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This Committee Report provides methodological, interpretive, and reporting guidance for researchers who use measures of heart rate (HR) and heart rate variability (HRV) in psychophysiological research. We provide brief summaries of best practices in measuring HR and HRV via electrocardiographic and photoplethysmographic signals in laboratory, field (ambulatory), and brain‐imaging contexts to address research questions incorporating measures of HR and HRV. The Report emphasizes evidence for the strengths and weaknesses of different recording and derivation methods for measures of HR and HRV. Along with this guidance, the Report reviews what is known about the origin of the heartbeat and its neural control, including factors that produce and influence HRV metrics. The Report concludes with checklists to guide authors in study design and analysis considerations, as well as guidance on the reporting of key methodological details and characteristics of the samples under study. It is expected that rigorous and transparent recording and reporting of HR and HRV measures will strengthen inferences across the many applications of these metrics in psychophysiology. The prior Committee Reports on HR and HRV are several decades old. Since their appearance, technologies for human cardiac and vascular monitoring in laboratory and daily life (i.e., ambulatory) contexts have greatly expanded. This Committee Report was prepared for the Society for Psychophysiological Research to provide updated methodological and interpretive guidance, as well as to summarize best practices for reporting HR and HRV studies in humans. [ABSTRACT FROM AUTHOR]

Threats to social connectedness in the form of social and societal rejection, and the permanent loss of social bonds, are inevitable and common sources of social pain. However, sensitivity to social pain, also known as algesia, differs across individuals and contexts. Such sensitivity has implications for health, well-being, and the maintenance of social connection over time. What biological factors predict differences in sensitivity to social pain? Based on long-standing translational perspectives and emerging findings, the current review highlights blood pressure as a novel predictor of sensitivity to social pain: Higher resting blood pressure appears to relate to lower sensitivity to social pain. Despite evidence for this association, possible psychobiological bases and moderating influences are not yet established. Moreover, although higher blood pressure may afford tolerance for life's many pains, the health-related implications and trade-offs of such an effect are unknown. [ABSTRACT FROM AUTHOR]

Social pain is a common experience that has potent implications for health. However, individuals differ in their sensitivity to social pain. Recent evidence suggests that sensitivity to social pain varies according to a biological factor that modulates sensitivity to physical pain: resting (tonic) blood pressure. The current studies extended this evidence by testing whether blood pressure relates to sensitivity to imagined (Study 1: N = 762, 51% female adults) and acute (Study 2, preregistered: N = 204, 57% female adults) experiences of social pain and whether associations extend to general emotional responding (Studies 1–3; Study 3: N = 162, 59% female adults). In line with prior evidence, results showed that higher resting blood pressure was associated with lower sensitivity to social pain. Moreover, associations regarding blood pressure and sensitivity to social pain did not appear to be explained by individual differences in general emotional responding. Findings appear to be compatible with the interpretation that social and physical pain share similar cardiovascular correlates and may be modulated by convergent interoceptive pathways. [ABSTRACT FROM AUTHOR]

Resting heart rate may confer risk for cardiovascular disease (CVD) and other adverse cardiovascular events. While the brainstem's autonomic control over heart rate is well established, less is known about the regulatory role of higher level cortical and subcortical brain regions, especially in humans. This study sought to characterize the brain networks that predict variation in prevailing heart rate in otherwise healthy adults. We used machine learning approaches designed for complex, high‐dimensional data sets, to predict variation in instantaneous heart period (the inter‐heartbeat‐interval) from whole‐brain hemodynamic signals measured by fMRI. Task‐based and resting‐state fMRI, as well as peripheral physiological recordings, were taken from two data sets that included extensive repeated measurements within individuals. Our models reliably predicted instantaneous heart period from whole‐brain fMRI data both within and across individuals, with prediction accuracies being highest when measured within‐participants. We found that a network of cortical and subcortical brain regions, many linked to visceral motor and visceral sensory processes, were reliable predictors of variation in heart period. This adds to evidence on brain–heart interactions and constitutes an incremental step toward developing clinically applicable biomarkers of brain contributions to CVD risk. Using whole‐brain fMRI data, we reliably predicted instantaneous heart period within and across individuals from the activity of a network of cortical and subcortical brain regions, many linked to visceral motor and visceral sensory processes. This adds to existing evidence on brain–heart interactions and constitutes a step toward developing clinically applicable biomarkers of brain contributions to CVD risk. [ABSTRACT FROM AUTHOR]

This study tested whether brain activity patterns evoked by affective stimuli relate to individual differences in an indicator of pre-clinical atherosclerosis: carotid artery intima-media thickness (CA-IMT). Adults (aged 30–54 years) completed functional magnetic resonance imaging (fMRI) tasks that involved viewing three sets of affective stimuli. Two sets included facial expressions of emotion, and one set included neutral and unpleasant images from the International Affective Picture System (IAPS). Cross-validated, multivariate and machine learning models showed that individual differences in CA-IMT were partially predicted by brain activity patterns evoked by unpleasant IAPS images, even after accounting for age, sex and known cardiovascular disease risk factors. CA-IMT was also predicted by brain activity patterns evoked by angry and fearful faces from one of the two stimulus sets of facial expressions, but this predictive association did not persist after accounting for known cardiovascular risk factors. The reliability (internal consistency) of brain activity patterns evoked by affective stimuli may have constrained their prediction of CA-IMT. Distributed brain activity patterns could comprise affective neural correlates of pre-clinical atherosclerosis; however, the interpretation of such correlates may depend on their psychometric properties, as well as the influence of other cardiovascular risk factors and specific affective cues. [ABSTRACT FROM AUTHOR]

Psychological stress still attracts scientific, clinical, and public interest because of its suspected connection to health, particularly cardiovascular health. Psychological stress is thought to arise from appraisal processes that imbue events and contexts with personal significance and threat-related meaning. These appraisal processes are also thought to be instantiated in brain systems that generate and control peripheral physiological stress reactions through visceral motor (brain-to-body) and visceral sensory (body-to-brain) mechanisms. In the short term, physiological stress reactions may enable coping and adaptive action. Among some individuals, however, the patterning of these reactions may predict or contribute to pathology in multiple organ systems, including the cardiovascular system. At present, however, we lack a precise understanding of the brain systems and visceral control processes that link psychological appraisals to patterns of stress physiology and physical health. This understanding is important: A mechanistic account of how the brain connects stressful experiences to bodily changes and health could help refine biomarkers of risk and targets for cardiovascular disease prevention and intervention. We review research contributing to this understanding, focusing on the neurobiology of cardiovascular stress reactivity and cardiovascular health. We suggest that a dysregulation of visceral motor and visceral sensory processes during stressful experiences may confer risk for poor cardiovascular health among vulnerable individuals. We further describe a need for new interpretive frameworks and markers of this brain-body dysregulation in cardiovascular behavioral medicine. [ABSTRACT FROM AUTHOR]

