereby producing new virus particles that kill cells. Persistent infections fuel chronic inflammatory responses, which in turn are linked to a range of age-related diseases (Steptoe et al., 2007). SES researchers have focused on Epstein-Barr virus (EBV), herpes simplex virus type 1 (HSV-1), and cytomegalovirus (CMV) infections (Simanek, Dowd, & Aiello, 2009; Steptoe, et al., 2007; Stowe, et al., 2010); these herpesviruses are ubiquitous in adults. More than 90% of adults are EBV seropositive (previously infected) (Glaser & Kiecolt-Glaser, 1994), and more than 90% of individuals have antibody to HSV-1 by their forties (Nahmias & Roizman, 1973). Lower SES individuals are more likely to be infected with each of these herpesviruses earlier in life than higher SES individuals; they are also more likely to be seropositive for multiple pathogens, and to show evidence of viral reactivation (Stowe, et al., 2010). Psychological stress and depression can drive herpesvirus reactivation or replication by impairing the ability of the cellular immune system to control viral latency (Glaser & Kiecolt-Glaser, 1994). Both stress and depression are higher among those with lower incomes and less education (Adler & Rehkopf, 2008). When the cellular immune system is compromised, EBV and other herpesviruses reactivate; the increased antiviral antibody production reflects the immune system’s response to heightened herpesvirus replication (Glaser & Kiecolt-Glaser, 1994). Supportive interpersonal relationships can buffer the negative effects of stress on the cellular immune system and herpesvirus latency. For example, dementia spousal caregivers who reported lower levels of social support upon entry into a longitudinal study showed greater negative changes in immune function a year later, including increases in EBV antibody titers (Kiecolt-Glaser, Dura, Speicher, Trask, & Glaser, 1991). Lonelier medical students had higher EBV antibody titers than their fellow students who were not as lonely (Kiecolt-Glaser et al., 1984). The experience of awaiting or receiving a breast cancer diagnosis is highly stressful, and supportive interpersonal relationships can buffer this distress (Hegel et al., 2006). Indeed, one study found that the elevated distress observed before a diagnostic breast biopsy remained high after the biopsy, regardless of the diagnostic outcome (Witek-Janusek, Gabram, & Mathews, 2007). Supportive interpersonal relationships predict better adjustment among women diagnosed with breast cancer (Arora, Finney Rutten, Gustafson, Moser, & Hawkins, 2007; Burgess et al., 2005; Epplein et al., 2010). Lower SES individuals may not obtain the same stress reducing benefits from social support as higher SES individuals (Riley & Eckenrode, 1986). Lower SES people receive lower quality support from others than those who are higher SES (Belle, 1982, 1990; Krause & Borawski-Clark, 1995). Higher SES individuals are more likely to seek support in times of high stress compared to those who are lower SES (Krause, 1997). This difference is important because people benefit most from social support when they experience stress (Cohen & Wills, 1985). Accordingly, SES may moderate the link between social support and health. This study investigated how SES and social support were related to cellular immune function in a highly stressed sample of newly diagnosed breast cancer patients or those awaiting a potential breast cancer diagnosis. Specifically, we addressed the question of whether SES moderated the association between social support and EBV antibody titers. Psychological stress and depression can drive herpesvirus reactivation, and people benefit most from social support when stressed (Cohen, 2004; Cohen & Wills, 1985). Given the heightened distress surrounding an abnormal mammogram or breast cancer diagnosis, we studied these relationships in both groups. Although we did not expect differential results between those awaiting a breast cancer diagnosis or newly diagnosed with breast cancer based on related studies (Witek-Janusek, et al., 2007), we tested for these differences. As an ancillary analysis, we also assessed relationships between SES, social support, and blood pressure.

