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Supplemental material, sj-docx-1-pss-10.1177_09567976211061107 for Resting (Tonic) Blood Pressure Is Associated With Sensitivity to Imagined and Acute Experiences of Social Pain: Evidence From Three Studies by Tristen K. Inagaki and Peter J. Gianaros in Psychological Science

Supplemental material, sj-pptx-1-pss-10.1177_0956797621989730 for Functional MRI Can Be Highly Reliable, but It Depends on What You Measure: A Commentary on Elliott et al. (2020) by Philip A. Kragel, Xiaochun Han, Thomas E. Kraynak, Peter J. Gianaros and Tor D. Wager in Psychological Science

Understanding the association between autonomic nervous system [ANS] function and brain morphology across the lifespan provides important insights into neurovisceral mechanisms underlying health and disease. Resting state ANS activity, indexed by measures of heart rate [HR] and its variability [HRV] has been associated with brain morphology, particularly cortical thickness [CT]. While findings have been mixed regarding the anatomical distribution and direction of the associations, these inconsistencies may be due to sex and age differences in HR/HRV and CT. Previous studies have been limited by small sample sizes, which impede the assessment of sex differences and aging effects on the association between ANS function and CT. To overcome these limitations, 20 groups worldwide contributed data collected under similar protocols of CT assessment and HR/HRV recording to be pooled in a mega-analysis (N = 1,218 (50.5% female), mean age 36.7 years (range: 12-87)). Findings suggest a decline in HRV as well as CT with increasing age. CT, particularly in the orbitofrontal cortex, explained additional variance in HRV, beyond the effects of aging. This pattern of results may suggest that the decline in HRV with increasing age is related to a decline in orbitofrontal CT. These effects were independent of sex and specific to HRV; with no significant association between CT and HR. Greater CT across the adult lifespan may be vital for the maintenance of healthy cardiac regulation via the ANS – or greater cardiac vagal activity as indirectly reflected in HRV may slow brain atrophy. Findings reveal an important association between cortical thickness and cardiac parasympathetic activity with implications for healthy aging and longevity that should be studied further in longitudinal research.

Understanding the association between autonomic nervous system [ANS] function and brain morphology across the lifespan provides important insights into neurovisceral mechanisms underlying health and disease. Resting-state ANS activity, indexed by measures of heart rate [HR] and its variability [HRV] has been associated with brain morphology, particularly cortical thickness [CT]. While findings have been mixed regarding the anatomical distribution and direction of the associations, these inconsistencies may be due to sex and age differences in HR/HRV and CT. Previous studies have been limited by small sample sizes, which impede the assessment of sex differences and aging effects on the association between ANS function and CT. To overcome these limitations, 20 groups worldwide contributed data collected under similar protocols of CT assessment and HR/HRV recording to be pooled in a mega-analysis (N = 1,218 (50.5% female), mean age 36.7 years (range: 12-87)). Findings suggest a decline in HRV as well as CT with increasing age. CT, particularly in the orbitofrontal cortex, explained additional variance in HRV, beyond the effects of aging. This pattern of results may suggest that the decline in HRV with increasing age is related to a decline in orbitofrontal CT. These effects were independent of sex and specific to HRV; with no significant association between CT and HR. Greater CT across the adult lifespan may be vital for the maintenance of healthy cardiac regulation via the ANS-or greater cardiac vagal activity as indirectly reflected in HRV may slow brain atrophy. Findings reveal an important association between CT and cardiac parasympathetic activity with implications for healthy aging and longevity that should be studied further in longitudinal research.

BACKGROUND: Mindfulness meditation training interventions have been shown to improve markers of health, but the underlying neurobiological mechanisms are not known. Building on initial cross-sectional research showing that mindfulness meditation may increase default mode network (DMN) resting-state functional connectivity (rsFC) with regions important in top-down executive control (dorsolateral prefrontal cortex [dlPFC]), here we test whether mindfulness meditation training increases DMN-dlPFC rsFC and whether these rsFC alterations prospectively explain improvements in interleukin (IL)-6 in a randomized controlled trial. METHODS: Stressed job-seeking unemployed community adults (n = 35) were randomized to either a 3-day intensive residential mindfulness meditation or relaxation training program. Participants completed a 5-minute resting-state scan before and after the intervention program. Participants also provided blood samples at preintervention and at 4-month follow-up, which were assayed for circulating IL-6, a biomarker of systemic inflammation. RESULTS: We tested for alterations in DMN rsFC using a posterior cingulate cortex seed-based analysis and found that mindfulness meditation training, and not relaxation training, increased posterior cingulate cortex rsFC with left dlPFC (p < .05, corrected). These pretraining to posttraining alterations in posterior cingulate cortex-dlPFC rsFC statistically mediated mindfulness meditation training improvements in IL-6 at 4-month follow-up. Specifically, these alterations in rsFC statistically explained 30% of the overall mindfulness meditation training effects on IL-6 at follow-up. CONCLUSIONS: These findings provide the first evidence that mindfulness meditation training functionally couples the DMN with a region known to be important in top-down executive control at rest (left dlPFC), which, in turn, is associated with improvements in a marker of inflammatory disease risk.