In this article, we argued that the term stress has served as a valuable heuristic, helping researchers to integrate traditions that illuminate different stages of the process linking stressful life events to disease. We provided a short history of three traditions in the study of stress: the epidemiological, psychological, and biological. The epidemiological tradition focuses on defining which circumstances and experiences are deemed stressful on the basis of consensual agreement that they constitute threats to social or physical well-being. The psychological tradition focuses on individuals' perceptions of the stress presented by life events on the basis of their appraisals of the threats posed and the availability of effective coping resources. The biological tradition focuses on brain-based perturbations of physiological systems that are otherwise essential for normal homeostatic regulation and metabolic control. The foci of these three traditions have informed elements of a stage model of disease, wherein events appraised as stressful are viewed as triggering affective states that in turn engender behavioral and biological responses having possible downstream implications for disease. [ABSTRACT FROM AUTHOR]

Recent studies indicate that mindfulness meditation training interventions reduce stress and improve stress-related health outcomes, but the neural pathways for these effects are unknown. The present research evaluates whether mindfulness meditation training alters resting state functional connectivity (rsFC) of the amygdala, a region known to coordinate stress processing and physiological stress responses. We show in an initial discovery study that higher perceived stress over the past month is associated with greater bilateral amygdala-subgenual anterior cingulate cortex (sgACC) rsFC in a sample of community adults (n¼130). A follow-up, single-blind randomized controlled trial shows that a 3-day intensive mindfulness meditation training intervention (relative to a well-matched 3-day relaxation training intervention without a mindfulness component) reduced right amygdala-sgACC rsFC in a sample of stressed unemployed community adults (n¼35). Although stress may increase amygdala-sgACC rsFC, brief training in mindfulness meditation could reverse these effects. This work provides an initial indication that mindfulness meditation training promotes functional neuroplastic changes, suggesting an amygdala-sgACC pathway for stress reduction effects. [ABSTRACT FROM AUTHOR]

Childhood trauma may confer risk for poorer adult health through changes in systemic inflammation. Emotion regulation may plausibly moderate associations between childhood trauma and adult psychological well‐being, but it remains unclear whether moderation effects extend to differences in systemic inflammation. To examine whether childhood trauma and emotion regulation separately and interactively predict prospective changes in C‐reactive protein (CRP) and interleukin‐6 (IL‐6) and whether biopsychosocial factors account for observed associations. Healthy midlife adults (N = 331) retrospectively reported on childhood trauma, current trait‐level cognitive reappraisal and expressive suppression, and had their blood drawn. At baseline and then a median of 2.85 years later, 279 of the 331 participants had their blood drawn, body mass index calculated, and reported on health behaviours (smoking, sleep), psychological distress (perceived stress, depressive symptoms), and years of education. Childhood trauma predicted prospective increases in CRP (B = 0.004, p = 0.049), which were partially accounted for by differences in adiposity, psychological distress, and health behaviours. In contrast, cognitive reappraisal predicted prospective decreases in IL‐6 (B = −0.007, p = 0.006), which were independent of biopsychosocial influences. Cognitive reappraisal further moderated the association between childhood trauma and prospective changes in IL‐6 (B = −0.001, p = 0.012) such that childhood trauma predicted greater IL‐6 increases but only among adults lower in cognitive reappraisal (B = 0.006, p = 0.007). There were no main or moderation effects of expressive suppression (ps > 0.05). Cognitive reappraisal may attenuate IL‐6 changes over time and may moderate the prospective association between childhood trauma and systemic inflammation in midlife. [ABSTRACT FROM AUTHOR]

Psychological stress is thought to arise from appraisal processes that ascribe threat-related meaning to experiences that tax or exceed our coping ability. Neuroimaging research indicates that these appraisal processes originate in brain systems that also control physiological stress reactions in the body. Separate lines of research in health psychology and behavioral medicine indicate that these physiological stress reactions confer risk for physical disease. Accordingly, integrative research that cuts across historically separated disciplines may help to define the brain-body pathways linking psychological stress to physical health. We describe recent studies aimed at this goal, focusing on studies of the brain bases of stressor-evoked cardiovascular-system reactions and heart disease risk. We also outline an interpretive framework for these studies, as well as needs for next-generation models and metrics to better understand how the brain encodes and embodies stress in relation to health. [ABSTRACT FROM AUTHOR]

Background: Inflammation is linked to cognitive decline in midlife, but the neural basis for this link is unclear. One possibility is that inflammation associates with adverse changes in brain morphology, which accelerates cognitive aging and later dementia risk. Clear evidence is lacking, however, regarding whether inflammation relates to cognition in midlife via changes in brain morphology. Accordingly, the current study examines whether associations of inflammation with cognitive function are mediated by variation in cortical gray matter volume among midlife adults. Methods: Plasma levels of interleukin (IL)-6 and C-reactive protein (CRP), relatively stable markers of peripheral systemic inflammation, were assessed in 408 community volunteers aged 30–54 years. All participants underwent structural neuroimaging to assess global and regional brain morphology and completed neuropsychological tests sensitive to early changes in cognitive function. Measurements of brain morphology (regional tissue volumes and cortical thickness and surface area) were derived using Freesurfer. Results: Higher peripheral inflammation was associated with poorer spatial reasoning, short term memory, verbal proficiency, learning and memory, and executive function, as well as lower cortical gray and white matter volumes, hippocampal volume and cortical surface area. Mediation models with age, sex and intracranial volume as covariates showed cortical gray matter volume to partially mediate the association of inflammation with cognitive performance. Exploratory analyses of body mass suggested that adiposity may be a source of the inflammation linking brain morphology to cognition. Conclusions: Inflammation and adiposity might relate to cognitive decline via influences on brain morphology. [ABSTRACT FROM AUTHOR]

Neuroimaging has identified many correlates of emotion but has not yet yielded brain representations predictive of the intensity of emotional experiences in individuals. We used machine learning to identify a sensitive and specific signature of emotional responses to aversive images. This signature predicted the intensity of negative emotion in individual participants in cross validation (n =121) and test (n = 61) samples (high–low emotion = 93.5% accuracy). It was unresponsive to physical pain (emotion–pain = 92% discriminative accuracy), demonstrating that it is not a representation of generalized arousal or salience. The signature was comprised of mesoscale patterns spanning multiple cortical and subcortical systems, with no single system necessary or sufficient for predicting experience. Furthermore, it was not reducible to activity in traditional “emotion-related” regions (e.g., amygdala, insula) or resting-state networks (e.g., “salience,” “default mode”). Overall, this work identifies differentiable neural components of negative emotion and pain, providing a basis for new, brain-based taxonomies of affective processes. [ABSTRACT FROM AUTHOR]

Health neuroscience is a new field that is at the interface of health psychology and neuroscience. It is concerned with the interplay between the brain and physical health over the life span. A chief goal of health neuroscience is to characterize bidirectional and dynamic brain-behavior and brain-physiology relationships that are determinants, markers, and consequences of physical-health states across the life span. The motivation behind this goal is that a better understanding of these relationships will provide mechanistic insights into how the brain links multilevel genetic, biological, psychological, behavioral, social, and environmental factors with physical health—especially vulnerability to and resilience against clinical illnesses. This review provides a conceptual introduction to health neuroscience, focusing on its major themes, representative studies, methodologies, and future directions. [ABSTRACT FROM PUBLISHER]