Inflammation increases with age and is associated with many chronic diseases that are prevalent among older adults. Persistent pathogens such as latent herpesviruses and chronic bacterial infections can act as a source of inflammation. Herpesviruses, including Epstein-Barr virus (EBV) and cytomegalovirus (CMV), establish latent infections following primary infection and reactivate when the cellular immune system is compromised. EBV and CMV replication can induce proinflammatory cytokine production and thus could influence systemic inflammation. The present study addressed relationships among EBV and CMV antibody titers, and levels of C-reactive protein (CRP) and interleukin-6 (IL-6) in a sample of 222 community dwelling older adults (meanage= 64.1 ± 14.1 years). Participants were divided into two groups based on whether they were EBV seropositive and CMV seronegative (EBV+CMV−), or EBV and CMV seropositive (EBV+CMV+). Among individuals who were EBV+CMV−, EBV antibody titers were not associated with either CRP or IL-6 levels. However, among those who were EBV+CMV+, higher EBV antibody titers were related to elevated levels of CRP and IL-6 in those individuals with higher CMV antibody titers; there was no relationship between EBV antibody titers and CRP or IL-6 levels in those participants with lower CMV antibody titers. These data suggest that the combination of latent EBV and CMV reactivation (indexed by antibody titers) may boost CRP and IL-6 production. Thus, reactivation of multiple herpesviruses may drive inflammation and could contribute to poorer health among older adults.

Objective We examined the effects of caffeine and a psychological stressor on salivary α-amylase (sAA) in healthy young males (age 18–30 years) who consumed caffeine on a daily basis. Methods Using a between-subjects, double-blind, placebo-controlled design, 45 participants received either 200 or 400 mg of caffeine (Vivarin®) or placebo, rested for 20 min, and then performed 20 min of mental arithmetic. Saliva samples (assayed for sAA and caffeine), blood pressure, and heart rate were taken before (baseline) and 15 min after the math stressor (stress). Results Baseline sAA activity did not differ among the treatment groups; however, there was a statistically significant time by caffeine group interaction. Changes in sAA activity across the session were dependent on the amount of caffeine consumed. Following the challenge period, sAA activity among the placebo group was the lowest and sAA activity among the 400 mg treatment group was the highest. Separate repeated-measures ANOVAs conducted for each drug treatment group revealed that sAA activity increased in response to stress and caffeine (i.e., 200 and 400 mg groups) but not to stress alone (i.e., placebo group). Conclusions Findings provide evidence for acute sAA changes in response to caffeine and stress in habitual caffeine users. Copyright © 2010 John Wiley & Sons, Ltd.

Behavioral characteristics closely associated with specific physiological profiles present an important area of research in understanding health disparities. In particular, glucocorticoid overproduction may be an important factor moderating disease progression; natural variance in production of this steroid has been proposed as one mechanism underlying individual differences in health and disease. In the current paper, we examined immune parameters in female rats of two different behavioral types previously shown to have differential glucocorticoid production and life spans. We categorized young female rats according to their behavioral response to novelty (high- or low-locomotion), and compared their glucocorticoid production, adrenal size, thymus size, tumor necrosis factor-alpha (TNF-alpha) production, tumor development and life span. As expected, high-locomotion females produced more glucocorticoids and had larger adrenal glands during young adulthood than did low-locomotion females. High-locomotion females had significantly smaller thymuses and reduced TNF-alpha levels compared to low-locomotion, suggesting altered immune function in young adulthood. Finally, high-locomotion females had shorter life spans than did low-locomotion females, and this was particularly true in females that developed pituitary tumors, but not in those that developed mammary tumors. These results, along with other published findings, suggest that high-locomotion rodent females experience life-long elevations in glucocorticoid responses to novelty, and that these elevated levels may be comparable to chronic stress. This naturally occurring endocrine profile may influence immune responses which in turn could affect disease susceptibility. Variance in immune function across personality types may be partially moderated by natural variance in glucocorticoid production.

Cigarette smoking continues to be the most preventable cause of illness and death. Current smokers have dysregulated hypothalamic–pituitary–adrenal (HPA) activity and elevated levels of inflammation compared to nonsmokers. To date, data in former smokers has been limited to observing persistent inflammation even years following cessation, yet there is little published on HPA function. This study examined cortisol and interleukin-6 (IL-6) responses to a laboratory stressor in breast cancer survivors who formerly smoked compared to their counterparts who had never smoked. Participants included 90 women (age = 51.4 ± 9.4 years) who had completed treatment for stage 0-IIIA breast cancer within the past three years and were at least two months post surgery, radiation or chemotherapy, whichever occurred last. Cortisol and IL-6 were evaluated in response to a standardized laboratory speech and mental arithmetic stressor. Former ( n = 25) and never ( n = 65) smokers did not differ by cancer stage, cancer treatment, comorbidities, time since treatment, depression, or stress. Despite having similar cortisol responses to the stressor, former smokers had exaggerated IL-6 responses two hours post-stressor compared to never smokers ( p