Association Between Vitamin D Supplementation and Fall Prevention.

Background: Falls occur frequently among older individuals, leading to high morbidity and mortality. This study was to assess the efficacy of vitamin D in preventing older individuals from falling. Methods: We searched the PubMed, Cochrane Library, and EMBASE databases systematically using the keywords "vitamin D" and "fall" for randomized controlled trials (RCTs) comparing the effects of vitamin D with or without calcium supplements with those of a placebo or no treatment on fall incidence in adults older than 50 years. A meta-analysis was performed to calculate risk ratios (RRs), absolute risk differences (ARDs) and 95% CIs with random-effects models. Results: A total of 38 RCTs involving 61 350 participants fulfilled the inclusion criteria. Compared with placebo, high-dose vitamin D (≥ 700 IU) can prevent falls [RR, 0.87 (95% CI 0.79 to 0.96); ARD, -0.06 (95% CI, -0.10 to -0.02)]. Low-dose vitamin D (<700 IU) was not significantly associated with falls. Subgroup analysis showed that supplemental calcium, 25(OH) D concentration and frequency influenced the effect of vitamin D in preventing falls. Sensitivity analysis showed that vitamin D prevented falls, which was consistent with the primary analysis. In addition, the active form of vitamin D also prevented falls. Conclusion: In this meta-analysis of RCTs, doses of 700 IU to 2000 IU of supplemental vitamin D per day were associated with a lower risk of falling among ambulatory and institutionalized older adults. However, this conclusion should be cautiously interpreted, given the small differences in outcomes. Systematic Review Registration: https://www.crd.york.ac.uk/prospero/, identifier CRD42020179390.

The impact of baseline potassium intake on the dose-response relation between sodium reduction and blood pressure change: systematic review and meta-analysis of randomized trials.

Sodium and potassium appear to interact with each other in their effects on blood pressure with potassium supplementation having a greater blood pressure lowering-effect when sodium intake is high. Whether the effect of sodium reduction on blood pressure varies according to potassium intake levels is unclear. We carried out a systematic review and meta-analysis to examine the impact of baseline potassium intake on blood pressure response to sodium reduction in randomized trials in adult populations, with sodium and potassium intake estimated from 24-h urine samples. We included 68 studies involving 5708 participants and conducted univariable and multivariable meta-regression. The median intake of baseline potassium was 67.7 mmol (Interquartile range: 54.6-76.4 mmol), and the mean reduction in sodium intake was 128 mmol (95% CI: 107-148). Multivariable meta-regression that included baseline 24-h urinary potassium excretion, age, ethnicity, baseline blood pressure, change in 24-h urinary sodium excretion, as well as the interaction between baseline 24-h urinary potassium excretion and change in 24-h urinary sodium excretion did not identify a significant association of baseline potassium intake levels with the blood pressure reduction achieved with a 50 mmol lowering of sodium intake (p > 0.05 for both systolic and diastolic blood pressure). A higher starting level of blood pressure was consistently associated with a greater blood pressure reduction from reduced sodium consumption. However, the nonsignificant findings may subject to the limitations of the data available. Additional studies with more varied potassium intake levels would allow a more confident exclusion of an interaction.

Chinese Herbal Medicine Interventions in Neurological Disorder Therapeutics by Regulating Glutamate Signaling.

Glutamate is the major excitatory neurotransmitter in the central nervous system, and its signaling is critical for excitatory synaptic transmission. The well-established glutamate system involves glutamate synthesis, presynaptic glutamate release, glutamate actions on the ionotropic glutamate receptors (NMDA, AMPA, and kainate receptors) and metabotropic glutamate receptors, and glutamate uptake by glutamate transporters. When the glutamate system becomes dysfunctional, it contributes to the pathogenesis of neurodegenerative and neuropsychiatric diseases such as Alzheimer's disease, Parkinson's disease, depression, epilepsy, and ischemic stroke. In this review, based on regulating glutamate signaling, we summarize the effects and underlying mechanisms of natural constituents from Chinese herbal medicines on neurological disorders. Natural constituents from Chinese herbal medicine can prevent the glutamate-mediated excitotoxicity via suppressing presynaptic glutamate release, decreasing ionotropic and metabotropic glutamate receptors expression in the excitatory synapse, and promoting astroglial glutamate transporter expression to increase glutamate clearance from the synaptic cleft. However, some natural constituents from Chinese herbal medicine have the ability to restore the collapse of excitatory synapses by promoting presynaptic glutamate release and increasing ionotropic and metabotropic glutamate receptors expression. These regulatory processes involve various signaling pathways, which lead to different mechanistic routes of protection against neurological disorders. Hence, our review addresses the underlying mechanisms of natural constituents from Chinese herbal medicines that regulate glutamate systems and serve as promising agents for the treatment of the above-mentioned neurological disorders.

[Effect of atorvastatin on cardiac function and TGF-ß1 signaling pathway after acute myocardial infarction in rats].

OBJECTIVE: To investigate the effect of atorvastatin on cardiac remodeling and function after acute myocardial infarction (AMI) in rats and whether this effect is mediated by transforming growth factor-ß1 (TGF-ß1) signaling pathway. METHODS: AMI was induced by left coronary artery ligation in 64 male Sprague-Dawley rats, and 45 surviving rats were randomized into control group (n=15), low-dose atorvastatin group (10 mg/kg, n=15) and high-dose atorvastatin group (20 mg/kg, n=15). Similar surgical procedure was performed in sham-operated rats (n=15) without coronary ligation. Atorvastatin was given daily by gavage from the first day after AMI. Eight weeks later, the cardiac function, left ventricular weight/body mass index (LVMI), collagen volume fraction (CVF), and the expressions of TGF-ß1 and Smad2 were compared between the groups. RESULTS: AMI caused significantly reduced cardiac function, increased LVMI and CVF, and upregulated expressions of TGF-ß1 and Smad2 mRNA and proteins in the control group (P<0.05). The cardiac function, LVMI, and CVF were improved by atorvastatin, which also down-regulated the expressions of TGF-ß1 and Smad2 (P<0.05), and the effects were more prominent in high-dose atorvastatin group (P<0.05). CONCLUSION: Atorvastatin can dose-dependently improve cardiac remodeling and function after AMI in rats, which is mediated by regulating the activity of TGF-ß1/Smad2 signaling pathway.