Background: Cognitive reappraisal is a form of emotion regulation that alters emotional responding by changing the meaning of emotional stimuli. Reappraisal engages regions of the prefrontal cortex that support multiple functions, including visceral control functions implicated in regulating the immune system. Immune activity plays a role in the preclinical pathophysiology of atherosclerotic cardiovascular disease (CVD), an inflammatory condition that is highly comorbid with affective disorders characterized by problems with emotion regulation. Here, we tested whether prefrontal engagement by reappraisal would be associated with atherosclerotic CVD risk and whether this association would be mediated by inflammatory activity. Methods: Community volunteers (n = 157; 30–54 years of age; 80 women) without DSM-IV Axis-1 psychiatric diagnoses or cardiovascular or immune disorders performed a functional neuroimaging task involving the reappraisal of negative emotional stimuli. Carotid artery intima-media thickness and inter-adventitial diameter were measured by ultrasonography and used as markers of preclinical atherosclerosis. Also measured were circulating levels of interleukin-6 (IL-6), an inflammatory cytokine linked to CVD risk and prefrontal neural activity. Results: Greater reappraisal-related engagement of the dorsal anterior cingulate cortex was associated with greater preclinical atherosclerosis and IL-6. Moreover, IL-6 mediated the association of dorsal anterior cingulate cortex engagement with preclinical atherosclerosis. These results were independent of age, sex, race, smoking status, and other known CVD risk factors. Conclusions: The cognitive regulation of emotion might relate to CVD risk through a pathway involving the functional interplay between the anterior cingulate region of the prefrontal cortex and inflammatory activity. [ABSTRACT FROM AUTHOR]

The present study compared neural activity in participants with blunted ( N = 9) or exaggerated ( N = 8) cardiac stress reactions. Neural activity was recorded with f MRI while participants performed a validated stress task and control task. Exaggerated reactors exhibited significant increases in heart rate from control to stress task, whereas blunted reactors had no change in heart rate. Blunted reactors also had reduced activation in the anterior midcingulate cortex and insula compared to exaggerated reactors during the stress condition, and a greater deactivation in the amygdala and posterior cingulate. The biological differences between groups in response to the stress task could not be explained by subjective measures of engagement, stressfulness, or difficulty. This study supports the notion that blunted peripheral physiological stress reactivity may be a marker of a corresponding under-recruitment of brain systems during behavioral states requiring motivated action. [ABSTRACT FROM AUTHOR]

The arterial baroreflex is a key mechanism for the homeostatic control of blood pressure (BP). In animals and humans, psychological stressors suppress the capacity of the arterial baroreflex to control short-term fluctuations in BP, reflected by reduced baroreflex sensitivity (BRS). While animal studies have characterized the brain systems that link stressor processing to BRS suppression, comparable human studies are lacking. Here, we measured beat-to-beat BP and heart rate (HR) in 97 adults who performed a multisource interference task that evoked changes in spontaneous BRS, which were quantified by a validated sequence method. The same 97 participants also performed the task during functional magnetic resonance imaging (fMRI) of brain activity. Across participants, task performance (i) increased BP and HR and (ii) reduced BRS. Analyses of fMRI data further demonstrated that a greater task-evoked reduction in BRS covaried with greater activity in brain systems important for central autonomic and cardiovascular control, particularly the cingulate cortex, insula, amygdala, and midbrain periaqueductal gray (PAG). Moreover, task performance increased the functional connectivity of a discrete area of the anterior insula with both the cingulate cortex and amygdala. In parallel, this same insula area showed increased task-evoked functional connectivity with midbrain PAG and pons. These novel findings provide human evidence for the brain systems presumptively involved in suppressing baroreflex functionality, with relevance for understanding the neurobiological mechanisms of stressor-related cardiovascular reactivity and associated risk for essential hypertension and atherosclerotic heart disease. Hum Brain Mapp, 2011. © 2011 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

The brain is the key organ of stress processes. It determines what individuals will experience as stressful, it orchestrates how individuals will cope with stressful experiences, and it changes both functionally and structurally as a result of stressful experiences. Within the brain, a distributed, dynamic, and plastic neural circuitry coordinates, monitors, and calibrates behavioral and physiological stress response systems to meet the demands imposed by particular stressors. These allodynamic processes can be adaptive in the short term (allostasis) and maladaptive in the long term (allostatic load). Critically, these processes involve bidirectional signaling between the brain and body. Consequently, allostasis and allostatic load can jointly affect vulnerability to brain-dependent and stress-related mental and physical health conditions. This review focuses on the role of brain plasticity in adaptation to, and pathophysiology resulting from, stressful experiences. It also considers interventions to prevent and treat chronic and prevalent health conditions via allodynamic brain mechanisms. [ABSTRACT FROM AUTHOR]

The brain is the key organ of stress reactivity, coping, and recovery processes. Within the brain, a distributed neural circuitry determines what is threatening and thus stressful to the individual. Instrumental brain systems of this circuitry include the hippocampus, amygdala, and areas of the prefrontal cortex. Together, these systems regulate physiological and behavioral stress processes, which can be adaptive in the short-term and maladaptive in the long-term. Importantly, such stress processes arise from bidirectional patterns of communication between the brain and the autonomic, cardiovascular, and immune systems via neural and endocrine mechanisms underpinning cognition, experience, and behavior. In one respect, these bidirectional stress mechanisms are protective in that they promote short-term adaptation ( allostasis). In another respect, however, these stress mechanisms can lead to a long-term dysregulation of allostasis in that they promote maladaptive wear-and-tear on the body and brain under chronically stressful conditions ( allostatic load), compromising stress resiliency and health. This review focuses specifically on the links between stress-related processes embedded within the social environment and embodied within the brain, which is viewed as the central mediator and target of allostasis and allostatic load. [ABSTRACT FROM AUTHOR]

Abstract: An individual''s tendency to show exaggerated or otherwise dysregulated cardiovascular reactions to acute stressors has long been associated with increased risk for clinical and preclinical endpoints of coronary heart disease (CHD). However, the ‘brain-body’ pathways that link stressor-evoked cardiovascular reactions to CHD risk remain uncertain. This review summarizes emerging neuroimaging research indicating that individual differences in stressor-evoked blood pressure reactivity (a particular form of cardiovascular reactivity) are associated with activation patterns in corticolimbic brain areas that are jointly involved in processing stressors and regulating the cardiovascular system. As supported empirically by activation likelihood estimates derived from a meta-analysis, these corticolimbic areas include divisions of the cingulate cortex, insula, and amygdala — as well as networked cortical and subcortical areas involved in mobilizing hemodynamic and metabolic support for stress-related behavioral responding. Contextually, the research reviewed here illustrates how behavioral medicine and health neuroscience methods can be integrated to help characterize the ‘brain-body’ pathways that mechanistically link stressful experiences with CHD risk. [Copyright &y& Elsevier]