Objective Examine the relationship between ectopic adiposity and markers of cardiometabolic risk, autonomic control, and subclinical cardiovascular disease (CVD). Methods Cross-sectional analyses of 324 overweight and obese subjects were performed. Single-slice CT images were analyzed to calculate thigh muscle attenuation (MA), a measure of ectopic adiposity. Autonomic control was assessed using low-frequency to respiratory-frequency heart rate variability (LFa/RFa ratio). Carotid intima-media thickness (IMT) was a marker of subclinical CVD. Results Among overweight participants, those with low MA had lower HDL-c, higher LFa/RFa ratio, and less subcutaneous thigh fat compared to high MA individuals despite no difference in visceral fat or insulin resistance. Significant associations were not observed in the class I obese group. In the class II obese group, those with high MA had higher triglycerides and insulin levels, yet there was no difference in visceral fat compared to the low MA group. Mean IMT was significantly higher in the low MA compared to the high MA overweight group (0.63 mm vs. 0.58 mm, p=0.04) but was similar between the low and high MA class II obese groups. Conclusions Excess ectopic adiposity in muscle tissue is associated with metabolic and autonomic risk factors and subclinical CVD, most notably in overweight individuals, independent of insulin resistance and visceral abdominal fat.

Resting high-frequency heart rate variability (HF-HRV) relates to cardiac vagal control and predicts individual differences in health and longevity, but its functional neural correlates are not well defined. The medial prefrontal cortex (mPFC) encompasses visceral control regions that are components of intrinsic networks of the brain, particularly the default mode network (DMN) and the salience network (SN). Might individual differences in resting HF-HRV covary with resting state neural activity in the DMN and SN, particularly within the mPFC? This question was addressed using fMRI data from an eyes-open, five-minute rest period during which echoplanar brain imaging yielded blood oxygen level dependent (BOLD) time series. Independent components analysis (ICA) yielded functional connectivity estimates defining the DMN and SN. HF-HRV was measured in a rest period outside of the scanner. Midlife (52% female) adults were assessed in two studies (Study 1, N = 107; Study 2, N = 112). Neither overall DMN nor SN connectivity strength was related to HF-HRV. However, HF-HRV related to connectivity of one region within mPFC shared by the DMN and SN; namely, the perigenual anterior cingulate cortex (pgACC), an area with connectivity to other regions involved in autonomic control. In sum, HF-HRV does not seem directly related to global resting state activity of intrinsic brain networks, but rather to more localized connectivity. A mPFC region was of particular interest as connectivity related to HF-HRV was shared by the DMN and SN. These findings may indicate a functional basis for the coordination of autonomic cardiac control with engagement and disengagement from the environment.

We aimed to investigate if trajectory components (baseline level, slope, and variability) of peripheral interleukin-6 (IL-6) over time were related to cognitive impairment and smaller hippocampal volume and if hippocampal volume explained the associations between IL-6 and cognitive impairment. Multivariable regression models were used to test the association between IL-6 trajectory components with change in neuroimaging measures of the hippocampus and with cognitive impairment among 135 older adults (70-79years at baseline) from the Healthy Brain Project over 14years. IL-6 variability was positively associated with cognitive impairment (odds ratio [OR]= 5.86, 95% confidence interval [CI]: 1.24, 27.61) and with greater decrease per year of gray matter volume of the hippocampus (β=-0.008, standard error= 0.004, p= 0.03). After adjustment for hippocampal volume, the OR of cognitive impairment decreased for each unit of IL-6 variability and CIs widened (OR= 4.36, 95% CI: 0.67, 28.29). Neither baseline levels nor slopes of IL-6 were related to cognitive impairment or hippocampal volume. We believe this has potential clinical and public health implications by suggesting adults with stable levels of peripheral IL-6 may be better targets for intervention studies for slowing or preventing cognitive decline.

