The objective of this study was to examine the efficacy of a novel binaural beat meditation technology for the treatment of anxiety symptoms in both psychiatric outpatients and nonpatients. Twenty psychiatric outpatients with anxiety disorder and eight individuals (nonpatients) in the healing professions were given the opportunity to use this meditation technology over the course of 2 weeks to 2 months. The State-Trait Anxiety Inventory scores were measured in all participants over the course of the study. Of the 20 outpatients who took part in the study, nine used the meditations as planned, whereas 11 did not for various reasons (could not download, forgot, did not have time, etc.), resulting in the formation of three treatment groups: psychiatry + meditation (n = 8), psychiatry only (n = 10), and meditation only (n = 8). The psychiatry + meditation group showed a 13.5-point (26.5%) decrease in State-Anxiety (t = 5.28, p = 0.001), a 14.1-point (24.7%) decrease in Trait-Anxiety (t = −5.12, p = 0.001), and a 27.6-point (25.6%) decrease in Total Anxiety (t = 7.63, p ≤ 0.001). The psychiatry-only group showed a 4.2-point (8.4%) decrease in State-Anxiety (t = −2.20, p = 0.05) and a 7.0-point (6.9%) decrease in Total Anxiety (t = −2.61, p = 0.02). The meditation only showed a 3.5-point (9.8%) decrease in Trait-Anxiety (t = −2.47, p = 0.04). In a multiple regression analysis controlling for sociodemographic factors, medications, and treatment-related variables, the only statistically significant improvement in anxiety was seen in the psychiatry + meditation group for the Total Anxiety score (p < 0.01). These findings suggest that use of this meditation technology may exhibit a positive effect on self-reported measures of anxiety in the context of a psychiatry/psychotherapy practice. However, larger-scale randomized, placebo-controlled trials are needed to confirm our findings.
Not enough research has been carried out on depression up to now in Latin America. The knowledge that has resulted from research activities in the USA or Europe offers limited generalizability to other regions of the world, including Latin America. In the Andean highlands of Ecuador, we found very high rates of moderate and severe depressive symptoms, a finding that must be interpreted within its cultural context. Somatic manifestations of depression predominated over cognitive manifestations, and higher education level was protective against depression. These findings call for an appreciation of culturally specific manifestations of depression and the social factors that influence them. These factors must be further studied in order to give them the deserved priority, allocate resources appropriately, and formulate innovative psychosocial interventions.
Glucocorticoids (GCs), the adrenal steroids secreted during stress, can compromise the ability of hippocampal neurons to survive numerous necrotic insults. We have previously observed that GCs worsen the deleterious effects of gp120, the glycoprotein of the acquired immune deficiency syndrome virus, which can indirectly damage neurons and which is thought to play a role in the neuropathological features of human immunodeficiency virus infection. Specifically, GCs augment gp120-induced calcium mobilization, ATP depletion, decline in mitochondrial potential, and neurotoxicity in fetal monolayer cultures from a number of brain regions. In the present report, we demonstrate a similar gp120/GC synergy in adult hippocampal and cortical explants. We generated explants from rats that were either adrenalectomized, adrenally intact, or intact and treated with corticosterone to produce levels seen in response to major stressors. Metabolic rates in explants were then indirectly assessed with silicon microphysiometry, and cytosolic calcium concentrations were assessed with fura-2 fluorescent microscopy. We observed that basal levels of GCs tonically augment the disruptive effects of gp120 on metabolism in the CA1 cell field of the hippocampus and in the cortex. Moreover, raising GC concentrations into the stress range exacerbated the ability of gp120 to mobilize cytosolic calcium in a number of hippocampal cell fields. Finally, we observed that the synthetic GC prednisone had similarly exacerbating effects on gp120. Thus, GCs can worsen the deleterious effects of gp120 in a system that is more physiologically relevant than the fetal monolayer culture and in a region-specific manner.
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