Background: Cardiovascular disease (CVD) is a major source of medical comorbidity for patients with mood and anxiety disorders, and it remains the leading public health burden for the general population in industrialized nations. Indirect neurobiological evidence suggests that preclinical risk for atherosclerosis, the main contributor to CVD, may be conferred by interindividual variation in the functionality of the amygdala, a brain system jointly involved in processing behaviorally salient stimuli and regulating the cardiovascular system. Methods: In a neuroimaging study of 36 middle-aged adults (18 women) who were screened for confounding clinical cardiovascular and psychiatric disorders, we examined the direct covariation between a marker of preclinical atherosclerosis, carotid artery intima-media thickness (IMT), and interindividual variation in amygdala reactivity and functional connectivity assessed during the processing of behaviorally salient stimuli (angry and fearful facial expressions). Results: After accounting for traditional CVD risk factors, a thickening of carotid IMT across individuals covaried with greater amygdala reactivity and a more positive functional connectivity between the amygdala and perigenual anterior cingulate cortex, a corticolimbic area also implicated in behavioral salience processing and cardiovascular regulation. Conclusions: Individual differences in amygdala reactivity and functional connectivity may reflect facets of a novel, systems-level neural phenotype conferring risk for atherosclerosis and CVD. [Copyright &y& Elsevier]

Background: Converging animal findings suggest that higher peripheral levels of inflammation are associated with activation of central inflammatory mechanisms that result in hippocampal neurodegeneration and related impairment of memory function. We have recently shown, consistent with animal findings, an inverse association between peripheral levels of interleukin-6 (IL-6), a relatively stable marker of systemic inflammation, and memory function in mid-life adults. In the current study, we extend this work to test whether systemic inflammation is associated with reduced grey matter volume of the hippocampus. Methods: For this purpose, we used a computational structural neuroimaging method (optimized voxel-based morphometry) to evaluate the relationship between plasma IL-6 levels and hippocampal grey matter volume in a sample of 76 relatively healthy community volunteers ages 30–54. Results: Peripheral levels of IL-6 covaried inversely with hippocampal grey matter volume, and this relationship persisted after accounting for several possible confounders, including age, gender, race, years of education, percent body fat, blood pressure, smoking, physical activity, hours of sleep, alcohol use, and total grey matter volume. Conclusions: To our knowledge, this is the first report of a relationship between a peripheral marker of IL-6 and hippocampal grey matter volume, raising the possibility that low-grade systemic inflammation could plausibly presage subclinical cognitive decline in part via structural neural pathways. [Copyright &y& Elsevier]

Socioeconomic disadvantage during childhood and adolescence predicts poor mental and physical health and premature death by major medical diseases in adulthood. However, the neural pathways through which socioeconomic factors may exert a developmental influence on health and longevity remain largely unknown. This fMRI study provides novel evidence of a unique relationship between the perception that one's parents had a relatively low social standing—a putative indicator of early socioeconomic disadvantage—and greater amygdala reactivity to threatening facial expressions. This relationship was not explained by several possible confounders, including sex, ethnicity, dispositional emotionality, symptoms of depression and anxiety, parental education and participants’ perceptions of their own social standing. The amygdala expresses marked developmental plasticity and plays instrumental roles in processing emotional information, regulating emotion-related behaviors and orchestrating biobehavioral stress responses throughout life. Thus, these findings may provide insight into the neurodevelopmental pathways impacting socioeconomic disparities in health. [ABSTRACT FROM PUBLISHER]

Individuals who exhibit exaggerated blood pressure reactions to psychological stressors are at risk for hypertension, ventricular hypertrophy, and premature atherosclerosis; however, the neural systems mediating exaggerated blood pressure reactivity and associated cardiovascular risk in humans remain poorly defined. Animal models indicate that the amygdala orchestrates stressor-evoked blood pressure reactions via reciprocal signaling with corticolimbic and brainstem cardiovascular-regulatory circuits. Based on these models, we used a multimodal neuroimaging approach to determine whether human individual differences in stressor-evoked blood pressure reactivity vary with amygdala activation, gray matter volume, and functional connectivity with corticolimbic and brainstem areas implicated in stressor processing and cardiovascular regulation. We monitored mean arterial pressure (MAP) and concurrent functional magnetic resonance imaging BOLD signal changes in healthy young individuals while they completed a Stroop color-word stressor task, validated previously in epidemiological studies of cardiovascular risk. Individuals exhibiting greater stressor-evoked MAP reactivity showed (1) greater amygdala activation, (2) lower amygdala gray matter volume, and (3) stronger positive functional connectivity between the amygdala and perigenual anterior cingulate cortex and brainstem pons. Individual differences in amygdala activation, gray matter volume, and functional connectivity with corticolimbic and brainstem circuitsmaypartly underpin cardiovascular disease risk by impacting stressor-evoked blood pressure reactivity. [ABSTRACT FROM AUTHOR]

Low socioeconomic status (SES) increases the risk for developing psychiatric and chronic medical disorders. A stress-related pathway by which low SES may affect mental and physical health is through the perception of holding a low social standing, termed low subjective social status. This proposal implicates overlapping brain regions mediating stress reactivity and socioemotional behaviors as neuroanatomical substrates that could plausibly link subjective social status to health-related outcomes. In a test of this proposal, we used a computational structural neuroimaging method (voxel-based morphometry) in a healthy community sample to examine the relationships between reports of subjective social status and regional gray matter volume. Results showed that after accounting for potential demographic confounds, subclinical depressive symptoms, dispositional forms of negative emotionality and conventional indicators of SES, self-reports of low subjective social status uniquely covaried with reduced gray matter volume in the perigenual area of the anterior cingulate cortex (pACC)—a brain region involved in experiencing emotions and regulating behavioral and physiological reactivity to psychosocial stress. The pACC may represent a neuroanatomical substrate by which perceived social standing relates to mental and physical health. [ABSTRACT FROM PUBLISHER]

Abstract: Background: In animals, dendritic arborization and levels of brain derived neurotrophic factor are positively associated with intake of the omega-3 fatty acids. Here, we test whether omega-3 fatty acid intake in humans varies with individual differences in gray matter volume, an in vivo, systems-level index of neuronal integrity. Methods: Fifty-five healthy adults completed two 24h dietary recall interviews. Intake of long-chain omega-3 fatty acids was categorized by tertiles. Regional gray matter volumes in a putative emotional brain circuitry comprised of the anterior cingulate cortex (ACC), amygdala and hippocampus were calculated using optimized voxel-based morphometry on high-resolution structural magnetic resonance images. Results: Region of interest analyses revealed positive associations between reported dietary omega-3 intake and gray matter volume in the subgenual ACC, the right hippocampus and the right amygdala, adjusted for total gray matter volume of brain. Unconstrained whole-brain analyses confirmed that higher intake of omega-3 fatty acids was selectively associated with increased greater gray matter volume in these and not other regions. Conclusions: Higher reported consumption of the long-chain omega-3 fatty acids is associated with greater gray matter volume in nodes of a corticolimbic circuitry supporting emotional arousal and regulation. Such associations may mediate previously observed effects of omega-3 fatty acids on memory, mood and affect regulation. [Copyright &y& Elsevier]

