Objective Increased inflammation and oxidative stress have been shown in Major Depressive Disorder (MDD), although there is significant heterogeneity across studies. Whether markers of inflammation and oxidative stress are associated with antidepressant treatment response in MDD is currently unclear. The goals of the present study are to investigate markers of inflammation and oxidative stress in unmedicated MDD subjects and controls and test the relationship between these markers and antidepressant response in MDD subjects. Methods Interleukin (IL)-6, tumor necrosis factor (TNF)-α, C-reactive protein, F2-isoprostanes, 8-OH 2-deoxyguanosine (8-OHdG), glutathione peroxidase, glutathione, and vitamin C were quantified in blood samples from 50 unmedicated MDD subjects and 55 healthy controls. Depression symptom severity was rated with the 17-item Hamilton Depression Rating Scale (HDRS). All subjects were somatically healthy and free from medications that could interfere with inflammation and oxidative stress markers. A subgroup of 22 MDD subjects underwent open-label selective serotonin reuptake inhibitor (SSRI) antidepressant treatment for eight weeks, after which blood sampling and the HDRS were repeated. Antidepressant treatment “response” was defined as ≥50% decrease in HDRS ratings over 8 weeks of treatment. Results After controlling for the effects of age, sex, body mass index and smoking, MDD subjects had significantly higher levels of IL-6 (p<0.001), TNF-α (p<0.001), 8-OHdG (p=0.018), and F2-isoprostanes (p=0.012). Compared to Responders, Non-responders to SSRI antidepressant treatment had higher levels of F2-isoprostanes at baseline (p=0.006), and after eight weeks of treatment (p=0.031). Non-responders showed a significant increase in 8-OHdG over the course of treatment (p=0.021), whereas Responders showed a significant decrease in IL-6 over the course of treatment (p=0.019). Conclusion Our results are in line with previous reports of increased levels of markers of inflammation and oxidative stress in MDD. Moreover, poorer antidepressant treatment response was related to higher baseline levels of the major oxidative stress marker, F2-isoprostanes, in vivo. Further, antidepressant response was associated with changes in oxidative (8-OHdG) and inflammatory (IL-6) markers.

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Objectives Family dementia caregivers are at high risk of depression and burnout. We aimed to assess the feasibility of Central Meditation and Imagery Therapy for Caregivers (CMIT-C), a novel 8-week group meditation and guided imagery group therapy program, for dementia caregivers reporting stress due to caregiving responsibilities. Methods 12 family dementia caregivers enrolled in CMIT-C. Primary outcomes included depression and anxiety, and secondary included insomnia, quality of life, and mindfulness. Changes over the study and three month follow-up were analyzed with non-parametric related samples tests. Correlations of feeling state changes from meditation diaries at 1 week were made with symptom changes post meditation training. Results 10 participants completed the study. Completers came to an average of 7 ± 1 sessions out of a possible 8, and turned in home practice logs 90 ± 10% of the time. Anxiety, depression and insomnia symptoms decreased, and mindfulness ratings improved with large effects (all p < 0.05 and Cohen's d ≥ 0.7). Gains were stable at 3 months. Early response during the first week of meditation practice was associated with subsequent home meditation practice, anxiety change at eight weeks, and endpoint satisfaction with CMIT-C. Conclusions CMIT-C is a feasible intervention for dementia caregivers. Results suggest that this therapeutic technique can reduce symptoms of anxiety, depression, and insomnia, and increase levels of mindfulness. Early response to meditation practice predicted those with the greatest short-term benefits, and this may inform future studies of meditation. Larger, controlled efficacy studies of CMIT-C for dementia caregivers are warranted.

Variations in heart rate variability (HRV) have been associated with major depressive disorder (MDD), but the relationship of baseline HRV to treatment outcome in MDD is unclear. We conducted a pilot study to examine associations between resting baseline HRV and MDD treatment outcome. We retrospectively tested several parameters of HRV in an MDD treatment study with escitalopram (ESC, N=26) to generate a model of how baseline HRV related to treatment outcome, and cross-validated the model in a separate trial of MDD treatment with Iyengar yoga (IY, N=16). Lower relative power of very low frequency (rVLF) HRV at baseline predicted improvement in depressive symptoms when adjusted for age and gender (R2>.43 and p<0.05 for both trials). Although vagal parasympathetic measures were correlated with antidepressant treatment outcome, their predictive power was not significant after adjusting for age and gender. In conclusion, baseline resting rVLF was associated with depression treatment outcome in two independent MDD treatment studies. These results should be interpreted with caution due to limited sample size, but a strength of this study is its validation of the rVLF predictor in an independent sample. rVLF merits prospective confirmation as a candidate biomarker.