The effect of non-pharmacological interventions on sleep quality in people with sleep disturbances: A systematic review and a meta-analysis.

Sleep is the elixir of life. Both healthy populations and patients with chronic diseases experience sleep disturbances in their lifetime. Pharmacological agents to induce sleep in individuals with sleep disturbances pose side effects like tolerance and dependence, warranting the development of alternative non-pharmacological interventions with less or no adverse effects. However, deciphering comprehensive evidence on the translational potential of these alternative therapies remains difficult. In the current paper, we systematically reviewed the recent literature on the effect of non-pharmacological interventions (NPIs) on improving sleep quality in both healthy and diseased populations experiencing sleep disturbances. We searched PubMed, Science Direct, Cochrane Controlled Trials, and Web of Science databases from inception to June 2022 for randomized controlled trials and cohort studies evaluating the sleep quality of individuals. We performed a meta-analysis using the random effects model with Pittsburgh Sleep Quality Index (PSQI) as an outcome measure to evaluate the effect of five distinct NPIs on sleep quality in normal and people with different medical conditions. Subgroup analyses and sensitivity analyses were done for heterogeneity analysis and to check the consistency of results, respectively. In 16 trials reporting on 1885 subjects, that all NPIs like Resistance Training (SMD -0.29, 95% CI -0.64 to 0.05; p = 0.09); Yoga (SMD -0.48, 95% CI -0.72 to -0.25; p < 0.0001); Cognitive Behavioral Therapy (SMD -1.69, 95% CI -2.70 to -0.68; p = 0.001); Music (SMD -1.42, 95% CI -1.99 to -0.85; p < 0.00001); Light (SMD -0.43, 95% CI -0.77 to -0.09; p = 0.01) have substantially decreased the global PSQI scores. The findings of the randomized studies and a cohort study included in qualitative synthesis demonstrated that the global PSQI scores improved significantly as compared to the placebo groups. Despite the limitations of clinical heterogeneity in subjects, our results demonstrate a positive impact of the studied NPIs on sleep quality in individuals experiencing sleep disturbances. However, comprehensive double-blinded controlled trials are indispensable in the future, emphasizing the objective sleep quality and inter-individual differences in response to the intervention.

Hypobaric Hypoxia Induces Deficits in Adult Neurogenesis and Social Interaction via Cyclooxygenase-1/ EP1 Receptor Pathway Activating NLRP3 Inflammasome.

Low oxygen environments, like hypobaric hypoxia (HH), are common nodes in a number of diseases characterized by neuroinflammation, which is detrimental to the structural and functional aspects of hippocampal circuitry. Hypoxic conditions lead to elevation of inflammasome-mediated inflammation that may contribute to cognitive deficits. However, a systematic investigation of the impact of inflammasome-mediated neuroinflammation on the components of neurogenic niche during HH remains to be elusive. Cerebral hypoxia was induced in adult male Sprague Dawley rats via decreasing partial pressure of oxygen. The effect of HH (1, 3, and 7 days at 25,000 ft) on social memory, anxiety, adult neurogenesis, and NLRP3- (NLR family pyrin domain containing 3) mediated neuroinflammation in the dentate gyrus (DG) was explored in detail. Furthermore, we explored the therapeutic efficacy of cyclooxygenase-1 inhibitor (valeryl salicylate, 5 mg/kg/day, i.p.) and EP1 receptor (EP1R) antagonist (SC19220, 1 mg/kg/day, i.p.) on HH-induced deficits. Seven days of HH exposure induced alteration in social and anxiety-like behavior along with perturbation in adult neurogenesis. Elevation in NLRP3, caspase-1, and IL-1ß levels was observed during HH from day 1. A notable increase in the COX-1/EP1R pathway in activated glial cells in DG was evident during HH. COX-1 inhibitor and EP1R antagonist mitigated the detrimental effects of HH on social memory, adult neurogenesis via blunting NLRP3-mediated inflammation. Our data showed induction of the COX-1/EP1R pathway in the glial cells, which is detrimental to neurogenesis and social memory, opening up the possibility that the COX-1/EP1R pathway is a plausible target for inflammasome-related neurogenesis impairments.