Abstract: Chronic stress in non-human animals decreases the volume of the hippocampus, a brain region that supports learning and memory and that regulates neuroendocrine activity. In humans with stress-related psychiatric syndromes characterized by impaired learning and memory and dysregulated neuroendocrine activity, surrogate and retrospective indicators of chronic stress are also associated with decreased hippocampal volume. However, it is unknown whether chronic stress is associated with decreased hippocampal volume in those without a clinical syndrome. We tested whether reports of life stress obtained prospectively over an approximate 20-year period predicted later hippocampal grey matter volume in 48 healthy postmenopausal women. Women completed the Perceived Stress Scale repeatedly from 1985 to 2004; in 2005 and 2006, their hippocampal grey matter volume was quantified by voxel-based morphometry. Higher Perceived Stress Scale scores from 1985 to 2004 — an indicator of more chronic life stress - predicted decreased grey matter volume in the right orbitofrontal cortex and right hippocampus. These relationships persisted after accounting for age, total grey matter volume, time since menopause, use of hormone therapy, subclinical depressive symptoms, and other potentially confounding behavioral and age-related cerebrovascular risk factors. The relationship between chronic life stress and regional grey matter volume – particularly in the hippocampus and orbitofrontal cortex – appears to span a continuum that extends to otherwise healthy individuals. Consistent with animal and human clinical evidence, we speculate that chronic-stress-related variations in brain morphology are reciprocally and functionally related to adaptive and maladaptive changes in cognition, neuroendocrine activity, and psychiatric vulnerability. [Copyright &y& Elsevier]

Abstract: Hypertension is a risk factor for diffuse brain atrophy. Yet, there is little evidence that higher blood pressure predicts focal brain atrophy, as indicated by a lower volume of regional brain tissue. This voxel-based morphometry study tested (a) whether higher blood pressure predicts lower regional grey or white matter volume and (b) whether a blood-pressure-related reduction in regional brain tissue volume predicts poorer neuropsychological test performance. Participants were 76 men (M age = 61.33, SD = 4.95 years) and 58 women (M age = 59.86, SD = 5.10 years) without a cardiovascular, cerebrovascular, or neuropsychiatric disease. Results showed that among men, higher resting systolic blood pressure predicted lower grey matter volume in the supplementary motor area and adjacent superior frontal gyrus, the anterior cingulate cortex, and middle temporal gyrus. Among men, lower grey matter volume in the supplementary motor area also predicted a slower time to complete the Trail Making Part B Test of executive control and a poorer recall of items from the Four-word Short-term Memory Test of working memory. These relationships were independent of age, total brain tissue volume, educational history, severity of carotid atherosclerosis, and the extent of periventricular and subcortical white matter lesions. Among women, no statistically significant relationships were found between blood pressure, regional brain tissue volume, and cognitive function. These findings suggest a functional relationship among men between higher blood pressure, lower regional grey matter volume, and poorer cognitive function that is independent of other risk factors and confounding medical conditions. [Copyright &y& Elsevier]

The anterior cingulate cortex presumptively regulates blood pressure reactions to behavioral stressors. There is little evidence in humans, however, that stressor-evoked changes in blood pressure correlate with concurrent changes in anterior cingulate activity. Using fMRI, we tested whether changes in mean arterial blood pressure correlate with ongoing changes in blood oxygen level dependent (BOLD) activation in 9 women and 11 men who completed a stressful Stroop color-word interference task. Higher mean arterial pressure during the Stroop task correlated with greater BOLD activation in two regions of the cingulate cortex (perigenual and mid-anterior) and in other networked brain regions, including the insula, thalamus, and periaqueductal gray. These results support the hypothesis that the anterior cingulate cortex regulates blood pressure reactions to behavioral stressors in humans. [ABSTRACT FROM AUTHOR]

The aim of the present study was to characterize the functional relationships between behaviorally evoked regional brain activation and cardiac autonomic activity in humans. Concurrent estimates of regional cerebral blood flow (rCBF; obtained by positron emission tomography), heart period, and high-frequency heart period variability (HF-HPV; an indicator of cardiac parasympathetic activity) were examined in 93 adults (aged 50–70 years) who performed a series of increasingly difficult working-memory tasks. Increased task difficulty resulted in decreased heart period (indicating cardioacceleration) and decreased HF-HPV (indicating decreased cardiac parasympathetic activity). Task-induced decreases in heart period and HF-HPV were associated with concurrent increases and decreases in rCBF to cortical and subcortical brain regions that are speculated to regulate cardiac autonomic activity during behavioral processes: the medial-prefrontal, insular, and anterior cingulate cortices, the amygdala–hippocampal complex, and the cerebellum. These findings replicate and extend a small number of functional neuroimaging studies that suggest an important role for both cortical and subcortical brain systems in human cardiac autonomic regulation. [ABSTRACT FROM AUTHOR]

Chemotherapy-induced nausea has been associated with a time-related decrease in cardiac parasympathetic activity. We tested the hypothesis that a time-related decrease in cardiac parasympathetic activity would also be associated with nausea and other motion sickness symptoms during illusory self-motion (vection). Fifty-nine participants (aged 18 u34 years:25 male) were exposed to a rotating optokinetic drum to induce vection. Symptoms of motion sickness and an estimate of cardiac parasympathetic activity (respiratory sinus arrhythmia; RSA) were obtained at baseline and throughout a drum-rotation period. As expected, motion sickness symptoms increased and RSA decreased over time during drum rotation. Moreover, greater decreases in RSA over time correlated with greater motion sickness severity. These results suggest that a time-related decrease in cardiac parasympathetic activity may be an important correlate of nausea and motion sickness across different evocative contexts. [ABSTRACT FROM AUTHOR]

Discusses results of a study evaluating the effects of speech preparation and isometric handgrip stress on gastric myoelectrical and autonomic cardiac activity in individuals with affective disorders. Respiratory sinus arrhythmia; Gastric tachyarrythmia.

Reports on a study conducted by researchers in the U.S., which determines the autonomic origins of a bradycardiac response to a moderate intensity nonsignal auditory stimulus and the changes in autonomic cardiac control of the response as a function of habituation. Presentation of pure tone stimuli to participants while phasic changes in heart period, preejection period and respiratory sinus arrhythmia were observed.

Discusses the detection of the onset of the lateralized readiness potential (LRP) through a comparison of available methods and procedures. Different techniques found to be the most accurate and reliable for the analysis of stimulus- and response-locked data; Data indicating that regression-based methods can be used to analyze most LRP data.

