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Rationale : Chronic stress has been related to lower telomerase, an enzyme that helps preserve the integrity of DNA and slow immunological aging. However, it is unknown whether daily psychological processes reflecting healthy emotion regulation protect against stress-related immune-aging. Methods : We examined basal telomerase activity in a sample of 72 healthy premenopausal women across a range of stress levels, including 35 mothers caring for a child with autism and 37 low-stress control mothers of healthy children. Participants completed a nightly diary over the course of a week, reporting their exposure to positive and negative events. Then they rated the extent to which they employed various emotion-regulation strategies in response to these events. Within-subject weekly means for all measures were calculated. In addition, composite scores for positive affect in response to positive daily events and negative affect in response to daily stressors were calculated, and weekly means obtained. Depressive symptoms were assessed using the Inventory of Depressive Symptoms. On day 4 of the study week, a fasting blood draw was performed to measure peripheral blood mononuclear cells (PBMC) telomerase activity. Results : Higher telomerase activity was significantly associated with the use of more resilient emotion regulation strategies, including more positive emotional responses to positive daily events (r=0.27, p=0.02) and increased savoring of positive daily events (r=0.24, p=0.04). In general, negative emotional responses and rumination in response to daily stressors were not related to telomerase with two exceptions: lower telomerase was associated with greater emotional suppression (r= − 0.34, p

Chronic psychological stress increases inflammation, providing a mechanism for the elevated risk of infectious, autoimmune and cardiovascular diseases in chronically stressed persons. While the HPA axis plays an important role in mediating the link between stressful events and inflammatory processes, it is becoming increasingly clear that immune cells can become resistant to cortisol, resulting in diminished regulation of inflammation. One potential mechanism of cortisol resistance results from decreased glucocorticoid receptor (GR) expression in immune cells during elevated cortisol exposure. Chronic stress results in chronic high cortisol exposure leading to decreased immune cell GR expression that in turn is associated with greater immune activation. Using flow cytometry we measured immune activation and GR expression (geometric mean fluorescence intensity [gMFI]) in 10 immune cell subsets in 25 post-menopausal females (10 caregivers [CGs] and 15 controls [CNTLs]). Mann–Whitney and Pearson correlations were employed for statistical analysis with p