Tea Consumption Enhances Endothelial-Dependent Vasodilation; a Meta-Analysis

Abstract

BackgroundTea consumption is associated with a lower risk of cardiovascular disease including stroke. Direct effects of tea components on the vasculature, particularly the endothelium, may partly explain this association.ObjectiveWe performed a meta-analysis of controlled human intervention studies on the effect of tea on flow-mediated dilation (FMD) of the brachial artery, a measurement of endothelial function, which is suggested to be associated with cardiovascular risk.MethodsHuman intervention studies were identified by systematic search of the databases Medline, Embase, Chemical Abstracts and Biosis through March 2009 and by hand-searching related articles. Studies were selected based on predefined criteria: intervention with tea as the sole experimental variable, placebo-controlled design, and no missing data on FMD outcome or its variability. A random effects model was used to calculate the pooled overall effect on FMD due to the intake of tea. The impact of various subject and treatment characteristics was investigated in the presence of heterogeneity.ResultsIn total, 9 studies from different research groups were included with 15 relevant study arms. The overall absolute increase in FMD of tea vs. placebo was 2.6% of the arterial diameter (95% CI: 1.8-3.3%; P-value <0.001) for a median daily dose of 500 mL of tea (2–3 cups). This is a relative increase of approximately 40% compared to the average FMD of 6.3% measured under placebo or baseline conditions. There was significant heterogeneity between studies (P-value <0.001) that might partly be explained by the cuff position either distal or proximal to the area of FMD measurement. No indication for publication bias was found.ConclusionModerate consumption of tea substantially enhances endothelial-dependent vasodilation. This may provide a mechanistic explanation for the reduced risk of cardiovascular events and stroke observed among tea drinkers.

Coffee, Tea, and Cocoa and Risk of Stroke

“…In a meta-analysis of 9 RCTs (2 on green tea, 6 on black tea, and 1 on both types of tea), involving 213 participants, the overall absolute increase in FMD of tea consumption (median daily dose of 500 mL tea, equivalent to 2-3 cups) versus placebo was 2.6% of the arterial diameter. 19 This is a relative improvement of ≈40% compared with the average FMD of 6.3% measured under placebo or baseline conditions. 19 Results from a meta-analysis of 14 short-term (≤3 months) RCTs showed that green tea consumption lowered total and LDL cholesterol concentrations but had no effect on high-density lipoprotein cholesterol.…”

Association of flavonoid-rich foods and flavonoids with risk of all-cause mortality

“…These associations remained after adjusting for dietary pattern, suggesting that the 191 oxidative stress and inflammation [29][30][31][32][33] . The strongest beneficial relation with all-cause mortality 195 was observed with the frequency of red wine consumption, which remained even after adjusting 196 for total alcohol consumption, which has been shown to be a strong predictor of all-cause 197 mortality 34 .…”

The Effect of Black Tea and Caffeine on Regional Cerebral Blood Flow Measured with Arterial Spin Labeling

“…Each treatment was delivered in six capsules that were consumed in a single sitting. The ingestion of 2,820 mg tea solids is based on the upper intake limit of tea studies looking at vascular effects 5 and was chosen to maximize our chance of seeing an effect of tea on the brain.…”

“…3 Flow mediated dilation of the brachial artery is a measure of endothelial function and several intervention studies have shown beneficial effects of tea and other flavonoid-rich foods therein. 4,5 Small doses of flavonoids, equivalent to one cup of tea, already exert a substantial increase in flow mediated dilation. 6 A proposed mechanism is that flavonoids improve the bioavailability of nitric oxide (NO), a key mediator of endotheliumdependent vasodilation, by stimulating activity of endothelial NO synthase or by preventing superoxide-mediated NO breakdown.…”