Compared to others, individuals living in communities of socioeconomic disadvantage experience more atherosclerotic cardiovascular disease (CVD) and a greater extent of preclinical atherosclerosis. Although the mechanisms underlying these associations remain unclear, it is widely hypothesized that alterations in normative cortisol release from the Hypothalamic Pituitary Adrenal (HPA) axis may play a role in linking lower community socioeconomic position (C-SEP) to CVD risk. The current study examined this hypothesis in relation to a marker of preclinical atherosclerosis among 488 healthy midlife adults (30–54 years, Mean age= 43, 52% Female, 81% White). All participants were employed and without clinical CVD. C-SEP was estimated from census tract data, and atherosclerosis was measured as intima-medial thickness of the carotid arteries (cIMT) by duplex ultrasonography. Four indicators of HPA activity [cortisol at awakening and the cortisol awakening response (CAR), rate of diurnal decline in cortisol (diurnal slope), and total output expressed as area under the curve (AUC)] were derived from salivary cortisol measurements obtained from 5 samples on each of 3 working days. Path analyses were used to examine associations of C-SEP with cIMT and HPA activity and to test whether individual differences in HPA activity could account for any association of C-SEP with cIMT using bootstrapping (5000 iterations). All models were adjusted for age, sex, race, and composite measures of both individual-level socioeconomic position (income, education, occupation), and cardiometabolic risk (systolic and diastolic blood pressure, waist circumference, fasting lipids and glucose). Lower C-SEP was related to both greater cIMT (b = −0.004, p =.021) and a flatter diurnal slope of cortisol (b = −0.001, p =.039). An indirect effect showed attenuated diurnal slope to partially mediate the relationship between C-SEP and cIMT (95% CI = −0.0018 to −0.0001), and a residual direct effect of C-SEP on cIMT remained significant (95% CI = −0.0097 to −0.004). These results suggest that low C-SEP associations with preclinical atherosclerosis may be due in part to correlated variation in adrenocortical activity. • Individual residing in communities of lower socioeconomic position show greater atherosclerosis and alterations in typical HPA dynamics. • A flatter diurnal decline in cortisol partially mediates associations of community level socioeconomic position and atherosclerosis. • This relationship persists after accounting for individual-level socioeconomic position and standard cardiometabolic risk factors. [ABSTRACT FROM AUTHOR]

Metrics of heart period variability are widely used in the behavioral and biomedical sciences, although somewhat confusingly labeled as heart rate variability (HRV). Despite their wide use, HRV metrics are usually analyzed and interpreted without reference to prevailing levels of cardiac chronotropic state (i.e., mean heart rate or mean heart period). This isolated treatment of HRV metrics is nontrivial. All HRV metrics routinely used in the literature exhibit a known and positive relationship with the mean duration of the interval between two beats (heart period): as the heart period increases, so does its variability. This raises the question of whether HRV metrics should be "corrected" for the mean heart period (or its inverse, the heart rate). Here, we outline biological, quantitative, and interpretive issues engendered by this question. We provide arguments that HRV is neither uniformly nor simply a surrogate for heart period. We also identify knowledge gaps that remain to be satisfactorily addressed with respect to assumptions underlying existing HRV correction approaches. In doing so, we aim to stimulate further progress toward the rigorous use and disciplined interpretation of HRV. We close with provisional guidance on HRV reporting that acknowledges the complex interplay between the mean and variability of the heart period. [ABSTRACT FROM AUTHOR]

Exaggerated cardiovascular reactivity to acute psychological stress is associated with an increased risk of developing cardiovascular disease. The amygdala and hippocampus have been implicated in centrally mediating stressor‐evoked cardiovascular reactivity. However, little is known about the associations of amygdala and hippocampus morphology with stressor‐evoked cardiovascular reactivity. Forty (Mage = 19.05, SD = 0.22 years) healthy young women completed two separate testing sessions. Session 1 assessed multiple parameters of cardiovascular physiology at rest and during a validated psychological stress task (Paced Auditory Serial Addition Test), using electrocardiography, Doppler echocardiography, and blood pressure monitoring. In Session 2, 1 year later, structural MRI was conducted. Brain structural volumes were computed using automated segmentation methods. Regression analyses, following Benjamini‐Hochberg correction, showed that greater heart rate and cardiac output reactivity were associated with reduced amygdala and hippocampus gray matter volume. Systolic blood pressure reactivity was associated with reduced hippocampus volume. In contrast, no associations between diastolic blood pressure, mean arterial blood pressure, stroke volume, or total peripheral resistance reactivity with amygdala or hippocampus volumes were apparent. Comparison analyses examining insula volume found no significant associations. Some indicators of greater stressor‐evoked cardiovascular reactivity associate with reduced amygdala and hippocampus gray matter volume, but the mechanisms of this association warrant further study. [ABSTRACT FROM AUTHOR]

Background: The diet of most adults is low in fish and, therefore, provides limited quantities of the long-chain, omega-3 fatty acids (LCn-3FAs), eicosapentaenoic and docosahexaenoic acids (EPA, DHA). Since these compounds serve important roles in the brain, we sought to determine if healthy adults with low-LCn-3FA consumption would exhibit improvements in neuropsychological performance and parallel changes in brain morphology following repletion through fish oil supplementation. Methods: In a randomized, controlled trial, 271 mid-life adults (30–54 years of age, 118 men, 153 women) consuming ⩽300 mg/day of LCn-3FAs received 18 weeks of supplementation with fish oil capsules (1400 mg/day of EPA and DHA) or matching placebo. All participants completed a neuropsychological test battery examining four cognitive domains: psychomotor speed, executive function, learning/episodic memory, and fluid intelligence. A subset of 122 underwent neuroimaging before and after supplementation to measure whole-brain and subcortical tissue volumes. Results: Capsule adherence was over 95%, participant blinding was verified, and red blood cell EPA and DHA levels increased as expected. Supplementation did not affect performance in any of the four cognitive domains. Exploratory analyses revealed that, compared to placebo, fish oil supplementation improved executive function in participants with low-baseline DHA levels. No changes were observed in any indicator of brain morphology. Conclusions: In healthy mid-life adults reporting low-dietary intake, supplementation with LCn-3FAs in moderate dose for moderate duration did not affect neuropsychological performance or brain morphology. Whether salutary effects occur in individuals with particularly low-DHA exposure requires further study. [ABSTRACT FROM AUTHOR]

