Lonely older adults have increased expression of pro-inflammatory genes as well as increased risk for morbidity and mortality. Previous behavioral treatments have attempted to reduce loneliness and its concomitant health risks, but have had limited success. The present study tested whether the 8-week Mindfulness-Based Stress Reduction (MBSR) program (compared to a Wait-List control group) reduces loneliness and downregulates loneliness-related pro-inflammatory gene expression in older adults (N=40). Consistent with study predictions, mixed effect linear models indicated that the MBSR program reduced loneliness, compared to small increases in loneliness in the control group (treatment condition × time interaction: F(1,35)=7.86, p=.008). Moreover, at baseline, there was an association between reported loneliness and upregulated pro-inflammatory NF-κB-related gene expression in circulating leukocytes, and MBSR downregulated this NF-κB-associated gene expression profile at post-treatment. Finally, there was a trend for MBSR to reduce C Reactive Protein (treatment condition × time interaction: (F(1,33)=3.39, p=.075). This work provides an initial indication that MBSR may be a novel treatment approach for reducing loneliness and related pro-inflammatory gene expression in older adults.
Objective Cognitive behavioral therapy (CBT) is an empirically supported treatment for social phobia. However, not all individuals respond to treatment and many who show improvement do not maintain their gains over the long-term. Thus, alternative treatments are needed. Method The current study (N=87) was a 3-arm randomized clinical trial comparing CBT, Acceptance and Commitment therapy (ACT), and a waitlist control group (WL) in participants with a DSM-IV diagnosis of social phobia. Participants completed 12 sessions of CBT or ACT or a 12-week waiting period. All participants completed assessments at baseline and post-treatment, and participants assigned to CBT and ACT also completed assessments at 6 and 12 months following baseline. Assessments consisted of self-report measures, a public speaking task, and clinician ratings. Results Multilevel modeling was used to examine between-group differences on outcomes measures. Both treatment groups outperformed WL, with no differences observed between CBT and ACT on self-report, independent clinician, or public speaking outcomes. Lower self-reported psychological flexibility at baseline was associated with greater improvement by the 12-mo follow-up in CBT compared to ACT. Self-reported fear of negative evaluation significantly moderated outcomes as well, with trends for both extremes to be associated with superior outcomes from CBT and inferior outcomes from ACT. Across treatment groups, higher perceived control, and extraversion were associated with greater improvement, whereas comorbid depression was associated with poorer outcomes. Conclusions Implications for clinical practice and future research are discussed.
Neurocognitive studies have observed rIFC involvement in motor, cognitive, and affective inhibition, suggesting that rIFC is a common inhibitory mechanism across psychological domains. If true, intentional inhibition in one domain may have unintended inhibitory effects ('spillover') in other domains. The present study used an emotional go/no-go task that produces responses in both motor and affective domains, but induces intentional inhibition in only the motor domain. Data support the hypothesis that intentional inhibition in the motor domain, via rIFC, produces inhibitory spillover in the affective domain. Specifically, we observed increased rIFC along with reduced amygdala activity when participants intentionally inhibited motor responses during the presentation of negativelyvalenced stimuli, and greater inverse connectivity between these regions during motor inhibition in a PPI analysis. Given the absence of intentional affect regulation, these results suggest that intentional inhibition of a motor response dampens the amygdala activation coincident with affective stimuli to the extent that rIFC activation is higher.The human ability to inhibit unwanted thoughts, feelings, and behaviors is central to effective goal pursuit in daily life. On a process level, it might be efficient for inhibition of motor, cognitive, and affective responses to share a neurological mechanism, but the subjective experience of inhibiting each of these responses feels different from one another. It is therefore unclear whether these different forms of inhibition depend on common or disparate neurocognitive systems. Recent cognitive neuroscience research in each domain independently implicates right inferior frontal cortex (rIFC) and suggests that this region may be a point of convergence involved in various forms of inhibition. If rIFC is a common inhibitory mechanism across various domains, it is possible that intentional inhibition in one domain (e.g. inhibiting a motor response) may lead to incidental inhibitory "spillover" in another domain (e.g. suppressing affective responses). However, because the research to date has typically been limited to a single domain in each investigation, the spillover hypothesis remains untested.The role of rIFC in inhibition is best established in the domain of motor inhibition. Studies of motor inhibition have consistently identified a network of brain regions including rIFC, anterior cingulate cortex (ACC), and dorsolateral prefrontal cortex (DLPFC). These studies commonly use the go/no-go task during which participants press a button on most trials ('go') and thus form a prepotent response to press the button. However, on some trials ('no-go') a cue indicates Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. ...
Psychosocial resources have been tied to lower psychological and biological responses to stress. The present research replicated this relationship and extended it by examining how differences in dispositional reactivity of certain neural structures may underlie this relationship. Two hypotheses were examined: (a) psychosocial resources are tied to decreased sensitivity to threat and/or (b) psychosocial resources are associated with enhanced prefrontal inhibition of threat responses during threat regulation. Results indicated that participants with greater psychosocial resources exhibited significantly less cortisol reactivity following a stress task, as predicted. Analyses using functional magnetic resonance imaging revealed that psychosocial resources were associated with greater right ventrolateral prefrontal cortex and less amygdala activity during a threat regulation task but were not associated with less amygdala activity during a threat sensitivity task. Mediational analyses suggest that the relation of psychosocial resources to low cortisol reactivity was mediated by lower amygdala activity during threat regulation. Results suggest that psychosocial resources are associated with lower cortisol responses to stress by means of enhanced inhibition of threat responses during threat regulation, rather than by decreased sensitivity to threat.
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