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Background and Aims: Vitamin D deficiency impacts a significant proportion of the world's population, and this deficiency has been linked to various conditions characterized by imbalanced serotonin regulation. The objective of this systematic review and meta-analysis was to evaluate the effect of vitamin D supplementation on serum serotonin levels. Methods: We conducted a comprehensive search of PubMed, Scopus, Cochrane Central for Randomized Clinical Trials, and Web of Science up to September 2022, without any language restrictions. The effect sizes were calculated using the standard mean difference (SMD) and 95% confidence interval (CI). Results: Six randomized clinical trials involving 356 participants were included in the analysis. Our findings indicated no significant changes in serotonin levels between the intervention and control groups (SMD: 0.24 ng/mL, 95% CI: -0.28, 0.75, p > 0.10). Subgroup analysis also did not reveal any significant changes in serotonin levels among children, participants with autism spectrum disorders, interventions lasting 10 weeks or longer, or those receiving vitamin D doses below 4000 IU/day. Conclusion: Although the results obtained in this systematic review are inconclusive, they support the need for further well-designed randomized trials to assess the potential role of vitamin D supplementation in regulating serotonin levels and potentially ameliorating depression and related disorders.
ABSTRACT
Coronavirus disease (COVID-19) affects both the respiratory system and the body as a whole. Natural molecules, such as flavonoid quercetin, as potential treatment methods to help patients combat COVID-19. The aim of this systematic review and meta-analysis is to give a comprehensive overview of the impact of quercetin supplementation on inflammatory factors, hospital admission, and mortality of patients with COVID-19. The search has been conducted on PubMed, Scopus, Web of Science, EMBASE, and the Cochrane Library using relevant keywords until August 25, 2023. We included randomized controlled trials (RCTs) comparing COVID-19 patients who received quercetin supplementation versus controls. We included five studies summarizing the evidence in 544 patients. Meta-analysis showed that quercetin administration significantly reduced LDH activity (standard mean difference (SMD): -0.42, 95% CI: -0.82, -0.02, I 2 = 48.86%), decreased the risk of hospital admission by 70% (RR: 0.30, 95% CI: 0.14, 0.62, I 2 = 00.00%), ICU admission by 73% (RR: 0.27, 95% CI: 0.09, 0.78, I 2 = 20.66%), and mortality by 82% (RR: 0.18, 95% CI: 0.03, 0.98, I 2 = 00.00%). No significant changes in CRP, D-dimmer, and ferritin were found between groups. Quercetin was found to significantly reduce LDH levels and decrease the risk of hospital and ICU admission and mortality in patients with COVID-19 infection.
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PURPOSE: Dyslipidemia is considered as a known risk factor for cardiovascular disease. Yet various trials with wide ranges of doses and durations have reported contradictory results. We undertook this meta-analysis of randomized controlled trials (RCTs) to determine whether omega-3 supplementation can affect lipid profile in children and adolescents. METHODS: Cochrane Library, Embase, PubMed, and Scopus databases were searched up to March 2021. Meta-analysis was performed using random-effect method. Effect size was expressed as weighted mean difference (WMD) and 95% confidence interval (CI). Heterogeneity was assessed using the I2 index. In order to identification of potential sources of heterogeneity, predefined subgroup and meta-regression analysis was conducted. RESULTS: A total of 14 RCTs with 15 data sets were included. Based on the combination of effect sizes, there was a significant reduction in TG levels (WMD: -15.71 mg/dl, 95% CI: -25.76 to -5.65, P=0.002), with remarkable heterogeneity (I2=88.3%, P<0.001). However, subgroup analysis revealed that omega-3 supplementation significantly decreased TG only in studies conducted on participants ≤13 years old (WMD=-25.09, 95% CI: -43.29 to -6.90, P=0.007), (I2=84.6%, P<0.001) and those with hypertriglyceridemia (WMD=-28.26, 95% CI: -39.12 to -17.41, P<0.001), (I2=0.0%, P=0.934). Omega-3 supplementation had no significant effect on total cholesterol, HDL, and LDL levels. Also, results of nonlinear analysis showed significant effect of treatment duration on HDL status (Pnon-linearity=0.047). CONCLUSION: Omega-3 supplementation may significantly reduce TG levels in younger children and those with hypertriglyceridemia. Also, based on the HDL-related results, clinical trials with longer duration of intervention are recommended in this population.
Subject(s)
Dyslipidemias , Hypertriglyceridemia , Humans , Adolescent , Child , Lipids , Dietary Supplements , Randomized Controlled Trials as Topic , Dyslipidemias/drug therapy , Hypertriglyceridemia/drug therapyABSTRACT
OBJECTIVES: Neuroprotective effect of creatine (Cr) against ß-amyloid (Aß) is reported in an in vitro study. This study investigated the effect of Cr supplementation on ß-amyloid toxicity in vivo. MATERIALS AND METHODS: Thirty two, male Wistar rats were divided into 4 groups. During ten weeks of study, control group went through no surgical or dietary intervention. At the 4th week of study Sham group had a hippocampal normal saline injection, while Aß and AßCr groups had an ß-amyloid injection in the hippocampus. AßCr group were fed by Cr diet during the study. After 10 weeks, Morris water maze (MWM) test was administered to measure learning ability and memory retrieval. Animals were sacrificed for TUNEL anti apoptotic assay and staining of amyloid plaques by Thioflavin-T. RESULTS: There was a significant retention deficit among AßCr and Aß group while the escape latency and the distance traveled to the platform were significantly higher in AßCr group compared to Aß group. AßCr group had same percent of TUNEL positive neurons compared to Aß group. CONCLUSION: Cr supplementation before and after ß-amyloid injection into the CA1 area of hippocampus deteriorates the learning and memory impairment of rats and it does not protect neuronal apoptosis caused by ß-amyloid.