Background Subjective social status (SSS) refers to a person's perception of their social rank relative to others and is cross-sectionally linked to systemic inflammation independently of objective socioeconomic status. Purpose We test the extent to which SSS relates to multiyear changes in inflammation, or if associations differ by race or sex. Methods Healthy adults (N = 331; 30–51 years) completed a baseline visit and 278 participants returned for a second visit 2.85 years later. At both visits, participants underwent a fasting blood draw and completed community (SSSC) and US (SSSUS) versions of the MacArthur Scale. Multiple linear regression analyses examined change in interleukin-6 (IL-6) and C-reactive protein (CRP) predicted by each type of SSS, adjusting for time between visits, sex, race, age, body mass index, smoking, baseline inflammation, and objective socioeconomic status. Additional analyses further adjusted for hopelessness and depressive symptoms. Interactions examined moderations by sex and race. Results Lower SSSC was longitudinally associated with greater IL-6 independently of all covariates, including education and income (β = −0.06), hopelessness (β = −0.06), and depressive symptoms (β = −0.06). Lower SSSUS was longitudinally associated with greater IL-6 independently of demographic covariates including education and income (β = −0.06), but was slightly attenuated after adjusting for hopelessness (β = −0.06) and depressive symptoms (β = −0.06). There were no associations for CRP or moderation by race or sex. Conclusions Lower SSS may be associated with greater circulating markers of inflammation over time as suggested by increases in IL-6. [ABSTRACT FROM AUTHOR]

Objective: To examine the associations among socioeconomic factors, depressive symptoms, and cytokines in patients diagnosed with hepatocellular carcinoma (HCC).Methods: A total of 266 patients diagnosed with HCC were administered a battery of questionnaires including a sociodemographic questionnaire and the Center for Epidemiologic StudiesDepression (CES-D) scale. Blood samples were collected to assess serum levels of cytokines using Luminex. Descriptive statistics, Mann-Whitney U, Kruskal-Wallis, linear regression, and Bonferroni corrections were performed to test the hypotheses.Results: Of the 266 patients, 24% reported depressive symptoms in the clinical range (CES-D ≥ 22). Females had higher CES-D score than males (Mann-Whitney U = 7135, P = .014, Padj  = .028). Being unemployed/disabled (Kruskal-Wallis = 14.732, P = .001, Padj  = .005) was found to be associated with higher depressive symptoms in males but not in females. Serum level of IL-2 (Kruskal-Wallis = 17.261, P = .001, Padj  = .005) were found to be negatively associated with education level. Gender (β = .177, P = .035), income (β = -.252, P = .004), whether the patient's income met their basic needs (β = .180, P = .035), and IL-1β (β = -.165, P = .045) independently predicted depressive symptoms and together explained 19.4% of variance associated with depressive symptoms.Conclusions: Sociodemographic and socioeconomic factors were predictive of inflammation and depressive symptoms. Recommendations include the development of gender-targeted interventions for patients diagnosed with HCC who have low socioeconomic status (SES) and may suffer from depressive symptoms. [ABSTRACT FROM AUTHOR]

Background: Several personality traits increase the risk for atherosclerotic cardiovascular disease. Because many of these traits are correlated, their associations with disease risk could reflect shared variance, rather than unique contributions of each trait. We examined a higher‐order personality trait of Stability as related to preclinical atherosclerosis and tested whether any such relationship might be explained by correlated variation in cardiometabolic risk factors. Method: Among 798 community volunteers, lower‐order traits of Neuroticism, Agreeableness, and Conscientiousness were modeled as latent variables (from self‐ and informant ratings) and used to estimate the second‐order factor, Stability. Cardiometabolic risk was similarly modeled from indicators of glycemic control, blood pressure, adiposity, and lipids. Carotid artery atherosclerosis was measured as intima‐media thickness (IMT) by duplex ultrasonography. Result: A structural equation model incorporating direct and indirect effects showed lower Stability associated with greater IMT, and this relationship was accounted for by the indirect pathway via cardiometabolic risk. Secondary analyses showed that: (1) Neuroticism, Agreeableness, and Conscientiousness were unrelated to IMT independent of Stability; and (2) Stability predicted variation in IMT when estimated from informant‐, but not self‐rated, traits. Conclusion: Personality traits may associate with atherosclerotic burden through their shared, rather than unique, variance, as reflected in Stability. [ABSTRACT FROM AUTHOR]

In response to the COVID‐19 pandemic, prior studies have modified the Trier Social Stress Test to be conducted remotely. The current study aimed to extend these studies to test whether a remote Trier Social Stress Test (rTSST) can elicit (a) affective, (b) blood pressure, and (c) heart rate responses relative to a control condition and whether these responses were reliable when assessed 1 week later. Participants (N = 99, 19.7 ± 3.5 years, 55% female) were randomized to a control or stress condition. Participants received blood pressure monitors in person. Controls completed easier versions of the tasks with a single, friendly researcher. Stress participants performed more difficult versions of the task in front of two judges who participants believed were rating their performance. Blood pressure and heart rate were measured every 2 min throughout, while affect was assessed at baseline, after the final task, and following recovery. The rTSST was feasible to administer with minimal technical issues reported. Participants reported lower positive affect and higher negative affect during the tasks in the stress condition relative to controls. Similarly, stress participants had higher cardiovascular responses during the tasks relative to controls, except that blood pressure was not elevated during mental arithmetic in stress participants relative to controls. Cardiovascular responses demonstrated good test–retest reliability when assessed 1 week later, especially when computed using area under the curve methods. Overall, a rTSST can be used to elicit affective and cardiovascular reactivity and provides an opportunity to increase the accessibility of research participation among diverse populations. We demonstrate that the Trier Social Stress Test can evoke both affective and cardiovascular (heart rate and blood pressure) responses when delivered online and remotely. This protocol can be administered during the COVID‐19 pandemic and could be used to include underserved and other populations that may have less accessibility to participate in research protocols. [ABSTRACT FROM AUTHOR]

Background There is abundant evidence that offspring of depressed mothers are at increased risk for persistent behavior problems related to emotion regulation, but the mechanisms by which offspring incur this risk are not entirely clear. Early adverse caregiving experiences have been associated with structural alterations in the amygdala and hippocampus, which parallel findings of cortical regions altered in adults with behavior problems related to emotion regulation. This study examined whether exposure to maternal depression during childhood might predict increased aggression and/or depression in early adulthood, and whether offspring amygdala:hippocampal volume ratio might mediate this relationship. Methods Participants were 258 mothers and sons at socioeconomic risk for behavior problems. Sons' trajectories of exposure to maternal depression were generated from eight reports collected prospectively from offspring ages 18 months to 10 years. Offspring brain structure, aggression, and depression were assessed at age 20 ( n = 170). Results Persistent, moderately high trajectories of maternal depression during childhood predicted increased aggression in adult offspring. In contrast, stable and very elevated trajectories of maternal depression during childhood predicted depression in adult offspring. Increased amygdala: hippocampal volume ratios at age 20 were significantly associated with concurrently increased aggression, but not depression, in adult offspring. Offspring amygdala: hippocampal volume ratio mediated the relationship found between trajectories of moderately elevated maternal depression during childhood and aggression in adult offspring. Conclusions Alterations in the relative size of brain structures implicated in emotion regulation may be one mechanism by which offspring of depressed mothers incur increased risk for the development of aggression. [ABSTRACT FROM AUTHOR]

