Mindfulness-Based Stress Reduction Buffers Glucocorticoid Resistance Among Older Adults: A Randomized Controlled Trial.

OBJECTIVE: Mindfulness interventions have been effective for improving a range of health outcomes; however, pathways underlying these effects remain unclear. Inflammatory processes may play a role, possibly through increased resistance of immune cells to the anti-inflammatory effects of glucocorticoids (i.e., glucocorticoid resistance, or GCR). Here, we conducted an initial examination of whether mindfulness training mitigates GCR among lonely older adults. METHODS: Lonely older adults (65-85 years; n = 190) were randomly assigned to an 8-week Mindfulness-Based Stress Reduction (MBSR) or a matched Health Enhancement Program (HEP). Whole blood drawn before and after the intervention and at 3-month follow-up was incubated with endotoxin and varying concentrations of dexamethasone, and interleukin-6 production was assessed using enzyme-linked immunosorbent assay. GCR was assessed as the concentration of dexamethasone required to decrease the stimulated interleukin-6 response by 50% (half maximal inhibitory concentration), with higher concentrations indicating greater GCR. Mixed-effects linear models tested time (pre, post, follow-up) by condition (MBSR versus HEP) effects. RESULTS: There was no overall time by condition effect on GCR across all time points. However, a significant time by condition effect was observed from preintervention to postintervention (d = 0.29), such that MBSR buffered increases in GCR observed in the HEP group. Although MBSR showed small, nonsignificant reductions in GCR from preintervention to 3-month follow-up, group differences were not maintained at the 3-month follow-up (d = 0.10). CONCLUSIONS: Results suggest that MBSR may protect against declines in the sensitivity of immune cells to the anti-inflammatory effects of glucocorticoids among at-risk lonely older adults and show value in studying this biological mechanism in future trials.Trial Registration: Clinical Trials identifier NCT02888600.

Emotion Regulation as a Pathway Connecting Early Life Adversity and Inflammation in Adulthood: a Conceptual Framework.

Chronic inflammation is implicated in a variety of diseases (e.g., cardiovascular disease and cancer). Much evidence suggests that early life adversity (ELA), such as maltreatment or neglect, can increase risk for inflammation in adulthood. ELA may program proinflammatory activity via its effects on brain areas involved in emotion regulation. Of multiple emotion regulation strategies, some are considered maladaptive (e.g., expressive suppression), while others are generally adaptive (e.g., cognitive reappraisal). We propose a conceptual framework for how emotion regulation tendencies may affect vulnerability or resilience to inflammation in adults who experienced adversity in childhood and/or adolescence. In support of this framework, we summarize evidence for the relationships between emotion dysregulation and higher inflammation (i.e., vulnerability), as well as between cognitive reappraisal and lower inflammation (i.e., resilience), in healthy adults with a history of ELA. Plausible neurobiological, physiological, psychosocial, and ELA-specific factors, as well as interventions, contributing to these associations are discussed. Strengths and limitations of the extant research, in addition to ideas for future directions, are presented.