Varying associations are reported between Five-Factor Model (FFM) personality traits and cardiovascular disease risk. Here, we further examine dispositional correlates of cardiometabolic risk within a hierarchical model of personality that proposes higher-order traits of Stability (shared variance of Agreeableness, Conscientiousness, inverse Neuroticism) and Plasticity (Extraversion, Openness), and we test hypothesized mediation via biological and behavioral factors. In an observational study of 856 community volunteers aged 30-54 years (46% male, 86% Caucasian), latent variable FFM traits (using multiple-informant reports) and aggregated cardiometabolic risk (indicators: insulin resistance, dyslipidemia, blood pressure, adiposity) were estimated using confirmatory factor analysis (CFA). The cardiometabolic factor was regressed on each personality factor or higher-order trait. Cross-sectional indirect effects via systemic inflammation, cardiac autonomic control, and physical activity were tested. CFA models confirmed the Stability "meta-trait," but not Plasticity. Lower Stability was associated with heightened cardiometabolic risk. This association was accounted for by inflammation, autonomic function, and physical activity. Among FFM traits, only Openness was associated with risk over and above Stability, and, unlike Stability, this relationship was unexplained by the intervening variables. A Stability meta-trait covaries with midlife cardiometabolic risk, and this association is accounted for by three candidate biological and behavioral factors.

Although animal research has demonstrated seasonal changes in hippocampal volume, reflecting seasonal neuroplasticity, seasonal differences in human hippocampal volume have yet to be documented. Hippocampal volume has also been linked to depressed mood, a seasonally varying phenotype. Therefore, we hypothesized that seasonal differences in day-length (i.e., photoperiod) would predict differences in hippocampal volume, and that this association would be linked to low mood. Healthy participants aged 30–54 (M = 43; SD = 7.32) from the University of Pittsburgh Adult Health and Behavior II project (n = 404; 53% female) were scanned in a 3T MRI scanner. Hippocampal volumes were determined using an automated segmentation algorithm using FreeSurfer. A mediation model tested whether hippocampal volume mediated the relationship between photoperiod and mood. Secondary analyses included seasonally fluctuating variables (i.e., sleep and physical activity) which have been shown to influence hippocampal volume. Shorter photoperiods were significantly associated with higher BDI scores (R2= 0.01, β =−0.12, p = 0.02) and smaller hippocampal volumes (R2= 0.40, β = 0.08, p = 0.04). However, due to the lack of an association between hippocampal volume and Beck Depression Inventory scores in the current sample, the mediation hypothesis was not supported. This study is the first to demonstrate an association between season and hippocampal volume. These data offer preliminary evidence that human hippocampal plasticity could be associated with photoperiod and indicates a need for longitudinal studies.

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.

Being overweight or obese is associated with reduced white matter integrity throughout the brain. It is not yet clear which physiological systems mediate the association between inter-individual variation in adiposity and white matter. We tested whether composite indicators of cardiovascular, lipid, glucose, and inflammatory factors would mediate the adiposity-related variation in white matter microstructure, measured with diffusion tensor imaging on a group of neurologically healthy adults (N=155). A composite factor representing adiposity (comprised of body mass index and waist circumference) was associated with smaller fractional anisotropy and greater radial diffusivity throughout the brain, a pattern previously linked to myelin structure changes in non-human animal models. A similar global negative association was found for factors representing inflammation and, to a lesser extent, glucose regulation. In contrast, factors for blood pressure and dyslipidemia had positive associations with white matter in isolated brain regions. Taken together, these competing influences on the diffusion signal were significant mediators linking adiposity to white matter and explained up to fifty-percent of the adiposity-white matter variance. These results provide the first evidence for contrasting physiological pathways, a globally distributed immunity-linked negative component and a more localized vascular-linked positive component, that associate adiposity to individual differences in the microstructure of white matter tracts in otherwise healthy adults.