The neurovisceral integration hypothesis suggests in part that cerebral control of autonomic function conveys comparable control of executive function and, hence, correlation among vagally determined high frequency heart rate variability ( HF-HRV), executive function, and regional cerebral blood flow ( CBF). In 440 middle-aged men and women, resting HF-HRV was related to regional CBF derived from a resting arterial spin-labeled MRI scan and to seven neuropsychological tests of executive function. Despite some intercorrelations, regression modeling failed to support integrated central control of HF-HRV and executive function. Integration between autonomic and cognitive control appears more circumscribed than the general integration suggested by the neurovisceral integration hypothesis. [ABSTRACT FROM AUTHOR]

We examined the neural correlates of resting cardiac vagal activity in a sample of 432 participants (206 male; 61 African American; mean age 42 years). Pulsed arterial spin labeling was used to quantify whole brain and regional cerebral blood flow at rest. High-frequency heart rate variability ( HF- HRV) was used to measure cardiac vagal activity at rest. The primary aim was to determine whether brain regions implicated in regulating cardiac vagal reactions were also related to cardiac vagal activity at rest, and whether these associations varied by sex or race. Brain areas previously related to vagal reactivity were related to resting HF- HRV. Directionality of relationships differed between overall and regional flows. Some relationships were only observed in women and African Americans. There appears to be communality between brain regions associated with task-induced vagal reactivity and those associated with resting cardiac vagal activity. [ABSTRACT FROM AUTHOR]

Mindfulness, a psychological process reflecting attention and awareness to what is happening in the present moment, has been associated with increased well-being and decreased depression and anxiety in both healthy and patient populations. However, little research has explored underlying neural pathways. Recent work suggests that mindfulness (and mindfulness training interventions) may foster neuroplastic changes in cortico-limbic circuits responsible for stress and emotion regulation. Building on this work, we hypothesized that higher levels of dispositional mindfulness would be associated with decreased grey matter volume in the amgydala. In the present study, a self-report measure of dispositional mindfulness and structural MRI images were obtained from 155 healthy community adults. Volumetric analyses showed that higher dispositional mindfulness is associated with decreased grey matter volume in the right amygdala, and exploratory analyses revealed that higher dispositional mindfulness is also associated with decreased grey matter volume in the left caudate. Moreover, secondary analyses indicate that these amygdala and caudate volume associations persist after controlling for relevant demographic and individual difference factors (i.e., age, total grey matter volume, neuroticism, depression). Such volumetric differences may help explain why mindful individuals have reduced stress reactivity, and suggest new candidate structural neurobiological pathways linking mindfulness with mental and physical health outcomes. [ABSTRACT FROM AUTHOR]

We examined the reliability of measures of fMRI, subjective, and cardiovascular reactions to standardized versions of a Stroop color-word task and a multisource interference task. A sample of 14 men and 12 women (30-49 years old) completed the tasks on two occasions, separated by a median of 88 days. The reliability of fMRI BOLD signal changes in brain areas engaged by the tasks was moderate, and aggregating fMRI BOLD signal changes across the tasks improved test-retest reliability metrics. These metrics included voxel-wise intraclass correlation coefficients ( ICCs) and overlap ratio statistics. Task-aggregated ratings of subjective arousal, valence, and control, as well as cardiovascular reactions evoked by the tasks showed ICCs of 0.57 to 0.87 ( ps < .001), indicating moderate-to-strong reliability. These findings support using these tasks as a battery for fMRI studies of cardiovascular reactivity. [ABSTRACT FROM AUTHOR]

Maintaining brain health promotes successful aging. The main determinants of brain health are the preservation of cognitive function and remaining free from structural and metabolic abnormalities, including loss of neuronal synapses, atrophy, small vessel disease and focal amyloid deposits visible by neuroimaging. Promising studies indicate that these determinants are to some extent modifiable, even among adults seventy years and older. Converging animal and human evidence further suggests that inflammation is a shared mechanism, contributing to both cognitive decline and abnormalities in brain structure and metabolism. Thus, inflammation may provide a target for intervention. Specifically, circulating inflammatory markers have been associated with declines in cognitive function and worsening of brain structural and metabolic characteristics. Additionally, it has been proposed that older brains are characterized by a sensitization to neuroinflammatory responses, even in the absence of overt disease. This increased propensity to central inflammation may contribute to poor brain health and premature brain aging. Still unknown is whether and how peripheral inflammatory factors directly contribute to decline of brain health. Human research is limited by the challenges of directly measuring neuroinflammation in vivo. This review assesses the role that inflammation may play in the brain changes that often accompany aging, focusing on relationships between peripheral inflammatory markers and brain health among well- functioning, community-dwelling adults seventy years and older. We propose that monitoring and maintaining lower levels of systemic and central inflammation among older adults could help preserve brain health and support successful aging. Hence, we also identify plausible ways and novel experimental study designs of maintaining brain health late in age through interventions that target the immune system. [ABSTRACT FROM AUTHOR]

Abstract: Exaggerated cardiovascular reactivity to stress is a risk factor for cardiovascular disease. Further, individual differences in stressor-evoked cardiovascular reactivity covary with the functionality of corticolimbic brain systems, particularly areas of the cingulate cortex. What remains unclear, however, is how individual differences in personality traits interact with cingulate functionality in the prediction of stressor-evoked cardiovascular reactivity. Accordingly, we tested the associations between (i) a particular personality trait, Agreeableness, which is associated with emotional reactions to conflict, (ii) resting state functional connectivity within the cingulate cortex, and (iii) stressor-evoked blood pressure (BP) reactivity. Participants (N=39, 19 men, aged 20–37years) completed a resting functional connectivity MRI protocol, followed by two standardized stressor tasks that engaged conflict processing and evoked BP reactivity. Agreeableness covaried positively with BP reactivity across individuals. Moreover, connectivity analyses demonstrated that a more positive functional connectivity between the posterior cingulate (BA31) and the perigenual anterior cingulate (BA32) covaried positively with Agreeableness and with BP reactivity. Finally, statistical mediation analyses demonstrated that BA31–BA32 connectivity mediated the covariation between Agreeableness and BP reactivity. Functional connectivity within the cingulate appears to link Agreeableness and a risk factor for cardiovascular disease, stressor-evoked BP reactivity. [Copyright &y& Elsevier]

Central to Walter Cannon's challenge to peripheral theories of emotion was that bodily arousal responses are too undifferentiated to account for the wealth of emotional feelings. Despite considerable evidence to the contrary, this remains widely accepted and for nearly a century has left the issue of whether visceral afferent signals are essential for emotional experience unresolved. Here we combine functional magnetic resonance imaging and multiorgan physiological recording to dissect experience of two distinct disgust forms and their relationship to peripheral and central physiological activity. We show that experience of core and bodyboundary-violation disgust are dissociable in both peripheral autonomic and central neural responses and also that emotional experience specific to anterior insular activity encodes these different underlying patterns of peripheral physiological responses. These findings demonstrate that organ-specific physiological responses differentiate emotional feeling states and support the hypothesis that central representations of organism physiological homeostasis constitute a critical aspect of the neural basis of feelings. [ABSTRACT FROM AUTHOR]