Insulin resistance confers risk for diabetes mellitus and associates with a reduced capacity of the arterial baroreflex to regulate blood pressure. Importantly, several brain regions that comprise the central autonomic network, which controls the baroreflex, are also sensitive to the neuromodulatory effects of insulin. However, it is unknown whether peripheral insulin resistance relates to activity within central autonomic network regions, which may in turn relate to reduced baroreflex regulation. Accordingly, we tested whether resting cerebral blood flow within central autonomic regions statistically mediated the relationship between insulin resistance and an indirect indicator of baroreflex regulation; namely, baroreflex sensitivity. Subjects were 92 community-dwelling adults free of confounding medical illnesses (48 men, 30-50 years old) who completed protocols to assess fasting insulin and glucose levels, resting baroreflex sensitivity, and resting cerebral blood flow. Baroreflex sensitivity was quantified by measuring the magnitude of spontaneous and sequential associations between beat-by-beat systolic blood pressure and heart rate changes. Individuals with greater insulin resistance, as measured by the homeostatic model assessment, exhibited reduced baroreflex sensitivity (b = -0.16, p < .05). Moreover, the relationship between insulin resistance and baroreflex sensitivity was statistically mediated by cerebral blood flow in central autonomic regions, including the insula and cingulate cortex (mediation coefficients < -0.06, p-values < .01). Activity within the central autonomic network may link insulin resistance to reduced baroreflex sensitivity. Our observations may help to characterize the neural pathways by which insulin resistance, and possibly diabetes mellitus, relates to adverse cardiovascular outcomes.

Insulin resistance confers risk for diabetes mellitus and associates with a reduced capacity of the arterial baroreflex to regulate blood pressure. Importantly, several brain regions that comprise the central autonomic network, which controls the baroreflex, are also sensitive to the neuromodulatory effects of insulin. However, it is unknown whether peripheral insulin resistance relates to activity within central autonomic network regions, which may in turn relate to reduced baroreflex regulation. Accordingly, we tested whether resting cerebral blood flow within central autonomic regions statistically mediated the relationship between insulin resistance and an indirect indicator of baroreflex regulation; namely, baroreflex sensitivity. Subjects were 92 community-dwelling adults free of confounding medical illnesses (48 men, 30-50 years old) who completed protocols to assess fasting insulin and glucose levels, resting baroreflex sensitivity, and resting cerebral blood flow. Baroreflex sensitivity was quantified by measuring the magnitude of spontaneous and sequential associations between beat-by-beat systolic blood pressure and heart rate changes. Individuals with greater insulin resistance, as measured by the homeostatic model assessment, exhibited reduced baroreflex sensitivity (b = -0.16, p < .05). Moreover, the relationship between insulin resistance and baroreflex sensitivity was statistically mediated by cerebral blood flow in central autonomic regions, including the insula and cingulate cortex (mediation coefficients < -0.06, p-values < .01). Activity within the central autonomic network may link insulin resistance to reduced baroreflex sensitivity. Our observations may help to characterize the neural pathways by which insulin resistance, and possibly diabetes mellitus, relates to adverse cardiovascular outcomes.

We examined the reliability of measures of fMRI, subjective, and cardiovascular reactions to standardized versions of a Stroop color-word task and a multi-source 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 < 0.001), indicating moderate-to-strong reliability. These findings support using these tasks as a battery for fMRI studies of cardiovascular reactivity.

The Motion Sickness Assessment Questionnaire (MSAQ) was developed in order to assess the multiple dimensions of the motion sickness syndrome (gastrointestinal, central nervous system, peripheral, and sopite-related symptoms). The aim of this study was to evaluate the psychometric properties of the Greek version of the MSAQ.The MSAQ was translated into Greek and then translated back into English. Minor differences between the two texts were corrected. The Greek version was then administered to male subjects before and after nauseogenic motion stimulation. With the use of a motor driven rotating chair, the subjects were exposed to Coriolis cross-coupling stimulation. A battery of statistical tests was used to evaluate the psychometric properties of the MSAQ.There were 112 subjects who participated. Internal consistency, measured with Cronbach's alpha coefficient, was excellent for the total scale and subscales. The test-retest evaluation was done with Pearson's coefficient and Bland-Altman's plot for the total score and subscales and showed statistically significant results. Mean total MSAQ score was 19.04 before the exposure and 33.46 after the exposure, which was statistically significant.Results suggest the Greek-MSAQ is a valid instrument with satisfactory internal consistency, reliability, reproducibility, validity, and responsiveness and can be used in future studies of motion sickness in Greek speaking populations. Kousoulis P, Pantes A, Alevetsovitis G, Fydanaki O. Psychometric properties of the Greek version of the Gianaros Motion Sickness Assessment Questionaire. Aerosp Med Hum Perform. 2016; 87(11):954-957.